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Archive for the ‘Male Genetics’ Category

male pattern baldness and genetics? | Yahoo Answers

Please don't bother my friend!

I reckon that you are quiet young, so the thought of going bald scares you.

I had that too when I was in my early 20s, because baldness is a common thing too in my family.

I'm almost 40 now and YES I'm almost bald too LOL! But in reality going bald is a very slow process. Nobody (some rare cases excepted) is completely bald in their early 20s.

You see this is what I'm trying to say: -When you are 20 you don't wanna look like a bald old man (and that's not gonna happen I promise)

BUT: -When you are 40+ you don't wanna look like a 20 year old! (Although the media wants to make us believe that "young" is the way to be)

So when you reach the age of 40 you won't bother about a little or more baldness because all of of your male generation members have the same "problem" (which isn't a problem)

Since in prehistory man was hairy like an ape and now we are allmost hairless I think the ability of loosing hair is a step ahead in evolution! And I feel that being a little or more bald is very masculine!

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male pattern baldness and genetics? | Yahoo Answers

Male Y chromosomes not ‘genetic wastelands’ : NewsCenter

February 6, 2019

When researchers say they have sequenced the human genome, there is a caveat to this statement: a lot of the human genome is sequenced and assembled, but there are regions that are full of repetitive elements, making them difficult to map. One piece that is notoriously difficult to sequence is the Y chromosome.

Now, researchers from the University of Rochester have found a way to sequence a large portion of the Y chromosome in the fruit fly Drosophila melanogasterthe most that the Y chromosome has been assembled in fruit flies. The research, published in the journal GENETICS, provides new insights into the processes that shape the Y chromosome, and adds to the evidence that, far from a genetic wasteland, Y chromosomes are highly dynamic and have mechanisms to acquire and maintain genes, says Amanda Larracuente, an assistant professor of biology at Rochester.

Y chromosomes are sex chromosomes in males that are transmitted from father to son; they can be important for male fertility and sex determination in many species. Even though fruit fly and mammalian Y chromosomes have different evolutionary origins, they have parallel genome structures, says Larracuente, who co-authored the paper with her PhD student Ching-Ho Chang. Drosophila melanogaster is a premier model organism for genetics and genomics, and has perhaps the best genome assembly of any animal. Despite these resources, we know very little about the organization of the Drosophila Y chromosome because most of it is missing from the genome assembly.

Thats in part because most Y chromosomes do not undergo standard recombination. Typically, genes from the mother and father are shuffledor, cross overto produce a genetic combination unique to each offspring. But the Y chromosome does not undergo crossing over, and, as a result, its genes tend to degenerate, while repetitive DNA sequences accumulate.

Each chromosome is made up of DNA. When mapping a genome, traditional sequencing methods chop up strands of DNA and reador sequencethem, then try to infer the order of those sequences and assemble them back together.

But, there is a difference between sequencing a genome and assembling a genome, Larracuente says. There are so many repetitive strands on the Y chromosome that the pieces tend to look the same. It is difficult, therefore, to figure out where they come from and how to reassemble the strandslike trying to put together a puzzle when all of the pieces are exactly the same color. When we try to take those bits of DNA and assemble them to see what the chromosome looks like, we cant fill in some of those gaps. We might have the sequence, but we dont know where it goes.

Using sequence data generated by new technology that reads long strands of individual DNA molecules, Chang and Larracuente developed a strategy to assemble a large part of the Y chromosome and other repeat-dense regions. By assembling a large portion of the Y chromosome, they discovered that the Y chromosome has a lot of duplicated sequences, where genes are present in multiple copies. They also discovered that although the Y chromosome does not experience crossing over, it undergoes a different type of recombination called gene conversion. While crossing over involves the shuffle and exchange of genes between two different chromosomes, gene conversion is not reciprocal, Larracuente says. You dont have two chromosomes that exchange material, you have one chromosome that donates its sequence to the other part of the chromosome and the sequences become identical.

The Y chromosome has therefore found a way to maintain its genes via a process different from crossing over, Larracuente says. We usually think of the Y chromosome as a really harsh environment for a gene to survive in, yet these genes manage to get expressed and carry out their functions that are important for male fertility. This rampant gene conversion that were seeing is one way that we think genes might be able to survive on Y chromosomes.

Tags: Amanda Larracuente, Arts and Sciences, Department of Biology, genetics, research finding

Category: Science & Technology

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Male Y chromosomes not 'genetic wastelands' : NewsCenter

Male Pattern Baldness: Causes, Identification, and Prevention

Male pattern baldness, also called androgenic alopecia, is the most common type of hair loss in men. According to the U.S. National Library of Medicine (NLM), more than 50 percent of all men over the age of 50 will be affected by male pattern baldness to some extent.

One cause of male pattern baldness is genetics, or having a family history of baldness. Research has found that male pattern baldness is associated with male sex hormones called androgens. The androgens have many functions, including regulating hair growth.

Each hair on your head has a growth cycle. With male pattern baldness, this growth cycle begins to weaken and the hair follicle shrinks, producing shorter and finer strands of hair. Eventually, the growth cycle for each hair ends and no new hair grows in its place.

Inherited male pattern baldness usually has no side effects. However, sometimes baldness has more serious causes, such as certain cancers, medications, thyroid conditions, and anabolic steroids. See your doctor if hair loss occurs after taking new medications or when its accompanied by other health complaints.

Doctors use the pattern of hair loss to diagnose male pattern baldness. They may perform a medical history and exam to rule out certain health conditions as the cause, such as fungal conditions of the scalp or nutritional disorders.

Health conditions may be a cause of baldness when a rash, redness, pain, peeling of the scalp, hair breakage, patchy hair loss, or an unusual pattern of hair loss accompanies the hair loss. A skin biopsy and blood tests also may be necessary to diagnose disorders responsible for the hair loss.

Male pattern baldness can begin in your teenage years, but it more commonly occurs in adult men, with the likelihood increasing with age. Genetics plays a big role. Men who have close relatives with male pattern baldness are at a higher risk. This is particularly true when their relatives are on the maternal side of the family.

If your hair loss begins at the temples or the crown of the head, you may have male pattern baldness. Some men will get a single bald spot. Others experience their hairlines receding to form an M shape. In some men, the hairline will continue to recede until all or most of the hair is gone.

Medical treatment isnt necessary if other health conditions arent a cause. However, treatments are available for men who are unhappy with the way they look and would like the appearance of a fuller head of hair.

Men with limited hair loss can sometimes hide hair loss with the right haircut or hairstyle. Ask your hairstylist for a creative cut that will make thinning hair look fuller.

Wigs can cover thinning hair, receding hairlines, and complete baldness. They come in a variety of styles, colors, and textures. For a natural look, choose wig colors, styles, and textures that look similar to your original hair. Professional wig stylists can help style and fit wigs for an even more natural look.

Hair weaves are wigs that are sewn into your natural hair. You must have enough hair to sew the weave into. The advantage to weaves is they always stay on, even during activities such as swimming, showering, and sleeping. The disadvantages are they must be sewn again whenever new hair growth occurs, and the sewing process can damage your natural hair.

Minoxidil (Rogaine) is a topical medication applied to the scalp. Minoxidil slows hair loss for some men and stimulates the hair follicles to grow new hair. Minoxidil takes four months to one year to produce visible results. Hair loss often happens again when you stop taking the medication.

Possible side effects associated with minoxidil include dryness, irritation, burning, and scaling of the scalp. You should visit the doctor immediately if you have any of these serious side effects:

Finasteride (Propecia, Proscar) is an oral medication that slows hair loss in some men. It works by blocking the production of the male hormone responsible for hair loss. Finasteride has a higher success rate than minoxidil. When you stop taking finasteride, your hair loss returns.

You must take finasteride for three months to one year before you see results. If no hair growth occurs after one year, your doctor will likely recommend that you stop taking the medication. The side effects of finasteride include:

Although its rare, finasteride can cause breast cancer. You should have any breast pain or lumps evaluated by a doctor immediately.

Finasteride may affect prostate-specific antigen (PSA) tests used to screen for prostate cancer. The medication lowers PSA levels, which causes lower-than-normal readings. Any rise in PSA levels when taking finasteride should be evaluated for prostate cancer.

A hair transplant is the most invasive and expensive treatment for hair loss. Hair transplants work by removing hair from areas of the scalp that have active hair growth and transplanting them to thinning or balding areas of your scalp.

Multiple treatments are often necessary, and the procedure carries the risk of scarring and infection. The advantages of a hair transplant are that it looks more natural and its permanent.

Going bald can be a big change. You may have trouble accepting your appearance. You should seek counseling if you experience anxiety, low self-esteem, depression, or other emotional problems because of male pattern baldness.

Theres no known way to prevent male pattern baldness. A theory is that stress may cause hair loss by increasing the production levels of sex hormones in the body. You can reduce stress by participating in relaxing activities, such as walking, listening to calming music, and enjoying more quiet time.

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Male Pattern Baldness: Causes, Identification, and Prevention

Fertility Center & Applied Genetics of Florida

Fertility Center and Applied Genetics of Florida is a Fertility Center providing comprehensive fertility services (IVF, IUI, PGD, PGS, Family Balancing/Sex Selection, Reproductive Surgeries, egg donation, surrogacy) for Tampa Bay, Sarasota, Bradenton, Orlando, Ft. Myers, Naples, all Florida, U.S., and International patients. Dr. Pabon is a fertility doctor (Reproductive Endocrinologist and Infertility Specialist) specializing in IVF, Tubal Reversals, Preimplantation genetic diagnosis, egg donation, surrogacy, and general infertility with offices in Sarasota and Bonita Springs, Florida, U.S.A. We enjoy helping traditional couples, single men or women, and the LGBT community.

Dr. Pabon is a nationally recognized Reproductive Endocrinologist and Infertility Specialist that has received Top Doctor designation by U.S. News and World Report and by the Castle Connolly agency for 2013, 2014, 2015, 2016, 2017.

Medical Tourism IVF and Tubal Reversals at Fertility Center and Applied Genetics of Florida:

Tampa, Tampa Bay, Orlando, Sarasota, Bradenton, Ft. Myers, Naples, Florida, and many international patients from the United Kingdom, Spain, and Canada have discovered that we are a destination where the highest technology and current science come together in a uniquely personal and compassionate setting. Patients enjoy the care at one of the best IVF clinics while relaxing in Floridas West Coast. Miles and miles of white sandy beaches, fishing, golf, tennis, and sun sports are quite a draw for Medical treatment tourists.

Dr. Pabon is a nationally and internationally recognized physician, reproductive surgeon, author, lecturer, and a leader in the implementation of new technologies in his area of expertise. He is a graduate with honors of The Univ. of Texas at Austin, Baylor College of Medicine, The University of Louisville, and is a clinical assistant professor for Florida State University College of Medicine. He is the past president, current board member and secretary of the Florida Society of Reproductive Endocrinology and Infertility (FSREI).

Since our first IVF procedures in Sarasota in 1997, we have implemented new technologies such as office based IVF, ICSI, laser assisted hatching, egg donor IVF, surrogacy, Day 3 pre-implantation genetics, trophectoderm blastocyst day 5 & 6 biopsies for pre-implantation genetics, fluorescent in situ hybridization, complete genomic hybridization for 24 chromosome PGS/PGD, laser embryology, fast freeze vitrification, antagonist protocols, agonist triggers, all freeze IVF protocols, family balancing and vitrification. Dr. Pabon is also one of the most experienced tubal reversal surgeons in the world. He has perfected his technique for the outpatient procedure since 1992.

Our Mission Goals:

We are better because we genuinely care about each patient. We do not screen out challenging patients in order to pad our results. Patients are given realistic information about the limits of current technology. While we aim to please, patients must understand that not all clinics are a perfect fit for all patients and that there are some patients that dont succeed despite our best efforts. It is our privilege and honor to have our patients confidence to help build healthy families.

AWorld Class Center for excellence in Reproductive Technologies and Surgery Dr. Pabon is among the most experienced reproductive surgeons in the world. Moreover, our center is recognized as one of the most successful clinics in the United States with pregnancy rates consistently above the National average. Triplets and higher order pregnancies occur in less than 1% of our cases. Our first successful pregnancy after pre-implantation genetic diagnosis was achieved 1999-2000. We are proud to announce the first pregnancy in Florida (Oct 2009) using new PGD/PGS technology through the new microarray technology called gene security parental support and most recently in 2012 the progression of our pre-implantation genetic diagnosis program from the previous multicellular embryo biopsies (1999-2012) to laser assisted trophectoderm blastocyst biopsies and next generation sequencing of the genome of each embryo.

Dr. Pabon is one of the most experienced reproductive surgeons. He specializes in Outpatient Tubal Reversals with microsurgical techniques. Dr. Pabon is one of few surgeons who uses a microscope to perform these delicate surgeries in an outpatient setting. The surgical microscope technique gives the highest magnification possible for the highest accuracy in performing this surgery. He has been performing these surgeries with high success since 1992. He enjoys quite a following at TubalReversalSurgeon/Facebook.

Read What Patients Say About Their Experience:

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Fertility Center & Applied Genetics of Florida and the offices of Julio E. Pabon, M.D., P.A. (formerly Fertility Center of Sarasota) is an extremely uniqueprivate practice where patients receive personal care from one Reproductive Endocrinologist and Infertility Specialist. Our Medical and Laboratory Director, J. E. Pabon, M.D., F.A.C.O.G. takes the time to know his patients, their history and their specific needs. Dr. Pabon and the staff of FC & AG of FL are happy to serve Lee County and Collier County through our south office formerly in Naples (since 2004) and now through the new Bonita Springs office (since 2010)

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Fertility Center & Applied Genetics of Florida

Home – DNA Ancestry Project

After conducting the test, as expected, Mr. Brown verifies that all three have exactly the same Y-DNA STR marker profile. After speaking with his grand-uncle, he was able to trace distant relatives in Europe who share his surname. After contacting various members of his European line, he obtained 9 participants and the results of the test show the following:

Mr. Brown and his cousin share the same Y-DNA STR marker profile. He also shares the same Y-DNA STR marker profile as group 2 and group 5 of his European line. There is a single mutation in group 3 and group 4, indicating that although they are related, it is more distant, and that groups 3 and 4 are closely related to each other. Group 7, however is not related to this particular Brown family line.

After finding out this exciting information, his newfound European family lines were able to bring more extended family into the surname project, and within a few months, Mr. Brown was able to connect and piece together a large puzzle of his ancestry.

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Home - DNA Ancestry Project

genetics | History, Biology, Timeline, & Facts …

Genetics, study of heredity in general and of genes in particular. Genetics forms one of the central pillars of biology and overlaps with many other areas, such as agriculture, medicine, and biotechnology.

Since the dawn of civilization, humankind has recognized the influence of heredity and applied its principles to the improvement of cultivated crops and domestic animals. A Babylonian tablet more than 6,000 years old, for example, shows pedigrees of horses and indicates possible inherited characteristics. Other old carvings show cross-pollination of date palm trees. Most of the mechanisms of heredity, however, remained a mystery until the 19th century, when genetics as a systematic science began.

Genetics arose out of the identification of genes, the fundamental units responsible for heredity. Genetics may be defined as the study of genes at all levels, including the ways in which they act in the cell and the ways in which they are transmitted from parents to offspring. Modern genetics focuses on the chemical substance that genes are made of, called deoxyribonucleic acid, or DNA, and the ways in which it affects the chemical reactions that constitute the living processes within the cell. Gene action depends on interaction with the environment. Green plants, for example, have genes containing the information necessary to synthesize the photosynthetic pigment chlorophyll that gives them their green colour. Chlorophyll is synthesized in an environment containing light because the gene for chlorophyll is expressed only when it interacts with light. If a plant is placed in a dark environment, chlorophyll synthesis stops because the gene is no longer expressed.

Genetics as a scientific discipline stemmed from the work of Gregor Mendel in the middle of the 19th century. Mendel suspected that traits were inherited as discrete units, and, although he knew nothing of the physical or chemical nature of genes at the time, his units became the basis for the development of the present understanding of heredity. All present research in genetics can be traced back to Mendels discovery of the laws governing the inheritance of traits. The word genetics was introduced in 1905 by English biologist William Bateson, who was one of the discoverers of Mendels work and who became a champion of Mendels principles of inheritance.

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heredity

clear in the study of genetics. Both aspects of heredity can be explained by genes, the functional units of heritable material that are found within all living cells. Every member of a species has a set of genes specific to that species. It is this set of genes that provides

Although scientific evidence for patterns of genetic inheritance did not appear until Mendels work, history shows that humankind must have been interested in heredity long before the dawn of civilization. Curiosity must first have been based on human family resemblances, such as similarity in body structure, voice, gait, and gestures. Such notions were instrumental in the establishment of family and royal dynasties. Early nomadic tribes were interested in the qualities of the animals that they herded and domesticated and, undoubtedly, bred selectively. The first human settlements that practiced farming appear to have selected crop plants with favourable qualities. Ancient tomb paintings show racehorse breeding pedigrees containing clear depictions of the inheritance of several distinct physical traits in the horses. Despite this interest, the first recorded speculations on heredity did not exist until the time of the ancient Greeks; some aspects of their ideas are still considered relevant today.

Hippocrates (c. 460c. 375 bce), known as the father of medicine, believed in the inheritance of acquired characteristics, and, to account for this, he devised the hypothesis known as pangenesis. He postulated that all organs of the body of a parent gave off invisible seeds, which were like miniaturized building components and were transmitted during sexual intercourse, reassembling themselves in the mothers womb to form a baby.

Aristotle (384322 bce) emphasized the importance of blood in heredity. He thought that the blood supplied generative material for building all parts of the adult body, and he reasoned that blood was the basis for passing on this generative power to the next generation. In fact, he believed that the males semen was purified blood and that a womans menstrual blood was her equivalent of semen. These male and female contributions united in the womb to produce a baby. The blood contained some type of hereditary essences, but he believed that the baby would develop under the influence of these essences, rather than being built from the essences themselves.

Aristotles ideas about the role of blood in procreation were probably the origin of the still prevalent notion that somehow the blood is involved in heredity. Today people still speak of certain traits as being in the blood and of blood lines and blood ties. The Greek model of inheritance, in which a teeming multitude of substances was invoked, differed from that of the Mendelian model. Mendels idea was that distinct differences between individuals are determined by differences in single yet powerful hereditary factors. These single hereditary factors were identified as genes. Copies of genes are transmitted through sperm and egg and guide the development of the offspring. Genes are also responsible for reproducing the distinct features of both parents that are visible in their children.

In the two millennia between the lives of Aristotle and Mendel, few new ideas were recorded on the nature of heredity. In the 17th and 18th centuries the idea of preformation was introduced. Scientists using the newly developed microscopes imagined that they could see miniature replicas of human beings inside sperm heads. French biologist Jean-Baptiste Lamarck invoked the idea of the inheritance of acquired characters, not as an explanation for heredity but as a model for evolution. He lived at a time when the fixity of species was taken for granted, yet he maintained that this fixity was only found in a constant environment. He enunciated the law of use and disuse, which states that when certain organs become specially developed as a result of some environmental need, then that state of development is hereditary and can be passed on to progeny. He believed that in this way, over many generations, giraffes could arise from deerlike animals that had to keep stretching their necks to reach high leaves on trees.

British naturalist Alfred Russel Wallace originally postulated the theory of evolution by natural selection. However, Charles Darwins observations during his circumnavigation of the globe aboard the HMS Beagle (183136) provided evidence for natural selection and his suggestion that humans and animals shared a common ancestry. Many scientists at the time believed in a hereditary mechanism that was a version of the ancient Greek idea of pangenesis, and Darwins ideas did not appear to fit with the theory of heredity that sprang from the experiments of Mendel.

Before Gregor Mendel, theories for a hereditary mechanism were based largely on logic and speculation, not on experimentation. In his monastery garden, Mendel carried out a large number of cross-pollination experiments between variants of the garden pea, which he obtained as pure-breeding lines. He crossed peas with yellow seeds to those with green seeds and observed that the progeny seeds (the first generation, F1) were all yellow. When the F1 individuals were self-pollinated or crossed among themselves, their progeny (F2) showed a ratio of 3:1 (3/4 yellow and 1/4 green). He deduced that, since the F2 generation contained some green individuals, the determinants of greenness must have been present in the F1 generation, although they were not expressed because yellow is dominant over green. From the precise mathematical 3:1 ratio (of which he found several other examples), he deduced not only the existence of discrete hereditary units (genes) but also that the units were present in pairs in the pea plant and that the pairs separated during gamete formation. Hence, the two original lines of pea plants were proposed to be YY (yellow) and yy (green). The gametes from these were Y and y, thereby producing an F1 generation of Yy that were yellow in colour because of the dominance of Y. In the F1 generation, half the gametes were Y and the other half were y, making the F2 generation produced from random mating 1/4 Yy, 1/2 YY, and 1/4 yy, thus explaining the 3:1 ratio. The forms of the pea colour genes, Y and y, are called alleles.

Mendel also analyzed pure lines that differed in pairs of characters, such as seed colour (yellow versus green) and seed shape (round versus wrinkled). The cross of yellow round seeds with green wrinkled seeds resulted in an F1 generation that were all yellow and round, revealing the dominance of the yellow and round traits. However, the F2 generation produced by self-pollination of F1 plants showed a ratio of 9:3:3:1 (9/16 yellow round, 3/16 yellow wrinkled, 3/16 green round, and 1/16 green wrinkled; note that a 9:3:3:1 ratio is simply two 3:1 ratios combined). From this result and others like it, he deduced the independent assortment of separate gene pairs at gamete formation.

Mendels success can be attributed in part to his classic experimental approach. He chose his experimental organism well and performed many controlled experiments to collect data. From his results, he developed brilliant explanatory hypotheses and went on to test these hypotheses experimentally. Mendels methodology established a prototype for genetics that is still used today for gene discovery and understanding the genetic properties of inheritance.

Mendels genes were only hypothetical entities, factors that could be inferred to exist in order to explain his results. The 20th century saw tremendous strides in the development of the understanding of the nature of genes and how they function. Mendels publications lay unmentioned in the research literature until 1900, when the same conclusions were reached by several other investigators. Then there followed hundreds of papers showing Mendelian inheritance in a wide array of plants and animals, including humans. It seemed that Mendels ideas were of general validity. Many biologists noted that the inheritance of genes closely paralleled the inheritance of chromosomes during nuclear divisions, called meiosis, that occur in the cell divisions just prior to gamete formation.

It seemed that genes were parts of chromosomes. In 1910 this idea was strengthened through the demonstration of parallel inheritance of certain Drosophila (a type of fruit fly) genes on sex-determining chromosomes by American zoologist and geneticist Thomas Hunt Morgan. Morgan and one of his students, Alfred Henry Sturtevant, showed not only that certain genes seemed to be linked on the same chromosome but that the distance between genes on the same chromosome could be calculated by measuring the frequency at which new chromosomal combinations arose (these were proposed to be caused by chromosomal breakage and reunion, also known as crossing over). In 1916 another student of Morgans, Calvin Bridges, used fruit flies with an extra chromosome to prove beyond reasonable doubt that the only way to explain the abnormal inheritance of certain genes was if they were part of the extra chromosome. American geneticist Hermann Joseph Mller showed that new alleles (called mutations) could be produced at high frequencies by treating cells with X-rays, the first demonstration of an environmental mutagenic agent (mutations can also arise spontaneously). In 1931 American botanist Harriet Creighton and American scientist Barbara McClintock demonstrated that new allelic combinations of linked genes were correlated with physically exchanged chromosome parts.

In 1908 British physician Archibald Garrod proposed the important idea that the human disease alkaptonuria, and certain other hereditary diseases, were caused by inborn errors of metabolism, suggesting for the first time that linked genes had molecular action at the cell level. Molecular genetics did not begin in earnest until 1941 when American geneticist George Beadle and American biochemist Edward Tatum showed that the genes they were studying in the fungus Neurospora crassa acted by coding for catalytic proteins called enzymes. Subsequent studies in other organisms extended this idea to show that genes generally code for proteins. Soon afterward, American bacteriologist Oswald Avery, Canadian American geneticist Colin M. MacLeod, and American biologist Maclyn McCarty showed that bacterial genes are made of DNA, a finding that was later extended to all organisms.

A major landmark was attained in 1953 when American geneticist and biophysicist James D. Watson and British biophysicists Francis Crick and Maurice Wilkins devised a double helix model for DNA structure. This model showed that DNA was capable of self-replication by separating its complementary strands and using them as templates for the synthesis of new DNA molecules. Each of the intertwined strands of DNA was proposed to be a chain of chemical groups called nucleotides, of which there were known to be four types. Because proteins are strings of amino acids, it was proposed that a specific nucleotide sequence of DNA could contain a code for an amino acid sequence and hence protein structure. In 1955 American molecular biologist Seymour Benzer, extending earlier studies in Drosophila, showed that the mutant sites within a gene could be mapped in relation to each other. His linear map indicated that the gene itself is a linear structure.

In 1958 the strand-separation method for DNA replication (called the semiconservative method) was demonstrated experimentally for the first time by American molecular biologist Matthew Meselson and American geneticist Franklin W. Stahl. In 1961 Crick and South African biologist Sydney Brenner showed that the genetic code must be read in triplets of nucleotides, called codons. American geneticist Charles Yanofsky showed that the positions of mutant sites within a gene matched perfectly the positions of altered amino acids in the amino acid sequence of the corresponding protein. In 1966 the complete genetic code of all 64 possible triplet coding units (codons), and the specific amino acids they code for, was deduced by American biochemists Marshall Nirenberg and Har Gobind Khorana. Subsequent studies in many organisms showed that the double helical structure of DNA, the mode of its replication, and the genetic code are the same in virtually all organisms, including plants, animals, fungi, bacteria, and viruses. In 1961 French biologist Franois Jacob and French biochemist Jacques Monod established the prototypical model for gene regulation by showing that bacterial genes can be turned on (initiating transcription into RNA and protein synthesis) and off through the binding action of regulatory proteins to a region just upstream of the coding region of the gene.

Technical advances have played an important role in the advance of genetic understanding. In 1970 American microbiologists Daniel Nathans and Hamilton Othanel Smith discovered a specialized class of enzymes (called restriction enzymes) that cut DNA at specific nucleotide target sequences. That discovery allowed American biochemist Paul Berg in the early 1970s to make the first artificial recombinant DNA molecule by isolating DNA molecules from different sources, cutting them, and joining them together in a test tube. Shortly thereafter, American biochemists Herbert W. Boyer and Stanley N. Cohen came up with methods to produce recombinant plasmids (extragenomic circular DNA elements), which replicated naturally when inserted into bacterial cells. These advances allowed individual genes to be cloned (amplified to a high copy number) by splicing them into self-replicating DNA molecules, such as plasmids or viruses, and inserting these into living bacterial cells. From these methodologies arose the field of recombinant DNA technology that came to dominate molecular genetics. In 1977 two different methods were invented for determining the nucleotide sequence of DNA: one by American molecular biologists Allan Maxam and Walter Gilbert and the other by English biochemist Fred Sanger. Such technologies made it possible to examine the structure of genes directly by nucleotide sequencing, resulting in the confirmation of many of the inferences about genes originally made indirectly.

In the 1970s Canadian biochemist Michael Smith revolutionized the art of redesigning genes by devising a method for inducing specifically tailored mutations at defined sites within a gene, creating a technique known as site-directed mutagenesis. In 1983 American biochemist Kary B. Mullis invented the polymerase chain reaction, a method for rapidly detecting and amplifying a specific DNA sequence without cloning it. In the last decade of the 20th century, progress in recombinant DNA technology and in the development of automated sequencing machines led to the elucidation of complete DNA sequences of several viruses, bacteria, plants, and animals. In 2001 the complete sequence of human DNA, approximately three billion nucleotide pairs, was made public.

A time line of important milestones in the history of genetics is provided in the table.

Classical genetics, which remains the foundation for all other areas in genetics, is concerned primarily with the method by which genetic traitsclassified as dominant (always expressed), recessive (subordinate to a dominant trait), intermediate (partially expressed), or polygenic (due to multiple genes)are transmitted in plants and animals. These traits may be sex-linked (resulting from the action of a gene on the sex, or X, chromosome) or autosomal (resulting from the action of a gene on a chromosome other than a sex chromosome). Classical genetics began with Mendels study of inheritance in garden peas and continues with studies of inheritance in many different plants and animals. Today a prime reason for performing classical genetics is for gene discoverythe finding and assembling of a set of genes that affects a biological property of interest.

Cytogenetics, the microscopic study of chromosomes, blends the skills of cytologists, who study the structure and activities of cells, with those of geneticists, who study genes. Cytologists discovered chromosomes and the way in which they duplicate and separate during cell division at about the same time that geneticists began to understand the behaviour of genes at the cellular level. The close correlation between the two disciplines led to their combination.

Plant cytogenetics early became an important subdivision of cytogenetics because, as a general rule, plant chromosomes are larger than those of animals. Animal cytogenetics became important after the development of the so-called squash technique, in which entire cells are pressed flat on a piece of glass and observed through a microscope; the human chromosomes were numbered using this technique.

Today there are multiple ways to attach molecular labels to specific genes and chromosomes, as well as to specific RNAs and proteins, that make these molecules easily discernible from other components of cells, thereby greatly facilitating cytogenetics research.

Microorganisms were generally ignored by the early geneticists because they are small in size and were thought to lack variable traits and the sexual reproduction necessary for a mixing of genes from different organisms. After it was discovered that microorganisms have many different physical and physiological characteristics that are amenable to study, they became objects of great interest to geneticists because of their small size and the fact that they reproduce much more rapidly than larger organisms. Bacteria became important model organisms in genetic analysis, and many discoveries of general interest in genetics arose from their study. Bacterial genetics is the centre of cloning technology.

Viral genetics is another key part of microbial genetics. The genetics of viruses that attack bacteria were the first to be elucidated. Since then, studies and findings of viral genetics have been applied to viruses pathogenic on plants and animals, including humans. Viruses are also used as vectors (agents that carry and introduce modified genetic material into an organism) in DNA technology.

Molecular genetics is the study of the molecular structure of DNA, its cellular activities (including its replication), and its influence in determining the overall makeup of an organism. Molecular genetics relies heavily on genetic engineering (recombinant DNA technology), which can be used to modify organisms by adding foreign DNA, thereby forming transgenic organisms. Since the early 1980s, these techniques have been used extensively in basic biological research and are also fundamental to the biotechnology industry, which is devoted to the manufacture of agricultural and medical products. Transgenesis forms the basis of gene therapy, the attempt to cure genetic disease by addition of normally functioning genes from exogenous sources.

The development of the technology to sequence the DNA of whole genomes on a routine basis has given rise to the discipline of genomics, which dominates genetics research today. Genomics is the study of the structure, function, and evolutionary comparison of whole genomes. Genomics has made it possible to study gene function at a broader level, revealing sets of genes that interact to impinge on some biological property of interest to the researcher. Bioinformatics is the computer-based discipline that deals with the analysis of such large sets of biological information, especially as it applies to genomic information.

The study of genes in populations of animals, plants, and microbes provides information on past migrations, evolutionary relationships and extents of mixing among different varieties and species, and methods of adaptation to the environment. Statistical methods are used to analyze gene distributions and chromosomal variations in populations.

Population genetics is based on the mathematics of the frequencies of alleles and of genetic types in populations. For example, the Hardy-Weinberg formula, p2 + 2pq + q2 = 1, predicts the frequency of individuals with the respective homozygous dominant (AA), heterozygous (Aa), and homozygous recessive (aa) genotypes in a randomly mating population. Selection, mutation, and random changes can be incorporated into such mathematical models to explain and predict the course of evolutionary change at the population level. These methods can be used on alleles of known phenotypic effect, such as the recessive allele for albinism, or on DNA segments of any type of known or unknown function.

Human population geneticists have traced the origins and migration and invasion routes of modern humans, Homo sapiens. DNA comparisons between the present peoples on the planet have pointed to an African origin of Homo sapiens. Tracing specific forms of genes has allowed geneticists to deduce probable migration routes out of Africa to the areas colonized today. Similar studies show to what degree present populations have been mixed by recent patterns of travel.

Another aspect of genetics is the study of the influence of heredity on behaviour. Many aspects of animal behaviour are genetically determined and can therefore be treated as similar to other biological properties. This is the subject material of behaviour genetics, whose goal is to determine which genes control various aspects of behaviour in animals. Human behaviour is difficult to analyze because of the powerful effects of environmental factors, such as culture. Few cases of genetic determination of complex human behaviour are known. Genomics studies provide a useful way to explore the genetic factors involved in complex human traits such as behaviour.

Some geneticists specialize in the hereditary processes of human genetics. Most of the emphasis is on understanding and treating genetic disease and genetically influenced ill health, areas collectively known as medical genetics. One broad area of activity is laboratory research dealing with the mechanisms of human gene function and malfunction and investigating pharmaceutical and other types of treatments. Since there is a high degree of evolutionary conservation between organisms, research on model organismssuch as bacteria, fungi, and fruit flies (Drosophila)which are easier to study, often provides important insights into human gene function.

Many single-gene diseases, caused by mutant alleles of a single gene, have been discovered. Two well-characterized single-gene diseases include phenylketonuria (PKU) and Tay-Sachs disease. Other diseases, such as heart disease, schizophrenia, and depression, are thought to have more complex heredity components that involve a number of different genes. These diseases are the focus of a great deal of research that is being carried out today.

Another broad area of activity is clinical genetics, which centres on advising parents of the likelihood of their children being affected by genetic disease caused by mutant genes and abnormal chromosome structure and number. Such genetic counseling is based on examining individual and family medical records and on diagnostic procedures that can detect unexpressed, abnormal forms of genes. Counseling is carried out by physicians with a particular interest in this area or by specially trained nonphysicians.

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Icelanders – Wikipedia

This article is about Icelanders as an ethnic group. For information about residents or nationals of Iceland, see Demographics of Iceland.IcelandersslendingarTotal population383,500[1]465,000Regions with significant populationsIceland 295,672[2]Canada94,205[3]United States42,716[4]Denmark8,429[5]Norway8,274[5]Sweden5,454[5]United Kingdom2,225[5]Germany1,802[5]Spain1,122[5]Australia980[6]Brazil576[5]Poland492[5]Other countries combinedc.3,000[5]LanguagesIcelandicReligionLutheranism (mainly the Church of Iceland);[7] Neo-pagan; Roman Catholic and Eastern Orthodox minorities among other faiths; secular. Historically Norse paganism, Celtic Christianity (c. 1000) and Catholicism (c. 1000 1551). See Religion in IcelandRelated ethnic groupsOther Germanic peoples, especially Norwegians, Danes, Faroese Islanders

Icelanders (Icelandic: slendingar) are a North Germanic ethnic group and nation who are native to the island nation of Iceland and speak Icelandic.[8]

Icelanders established the country of Iceland in 930 A.D. when the Althingi (Parliament) met for the first time. Iceland came under the reign of Norwegian, Swedish and Danish kings but regained full sovereignty and independence from the Danish monarchy on 1 December 1918, when the Kingdom of Iceland was established. On 17 June 1944, the monarchy was abolished and the Icelandic republic was founded. The language spoken is Icelandic, a North Germanic language, and Lutheranism is the predominant religion. Historical and DNA records indicate that around 60 to 80 percent of the male settlers were of Norse origin (primarily from Western Norway) and a similar percentage of the women were of Gaelic stock from Ireland and peripheral Scotland.[9][10]

Icelanders have had a tumultuous history. Development of the island was slow due to a lack of interest from the countries controlling it for most of its history: Norway, DenmarkNorway, and ultimately Denmark. Through this time, Iceland had relatively little contact with the outside world.[11] The island became independent in personal union with the Kingdom of Denmark in 1918. Since 1944, Iceland has been a republic, and Icelandic society has undergone a rapid modernisation process in the post-independence era.

Iceland is a geologically young land mass, having formed an estimated 20 million years ago due to volcanic eruptions on the Mid-Atlantic ridge. One of the last larger islands to remain uninhabited, the first human settlement date is generally accepted to be 874 AD, although there is some evidence to suggest human activity prior to the Norse arrival.[12]

The first Viking to sight Iceland was Gardar Svavarsson, who went off course due to harsh conditions when sailing from Norway to the Faroe Islands. His reports led to the first efforts to settle the island. Flki Vilgerarson (b. 9th century) was the first Norseman to sail to Iceland intentionally. His story is documented in the Landnmabk manuscript, and he is said to have named the island sland (Iceland). The first permanent settler in Iceland is usually considered to have been a Norwegian chieftain named Inglfur Arnarson. He settled with his family in around 874, at a place he named "Bay of Smokes", or Reykjavk in Icelandic.[13]

Following Inglfur, and also in 874, another group of Norwegians set sail across the North Atlantic Ocean with their families, livestock, slaves, and possessions, escaping the domination of the first King of Norway, Harald Fairhair. They traveled 1,000km (600mi) in their Viking longships to the island of Iceland. These people were primarily of Norwegian, Irish or Gaelic Scottish origin. The Irish and the Scottish Gaels were either slaves or servants of the Norse chiefs, according to the Icelandic sagas, or descendants of a "group of Norsemen who had settled in Scotland and Ireland and intermarried with Gaelic-speaking people".[14] Genetic evidence suggests that approximately 62% of the Icelandic maternal gene pool is derived from Ireland and Scotland, which is much higher than other Scandinavian countries, although comparable to the Faroese, while 37% is of Nordic origin.[15] About 20-25% of the Icelandic paternal gene pool is of Gaelic origin, with the rest being Nordic.[16]

The Icelandic Age of Settlement (Icelandic: Landnmsld) is considered to have lasted from 874 to 930, at which point most of the island had been claimed and the Alingi (English: Althing), the assembly of the Icelandic Commonwealth, was founded at ingvellir.[17]

In 930, on the ingvellir (English: Thingvellir) plain near Reykjavk, the chieftains and their families met and established the Alingi, Iceland's first national assembly. However, the Alingi lacked the power to enforce the laws it made. In 1262, struggles between rival chieftains left Iceland so divided that King Haakon IV of Norway was asked to step in as a final arbitrator for all disputes, as part of the Old Covenant. This is known as the Age of the Sturlungs.[18]

Iceland was under Norwegian leadership until 1380, when the Royal House of Norway died out. At this point, both Iceland and Norway came under the control of the Danish Crown. With the introduction of absolute monarchy in Denmark, the Icelanders relinquished their autonomy to the crown, including the right to initiate and consent to legislation. This meant a loss of independence for Iceland, which led to nearly 300 years of decline: perhaps largely because Denmark and its Crown did not consider Iceland to be a colony to be supported and assisted. In particular, the lack of help in defense led to constant raids by marauding pirates along the Icelandic coasts.[11]

Unlike Norway, Denmark did not need Iceland's fish and homespun wool. This created a dramatic deficit in Iceland's trade, and no new ships were built as a result. In 1602 Iceland was forbidden to trade with other countries by order of the Danish Government, and in the 18th century climatic conditions had reached an all-time low since Settlement.[11]

In 178384 Laki, a volcanic fissure in the south of the island, erupted. The eruption produced about 15km (3.6mi) of basalt lava, and the total volume of tephra emitted was 0.91km.[19] The aerosols that built up caused a cooling effect in the Northern Hemisphere. The consequences for Iceland were catastrophic, with approximately 25-33% of the population dying in the famine of 1783 and 1784. Around 80% of sheep, 50% of cattle, and 50% of horses died of fluorosis from the 8 million tons of fluorine that were released.[20] This disaster is known as the Mist Hardship (Icelandic: Muharindin).

In 179899 the Alingi was discontinued for several decades, eventually being restored in 1844. It was moved to Reykjavk, the capital, after being held at ingvellir for over nine centuries.

The 19th century brought significant improvement in the Icelanders' situation. A protest movement was led by Jn Sigursson, a statesman, historian, and authority on Icelandic literature. Inspired by the romantic and nationalist currents from mainland Europe, Jn protested strongly, through political journals and self-publications, for 'a return to national consciousness' and for political and social changes to be made to help speed up Iceland's development.[21]

In 1854, the Danish government relaxed the trade ban that had been imposed in 1602, and Iceland gradually began to rejoin Western Europe economically and socially. With this return of contact with other peoples came a reawakening of Iceland's arts, especially its literature. Twenty years later in 1874, Iceland was granted a constitution. Icelanders today recognize Jn's efforts as largely responsible for their economic and social resurgence.[21]

Iceland gained full sovereignty and independence from Denmark in 1918 after World War I. It became the Kingdom of Iceland. The King of Denmark also served as the King of Iceland but Iceland retained only formal ties with the Danish Crown. On 17 June 1944 the monarchy was abolished and a republic was established on what would have been Jn Sigursson's 133rd birthday. This ended nearly six centuries of ties with Denmark.[21]

Due to their small founding population and history of relative isolation, Icelanders have often been considered highly genetically homogeneous as compared to other European populations. For this reason, along with the extensive genealogical records for much of the population that reach back to the settlement of Iceland, Icelanders have been the focus of considerable genomics research by both biotechnology companies and academic and medical researchers.[22][23] It was, for example, possible for researchers to reconstruct much of the maternal genome of Iceland's first known black inhabitant, Hans Jonatan, from the DNA of his present-day descendants partly because the distinctively African parts of his genome were unique in Iceland until very recent times.[24]

Genetic evidence shows that most DNA lineages found among Icelanders today can be traced to the settlement of Iceland, indicating that there has been relatively little immigration since. This evidence shows that the founder population of Iceland came from Ireland, Scotland, and Scandinavia: studies of mitochondrial DNA and Y-chromosomes indicate that 62% of Icelanders' matrilineal ancestry derives from Scotland and Ireland (with most of the rest being from Scandinavia), while 75% of their patrilineal ancestry derives from Scandinavia (with most of the rest being from the Irish and British Isles).[25] Despite Iceland's historical isolation, the genetic makeup of Icelanders today is still quite different from the founding population, due to founder effects and genetic drift.[26] One study found that the mean Norse ancestry among Iceland's settlers was 56%, whereas in the current population the figure was 70%.[27]

Other studies have identified other ancestries, however. One study of mitochondrial DNA, blood groups, and isozymes revealed a more variable population than expected, comparable to the diversity of some other Europeans.[28] Another study showed that a tiny proportion of samples of contemporary Icelanders carry a more distant lineage, which belongs to the haplogroup C1e, which can possibly be traced to the settlement of the Americas around 14,000 years ago. This hints a small proportion of Icelanders have some Native American ancestry arising from Norse colonization of Greenland and North America.[29]

The first Europeans to emigrate to and settle in Greenland were Icelanders who did so under the leadership of Erik the Red in the late 10th century CE and numbered around 500 people. Isolated fjords in this harsh land offered sufficient grazing to support cattle and sheep, though the climate was too cold for cereal crops. Royal trade ships from Norway occasionally went to Greenland to trade for walrus tusks and falcons. The population eventually reached a high point of perhaps 3,000 in two communities and developed independent institutions before fading away during the 15th century.[30] A papal legation was sent there as late as 1492, the year Columbus attempted to find a shorter spice route to Asia but instead encountered the Americas.

According to the Saga of Eric the Red, Icelandic immigration to North America dates back to Vinland circa 1006. The colony was believed to be short-lived and abandoned by the 1020s. [31] European settlement of the region was not archeologically and historically confirmed as more than legend until the 1960s. The former Norse site, now known as L'Anse aux Meadows, pre-dated the arrival of Colombus in the Americas by almost 500 years.

A more recent instance of Icelandic emigration to North America occurred in 1855, when a small group settled in Spanish Fork, Utah.[32] Another Icelandic colony formed in Washington Island, Wisconsin.[33] Immigration to the United States and Canada began in earnest in the 1870s, with most migrants initially settling in the Great Lakes area. These settlers were fleeing famine and overcrowding on Iceland.[34] Today, there are sizable communities of Icelandic descent in both the United States and Canada. Gimli, in Manitoba, Canada, is home to the largest population of Icelanders outside of the main island of Iceland.[35]

From the mid-1990s, Iceland experienced rising immigration. By 2017 the population of first-generation immigrants (defined as people born abroad with both parents foreign-born and all grandparents foreign-born) stood at 35,997 (10.6% of residents), and the population of second-generation immigrants at 4,473. Correspondingly, the numbers of foreign-born people acquiring Icelandic citizenship are markedly higher than in the 1990s, standing at 703 in 2016.[36][37] Correspondingly, Icelandic identity is gradually shifting towards a more multicultural form.[38]

Icelandic, a North Germanic language, is the official language of Iceland (de facto; the laws are silent about the issue). Icelandic has inflectional grammar comparable to Latin, Ancient Greek, more closely to Old English and practically identical to Old Norse.

Old Icelandic literature can be divided into several categories. Three are best known to foreigners: Eddic poetry, skaldic poetry, and saga literature, if saga literature is understood broadly. Eddic poetry is made up of heroic and mythological poems. Poetry that praises someone is considered skaldic poetry or court poetry. Finally, saga literature is prose, ranging from pure fiction to fairly factual history.[39]

Written Icelandic has changed little since the 13th century. Because of this modern readers can understand the Icelanders' sagas. The sagas tell of events in Iceland in the 10th and early 11th centuries. They are considered to be the best-known pieces of Icelandic literature.[40]

The elder or Poetic Edda, the younger or Prose Edda, and the sagas are the major pieces of Icelandic literature. The Poetic Edda is a collection of poems and stories from the late 10th century, whereas the younger or Prose Edda is a manual of poetry that contains many stories of Norse mythology.

Iceland embraced Christianity in c. AD 1000, in what is called the kristnitaka, and the country, while mostly secular in observance, is still predominantly Christian culturally. The Lutheran church claims some 84% of the total population.[41] While early Icelandic Christianity was more lax in its observances than traditional Catholicism, Pietism, a religious movement imported from Denmark in the 18th century, had a marked effect on the island. By discouraging all but religious leisure activities, it fostered a certain dourness, which was for a long time considered an Icelandic stereotype. At the same time, it also led to a boom in printing, and Iceland today is one of the most literate societies in the world.[21][42]

While Catholicism was supplanted by Protestantism during the Reformation, most other world religions are now represented on the island: there are small Protestant Free Churches and Catholic communities, and even a nascent Muslim community, composed of both immigrants and local converts. Perhaps unique to Iceland is the fast-growing satrarflag, a legally recognized revival of the pre-Christian Nordic religion of the original settlers. According to the Roman Catholic Diocese of Reykjavk, there were only approximately 30 Jews in Iceland as of 2001.[43] The former First Lady of Iceland Dorrit Moussaieff was an Israeli-born Bukharian Jew.

Icelandic cuisine consists mainly of fish, lamb, and dairy. Fish was once the main part of an Icelander's diet but has recently given way to meats such as beef, pork, and poultry.[20]

Iceland has many traditional foods called orramatur. These foods include smoked and salted lamb, singed sheep heads, dried fish, smoked and pickled salmon, and cured shark. Andrew Zimmern, a chef who has traveled the world on his show Bizarre Foods with Andrew Zimmern, responded to the question "What's the most disgusting thing you've ever eaten?" with the response "That would have to be the fermented shark fin I had in Iceland." Fermented shark fin is a form of orramatur.[44]

The earliest indigenous Icelandic music was the rmur, epic tales from the Viking era that were often performed a cappella. Christianity played a major role in the development of Icelandic music, with many hymns being written in the local idiom. Hallgrmur Ptursson, a poet and priest, is noted for writing many of these hymns in the 17th century. The island's relative isolation ensured that the music maintained its regional flavor. It was only in the 19th century that the first pipe organs, prevalent in European religious music, first appeared on the island.[45]

Many singers, groups, and forms of music have come from Iceland. Most Icelandic music contains vibrant folk and pop traditions. Some more recent groups and singers are Voces Thules, The Sugarcubes, Bjrk, Sigur Rs, and Of Monsters and Men.

The national anthem is " Gu vors lands" (English: "Our Country's God"), written by Matthas Jochumsson, with music by Sveinbjrn Sveinbjrnsson. The song was written in 1874, when Iceland celebrated its one thousandth anniversary of settlement on the island. It was originally published with the title A Hymn in Commemoration of Iceland's Thousand Years.[45]

Iceland's men's national football team participated in their first FIFA World Cup in 2018, after reaching the quarter finals of its first major international tournament, UEFA Euro 2016. The women's national football team has yet to reach a World Cup; its best result at a major international event was a quarterfinal finish in UEFA Women's Euro 2013. The country's first Olympic participation was in the 1912 Summer Olympics; however, they did not participate again until the 1936 Summer Olympics. Their first appearance at the Winter Games was at the 1948 Winter Olympics. In 1956, Vilhjlmur Einarsson won the Olympic silver medal for the triple jump.[46] The Icelandic national handball team has enjoyed relative success. The team received a silver medal at the 2008 Olympic Games and a 3rd place at the 2010 European Men's Handball Championship.

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Icelanders - Wikipedia

GNN – Genetics and Genomics Timeline

1910

Thomas Hunt Morgan (1866-1945) establishes the chromosomal theory of heredity

Thomas Hunt Morgan, an embryologist who had turned to research in heredity, in 1907 began to extensively breed the common fruit fly, Drosophila melanogaster. He hoped to discover large-scale mutations that would represent the emergence of new species. As it turned out, Morgan confirmed Mendelian laws of inheritance and the hypothesis that genes are located on chromosomes. He thereby inaugurated classical experimental genetics.

These results were suggestive for hypotheses of which Morgan himself was skeptical. He was at the time critical of the Mendelian theory of inheritance, mistrusted aspects of chromosomal theory, and did not believe that Darwin's concept of natural selection could account for the emergence of new species. But Morgan's discoveries with white- and red-eyed flies led him to reconsider each of these hypotheses.

In particular, Morgan began to entertain the possibility that association of eye color and sex in fruit flies had a physical and mechanistic basis in the chromosomes. The shape of one of Drosophila's four chromosome pairs was thought to be distinctive for sex determination. Males invariably possess the XY chromosome pair (Morgan used a more cumbersome notation) while flies with the XX chromosome are female. If the factor for eye color was located exclusively on the X chromosome, Morgan realized, Mendelian rules for inheritance of dominant and recessive traits could apply.

In brief, Morgan had discovered that eye color in Drosophila expressed a sex-linked trait. All first-generation offspring of a mutant white-eyed male and a normal red-eyed female would have red eyes because every chromosome pair would contain at least one copy of the X chromosome with the dominant trait. But half the females from this union would now possess a copy of the white-eyed male's recessive X chromosome. This chromosome would be transmitted, on average, to one-half of second-generation offspringone-half of which would be male. Thus, second-generation offspring would include one-quarter with white eyesand all of these would be male.

Intensive work led Morgan to discover more mutant traitssome two dozen between 1911 and 1914. With evidence drawn from cytology he was able to refine Mendelian laws and combine them with the theoryfirst suggested by Theodor Boveri and Walter Suttonthat the chromosomes carry hereditary information. In 1915, Morgan and his colleagues published The Mechanism of Mendelian Heredity. Its major tenets:

Discrete pairs of factors located on chromosomes like beads on a string bear hereditary information. These factorsMorgan would soon call them genessegregate in germ cells and combine during reproduction, essentially as predicted by Mendelian laws. However:

Certain characteristics are sex-linkedthat is, occur together because they arise on the same chromosome that determines gender. More generally:

Other characteristics are also sometimes associated because, as paired chromosomes separate during germ cell development, genes proximate to one another tend to remain together. But sometimes, as a mechanistic consequence of reproduction, this linkage between genes is broken, allowing for new combinations of traits.

Morgan's experimental and theoretical work inaugurated research in genetics and promoted a revolution in biology. Evidence he adduced from embryology and cell theory pointed the way toward a synthesis of genetics with evolutionary theory. Morgan himself explored aspects of these developments in later work, including Evolution and Genetics published in 1925, and The Theory of the Gene in 1926. He received the Nobel Prize in Physiology or Medicine in 1933.

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GNN - Genetics and Genomics Timeline

Neolithic Male Genetic Diversity Plummeted Heres Why …

Starting about 7,000 years ago, something weird seems to have happened to men: Over the next two millennia, recent studies suggest, their genetic diversity - specifically, the diversity of their Y chromosomes - collapsed. So extreme was that collapse that it was as if there was only one man left to mate for every 17 women.

Anthropologists and biologists were perplexed, but Stanford researchers now believe they've found a simple - if revealing - explanation. The collapse, they argue, was the result of generations of war between patrilineal clans, whose membership is determined by male ancestors.

The outlines of that idea came to Tian Chen Zeng, a Stanford undergraduate in sociology, after spending hours reading blog posts that speculated - unconvincingly, Zeng thought - on the origins of the "Neolithic Y-chromosome bottleneck," as the event is known. He soon shared his ideas with his high school classmate Alan Aw, also a Stanford undergraduate in mathematical and computational science.

"He was really waxing lyrical about it," Aw said, so the pair took their idea to Marcus Feldman, a professor of biology in Stanford's School of Humanities and Sciences. Zeng, Aw and Feldman published their results May 25 in Nature Communications .

"Woman Triumphant" by Rudolf Cronau. (1919). ( Public Domain )

It's not unprecedented for human genetic diversity to take a nosedive once in a while, but the Y-chromosome bottleneck, which was inferred from genetic patterns in modern humans, was an odd one. First, it was observed only in men - more precisely, it was detected only through genes on the Y chromosome, which fathers pass to their sons. Second, the bottleneck is much more recent than other biologically similar events, hinting that its origins might have something to do with changing social structures.

Certainly, the researchers point out, social structures were changing. After the onset of farming and herding around 12,000 years ago, societies grew increasingly organized around extended kinship groups, many of them patrilineal clans - a cultural fact with potentially significant biological consequences. The key is how clan members are related to each other. While women may have married into a clan, men in such clans are all related through male ancestors and therefore tend to have the same Y chromosomes. From the point of view of those chromosomes at least, it's almost as if everyone in a clan has the same father.

That only applies within one clan, however, and there could still be considerable variation between clans. To explain why even between-clan variation might have declined during the bottleneck, the researchers hypothesized that wars, if they repeatedly wiped out entire clans over time, would also wipe out a good many male lineages and their unique Y chromosomes in the process.

Cave art in Magura cave from between 10000-8000 years ago. ( Public Domain )

To test their ideas, the researchers turned to mathematical models and computer simulations in which men fought - and died - for the resources their clans needed to survive. As the team expected, wars between patrilineal clans drastically reduced Y chromosome diversity over time, while conflict between non-patrilineal clans - groups where both men and women could move between clans - did not.

Zeng, Aw and Feldman's model also accounted for the observation that among the male lineages that survived the Y-chromosome bottleneck, a few lineages underwent dramatic expansions, consistent with the patrilineal clan model, but not others.

Now the researchers are looking at applying the framework in other areas - anywhere "historical and geographical patterns of cultural interactions could explain the patterns you see in genetics," said Feldman, who is also the Burnet C. and Mildred Finley Wohlford Professor.

Feldman said the work was an unusual example of undergraduates driving research that was broad both in terms of the academic disciplines spanned - in this case, sociology, mathematics and biology - and in terms of its potential implications for understanding the role of culture in shaping human evolution. And, he said, "Working with these talented guys is a lot of fun."

Top image: Prehistoric Man Hunting Bears by Emmanuel Benner the Younger. Source: Public Domain

The article, originally titled Wars and clan structure may explain a strange biological event 7,000 years ago, was first published on Science Daily.

Stanford University. "Wars and clan structure may explain a strange biological event 7,000 years ago." ScienceDaily. ScienceDaily, 29 May 2018. http://www.sciencedaily.com/releases/2018/05/180529185356.htm

Tian Chen Zeng, Alan J. Aw, Marcus W. Feldman. Cultural hitchhiking and competition between patrilineal kin groups explain the post-Neolithic Y-chromosome bottleneck . Nature Communications , 2018; 9 (1) DOI: 10.1038/s41467-018-04375-6

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Neolithic Male Genetic Diversity Plummeted Heres Why ...

Learn About Men’s Health Issues and Genetics – Men’s …

The genetic causes of mens health issues cut both ways. On the one hand, it can make you resigned to the fact that youre going to have this or that problem. On the other hand, you can just blame it on your genes!

Having a certain type of genes doesnt mean that you will definitely develop the related disease or health issue. Very few genetic markers are like that. Most inherited genes only increase the risk of you getting the health problem. Lets look more closely at the known and suspected genetic causes of mens health issues.

The most common talking points about baldness are far from proven. They are only educated guesses with certain promising correlations shown in studies, though far from conclusive. These include hair follicles health, blood circulation in the head, eating too much greasy food, etc.

In comparison, male pattern baldness is definitively linked to genetics. You are more likely to go bald if your father is bald. This is also true concerning your grandfather and uncles on your mothers side of the family. A study using over 52,000 genetic data from the UK Biobank found that among the men in the top 10% highest risk pool, 58% of them had moderate to severe hair loss. There are many more such studies.

We are happy to report that research into the genetics of erectile dysfunction is in its infancy. This is probably because most types of ED are unlikely to be caused by genes.

There is a small chance that infertility has a genetic root, and thats only if the infertility is caused by Klinefelters syndrome, Y chromosome deletions, and cystic fibrosis gene mutation.

As for prostate cancer, about 5-10% of prostate cancers are genetic, according to the Memorial Sloan Kettering Cancer Center. However, your chances of getting prostate cancer can increase 5 times if two or more of your close male relatives have it.

And thats about it. Apart from baldness, how you live your life is often more influential than the genetic causes of mens health issues.

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Learn About Men's Health Issues and Genetics - Men's ...

Genetics of Kidney Cancer (Renal Cell Cancer) (PDQ …

More than 55% of VHL-affected individuals develop only multiple renal cell cysts. The VHL-associated RCCs that occur are characteristically multifocal and bilateral and present as a combined cystic and solid mass.[66] Among individuals with VHL, the cumulative RCC risk has been reported as 24% to 45% overall. RCCs smaller than 3 cm in this disease tend to be low grade (Fuhrman nuclear grade 2) and minimally invasive,[67] and their rate of growth varies widely.[68] An investigation of 228 renal lesions in 28 patients who were followed up for at least 1 year showed that transition from a simple cyst to a solid lesion was infrequent.[66] Complex cystic and solid lesions contained neoplastic tissue that uniformly enlarged. These data may be used to help predict the progression of renal lesions in VHL. Figure 1 depicts bilateral renal tumors in a patient with VHL.

Enlarge Figure 1. von Hippel-Lindau diseaseassociated renal cell cancers are characteristically multifocal and bilateral and present as a combined cystic and solid mass. Red arrow indicates a lesion with a solid and cystic component, and white arrow indicates a predominantly solid lesion.

Tumors larger than 3 cm may increase in grade as they grow, and metastasis may occur.[68,69] RCCs often remain asymptomatic for long intervals.

Patients can also develop pancreatic cysts, cystadenomas, and pancreatic NETs.[2] Pancreatic cysts and cystadenomas are not malignant, but pancreatic NETs possess malignant characteristics and are typically resected if they are 3 cm or larger (2 cm if located in the head of the pancreas).[70] A review of the natural history of pancreatic NETs shows that these tumors may demonstrate nonlinear growth characteristics.[71]

Retinal manifestations, first reported more than a century ago, were one of the first recognized aspects of VHL. Retinal hemangioblastomas (also known as capillary retinal angiomas) are one of the most frequent manifestations of VHL and are present in more than 50% of patients.[72] Retinal involvement is one of the earliest manifestations of VHL, with a mean age at onset of 25 years.[1,2] These tumors are the first manifestation of VHL in nearly 80% of affected individuals and may occur in children as young as 1 year.[2,73,74]

Retinal hemangioblastomas occur most frequently in the periphery of the retina but can occur in other locations such as the optic nerve, a location much more difficult to treat. Retinal hemangioblastomas appear as a bright orange spherical tumor supplied by a tortuous vascular supply. Nearly 50% of patients have bilateral retinal hemangioblastomas.[72] The median number of lesions per affected eye is approximately six.[75] Other retinal lesions in VHL can include retinal vascular hamartomas, flat vascular tumors located in the superficial aspect of the retina.[76]

Longitudinal studies are important for the understanding of the natural history of these tumors. Left untreated, retinal hemangioblastomas can be a major source of morbidity in VHL, with approximately 8% of patients [72] having blindness caused by various mechanisms, including secondary maculopathy, contributing to retinal detachment, or possibly directly causing retinal neurodegeneration.[77] Patients with symptomatic lesions generally have larger and more numerous retinal hemangioblastomas. Long-term follow-up studies demonstrate that most lesions grow slowly and that new lesions do not develop frequently.[75,78]

Hemangioblastomas are the most common disease manifestation in patients with VHL, affecting more than 70% of individuals. A prospective study assessed the natural history of hemangioblastomas.[79] The mean age at onset of CNS hemangioblastomas is 29.1 years (range, 773 y).[80] After a mean follow-up of 7 years, 72% of the 225 patients studied developed new lesions.[81] Fifty-one percent of existing hemangioblastomas remained stable. The remaining lesions exhibited heterogeneous growth rates, with cerebellar and brainstem lesions growing faster than those in the spinal cord or cauda equina. Approximately 12% of hemangioblastomas developed either peritumoral or intratumoral cysts, and 6.4% were symptomatic and required treatment. Increased tumor burden or total tumor number detected was associated with male sex, longer follow-up, and genotype (all P

Enlarge Figure 2. Hemangioblastomas are the most common disease manifestation in patients with von Hippel-Lindau disease. The left panel shows a sagittal view of brainstem and cerebellar lesions. The middle panel shows an axial view of a brainstem lesion. The right panel shows a cerebellar lesion (red arrow) with a dominant cystic component (white arrow).

Enlarge Figure 3. Hemangioblastomas are the most common disease manifestation in patients with von Hippel-Lindau disease. Multiple spinal cord hemangioblastomas are shown.

The rate of pheochromocytoma formation in the VHL patient population is 25% to 30%.[82,83] Of patients with VHL-associated pheochromocytomas, 44% developed disease in both adrenal glands.[84] The rate of malignant transformation is very low. Levels of plasma and urine normetanephrine are typically elevated in patients with VHL,[85] and approximately two-thirds will experience physical manifestations such as hypertension, tachycardia, and palpitations.[82] Patients with a partial loss of VHL function (Type 2 disease) are at higher risk of pheochromocytoma than are VHL patients with a complete loss of VHL function (Type 1 disease); the latter develop pheochromocytoma very rarely.[13,14,82,86] The rate of VHL germline pathogenic variants in nonsyndromic pheochromocytomas and paragangliomas was very low in a cohort of 182 patients, with only 1 of 182 patients ultimately diagnosed with VHL.[87]

Paragangliomas are rare in VHL patients but can occur in the head and neck or abdomen.[88] A review of VHL patients who developed pheochromocytomas and/or paragangliomas revealed that 90% of patients manifested pheochromocytomas and 19% presented with a paraganglioma.[84]

The mean age at diagnosis of VHL-related pheochromocytomas and paragangliomas is approximately 30 years,[83,89] and patients with multiple tumors were diagnosed more than a decade earlier than patients with solitary lesions in one series (19 vs. 34 y; P

VHL patients may develop multiple serous cystadenomas, pancreatic NETs, and simple pancreatic cysts.[1] VHL patients do not have an increased risk of pancreatic adenocarcinoma. Serous cystadenomas are benign tumors and warrant no intervention. Simple pancreatic cysts can be numerous and rarely cause symptomatic biliary duct obstruction. Endocrine function is nearly always maintained; occasionally, however, patients with extensive cystic disease requiring pancreatic surgery may ultimately require pancreatic exocrine supplementation.

Pancreatic NETs are usually nonfunctional but can metastasize (to lymph nodes and the liver). The risk of pancreatic NET metastasis was analyzed in a large cohort of patients, in which the mean age at diagnosis of a pancreatic NET was 38 years (range, 1668 y).[90] The risk of metastasis was lower in patients with small primary lesions (3 cm), in patients without an exon 3 pathogenic variant, and in patients whose tumor had a slow doubling time (>500 days). Nonfunctional pancreatic NETs can be followed by imaging surveillance with intervention when tumors reach 3 cm. Lesions in the head of the pancreas can be considered for surgery at a smaller size to limit operative complexity.

ELSTs are adenomatous tumors arising from the endolymphatic duct or sac within the posterior part of the petrous bone.[91] ELSTs are rare in the sporadic setting, but are apparent on imaging in 11% to 16% of patients with VHL. Although these tumors do not metastasize, they are locally invasive, eroding through the petrous bone and the inner ear structures.[91,92] Approximately 30% of VHL patients with ELSTs have bilateral lesions.[91,93]

ELSTs are an important cause of morbidity in VHL patients. ELSTs evident on imaging are associated with a variety of symptoms, including hearing loss (95% of patients), tinnitus (92%), vestibular symptoms (such as vertigo or disequilibrium) (62%), aural fullness (29%), and facial paresis (8%).[91,92] In approximately half of patients, symptoms (particularly hearing loss) can occur suddenly, probably as a result of acute intralabyrinthine hemorrhage.[92] Hearing loss or vestibular dysfunction in VHL patients can also present in the absence of radiologically evident ELSTs (approximately 60% of all symptomatic patients) and is believed to be a consequence of microscopic ELSTs.[91]

Hearing loss related to ELSTs is typically irreversible; serial imaging to enable early detection of ELSTs in asymptomatic patients and resection of radiologically evident lesions are important components in the management of VHL patients.[94,95] Surgical resection by retrolabyrinthine posterior petrosectomy is usually curative and can prevent onset or worsening of hearing loss and improve vestibular symptoms.[92,94]

Tumors of the broad ligament can occur in females with VHL and are known as papillary cystadenomas. These tumors are extremely rare, and fewer than 20 have been reported in the literature.[96] Papillary cystadenomas are histologically identical to epididymal cystadenomas commonly observed in males with VHL.[97] One important difference is that papillary cystadenomas are almost exclusively observed in patients with VHL, whereas epididymal cystadenomas in men can occur sporadically.[98] These tumors are frequently cystic, and although they become large, they generally have a fairly indolent behavior.

More than one-third of all cases of epididymal cystadenomas reported in the literature and most cases of bilateral cystadenomas have been reported in patients with VHL.[99] Among symptomatic patients, the most common presentation is a painless, slow-growing scrotal swelling. The differential diagnoses of epididymal tumors include adenomatoid tumor (which is the most common tumor in this site), metastatic ccRCC, and papillary mesothelioma.[100]

In a small series, histological analysis did not reveal features typically associated with malignancy, such as mitotic figures, nuclear pleomorphism, and necrosis. Lesions were strongly positive for CK7 and negative for RCC. Carbonic anhydrase IX (CAIX) was positive in all tumors. PAX8 was positive in most cases. These features were reminiscent of clear cell papillary RCC, a relatively benign form of RCC without known metastatic potential.[97]

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Homosexual behavior in animals – Wikipedia

Homosexual behavior in animals is sexual behavior among non-human species that is interpreted as homosexual or bisexual. This may include same-sex sexual activity, courtship, affection, pair bonding, and parenting among same-sex animal pairs.[1][2][3][4] Research indicates that various forms of this are found in every major geographic region and every major animal group. The sexual behavior of non-human animals takes many different forms, even within the same species, though homosexual behavior is best known from social species.

Scientists perceive homosexual behavior in animals to different degrees. The motivations for and implications of these behaviors have yet to be fully understood, since most species have yet to be fully studied.[5] According to Bruce Bagemihl, the animal kingdom engages in homosexual behavior "with much greater sexual diversity including homosexual, bisexual and nonreproductive sex than the scientific community and society at large have previously been willing to accept."[6] Bagemihl adds, however, that this is "necessarily an account of human interpretations of these phenomena".[7] Simon LeVay introduced caveat that "[a]lthough homosexual behavior is very common in the animal world, it seems to be very uncommon that individual animals have a long-lasting predisposition to engage in such behavior to the exclusion of heterosexual activities. Thus, a homosexual orientation, if one can speak of such thing in animals, seems to be a rarity."[8] One species in which exclusive homosexual orientation occurs, however, is that of domesticated sheep (Ovis aries).[9][10] "About 10% of rams (males), refuse to mate with ewes (females) but do readily mate with other rams."[10]

According to Bagemihl (1999), same-sex behavior (comprising courtship, sexual, pair-bonding, and parental activities) has been documented in over 450 species of animals worldwide.[11]

The term homosexual was coined by Karl-Maria Kertbeny in 1868 to describe same-sex sexual attraction and sexual behavior in humans.[12] Its use in animal studies has been controversial for two main reasons: animal sexuality and motivating factors have been and remain poorly understood, and the term has strong cultural implications in western society that are irrelevant for species other than humans.[13] Thus homosexual behavior has been given a number of terms over the years. According to Bruce Bagemihl, when describing animals, the term homosexual is preferred over gay, lesbian, and other terms currently in use, as these are seen as even more bound to human homosexuality.[14]

Bailey et al. says: "Homosexual: in animals, this has been used to refer to same-sex behavior that is not sexual in character (e.g. homosexual tandem running in termites), same-sex courtship or copulatory behavior occurring over a short period of time (e.g. homosexual mounting in cockroaches and rams) or long-term pair bonds between same-sex partners that might involve any combination of courting, copulating, parenting and affectional behaviors (e.g. homosexual pair bonds in gulls). In humans, the term is used to describe individual sexual behaviors as well as long-term relationships, but in some usages connotes a gay or lesbian social identity. Scientific writing would benefit from reserving this anthropomorphic term for humans and not using it to describe behavior in other animals, because of its deeply rooted context in human society".[15]

Animal preference and motivation is always inferred from behavior. In wild animals, researchers will as a rule not be able to map the entire life of an individual, and must infer from frequency of single observations of behavior. The correct usage of the term homosexual is that an animal exhibits homosexual behavior or even same-sex sexual behavior; however, this article conforms to the usage by modern research,[14][16][17][18][pageneeded][19]applying the term homosexuality to all sexual behavior (copulation, genital stimulation, mating games and sexual display behavior) between animals of the same sex. In most instances, it is presumed that the homosexual behavior is but part of the animal's overall sexual behavioral repertoire, making the animal "bisexual" rather than "homosexual" as the terms are commonly understood in humans.[18][pageneeded], but cases of homosexual preference and exclusive homosexual pairs are known.[20]

The observation of homosexual behavior in animals can be seen as both an argument for and against the acceptance of homosexuality in humans, and has been used especially against the claim that it is a peccatum contra naturam ("sin against nature"). For instance, homosexuality in animals was cited by the American Psychiatric Association and other groups in their amici curiae brief to the United States Supreme Court in Lawrence v. Texas, which ultimately struck down the sodomy laws of 14 states.[21][22]

A majority of the research available concerning homosexual behavior in animals lacks specification between animals that exclusively exhibit same-sex tendencies and those that participate in heterosexual and homosexual mating activities interchangeably. This lack of distinction has led to differing opinions and conflicting interpretations of collected data amongst scientists and researchers. For instance, Bruce Bagemihl, author of the book Biological Exuberence: Animal Homosexuality and Natural Diversity, emphasizes that there are no anatomical or endocrinological differences between exclusively homosexual and exclusively heterosexual animal pairs.[23][pageneeded] However, if the definition of "homosexual behavior" is made to include animals that participate in both same-sex and opposite-sex mating activities, hormonal differences have been documented among key sex hormones, such as testosterone and estradiol, when compared to those who participate solely in heterosexual mating.[24]

Many of the animals used in laboratory-based studies of homosexuality do not appear to spontaneously exhibit these tendencies often in the wild. Such behavior is often elicited and exaggerated by the researcher during experimentation through the destruction of a portion of brain tissue, or by exposing the animal to high levels of steroid hormones prenatally.[25][pageneeded] Information gathered from these studies is limited when applied to spontaneously occurring same-sex behavior in animals outside of the laboratory.[25]

Homosexual behaviour in animals has been discussed since classical antiquity. The earliest written mention of animal homosexuality appears to date back to 2,300 years ago, when Aristotle (384322 BC) described copulation between pigeons, partridges and quails of the same sex.[26] The Hieroglyphics of Horapollo, written in the 4th century AD by the Egyptian writer Horapollo, mentions "hermaphroditism" in hyenas and homosexuality in partridges.[26] The first review of animal homosexuality was written by the zoologist Ferdinand Karsch-Haack in 1900.[26]

Until recent times, the presence of same-sex sexual behavior was not "officially" observed on a large scale, possibly due to observer bias caused by social attitudes to same-sex sexual behavior,[27] innocent confusion, lack of interest, distaste, scientists fearing loss of their grants or even from a fear of "being ridiculed by their colleagues".[28][29] Georgetown University biologist Janet Mann states "Scientists who study the topic are often accused of trying to forward an agenda, and their work can come under greater scrutiny than that of their colleagues who study other topics."[30] They also noted "Not every sexual act has a reproductive function ... that's true of humans and non-humans."[30] It appears to be widespread amongst social birds and mammals, particularly the sea mammals and the primates. The true extent of homosexuality in animals is not known. While studies have demonstrated homosexual behavior in a number of species, Petter Bckman, the scientific advisor of the exhibition Against Nature? in 2007, speculated that the true extent of the phenomenon may be much larger than was then recognized:

No species has been found in which homosexual behaviour has not been shown to exist, with the exception of species that never have sex at all, such as sea urchins and aphis. Moreover, a part of the animal kingdom is hermaphroditic, truly bisexual. For them, homosexuality is not an issue.[28]

An example of overlooking homosexual behavior is noted by Bagemihl describing mating giraffes where nine out of ten pairings occur between males:

Every male that sniffed a female was reported as sex, while anal intercourse with orgasm between males was only "revolving around" dominance, competition or greetings.[31]

Some researchers believe this behavior to have its origin in male social organization and social dominance, similar to the dominance traits shown in prison sexuality. Others, particularly Bagemihl, Joan Roughgarden, Thierry Lod[32] and Paul Vasey suggest the social function of sex (both homosexual and heterosexual) is not necessarily connected to dominance, but serves to strengthen alliances and social ties within a flock. Others have argued that social organization theory is inadequate because it cannot account for some homosexual behaviors, for example, penguin species where male individuals mate for life and refuse to pair with females when given the chance.[33][34] While reports on many such mating scenarios are still only anecdotal, a growing body of scientific work confirms that permanent homosexuality occurs not only in species with permanent pair bonds,[19] but also in non-monogamous species like sheep.

One report on sheep cited below states:

Approximately 8% of rams exhibit sexual preferences [that is, even when given a choice] for male partners (male-oriented rams) in contrast to most rams, which prefer female partners (female-oriented rams). We identified a cell group within the medial preoptic area/anterior hypothalamus of age-matched adult sheep that was significantly larger in adult rams than in ewes...[35]

In fact, apparent homosexual individuals are known from all of the traditional domestic species, from sheep, cattle and horses to cats, dogs and budgerigars.[36][pageneeded]

A definite physiological explanation or reason for homosexual activity in animal species has not been agreed upon by researchers in the field. Numerous scholars are of the opinion that varying levels (either higher or lower) of the sex hormones in the animal,[37] in addition to the size of the animal's gonads,[24] play a direct role in the sexual behavior and preference exhibited by that animal. Others firmly argue no evidence to support these claims exists when comparing animals of a specific species exhibiting homosexual behavior exclusively and those that do not. Ultimately, empirical support from comprehensive endocrinological studies exist for both interpretations.[37][38] Researchers found no evidence of differences in the measurements of the gonads, or the levels of the sex hormones of exclusively homosexual western gulls and ring-billed gulls.[39] However, when analyzing these differences in bisexual rams, males were found to have lower levels of testosterone and estradiol in their blood, as well as smaller gonads than their heterosexual counterpart.[citation needed]

Additional studies pertaining to hormone involvement in homosexual behavior indicate that when administering treatments of testosterone and estradiol to female heterosexual animals, the elevated hormone levels increase the likelihood of homosexual behavior. Additionally, boosting the levels of sex hormones during an animal's pregnancy appears to increase the likelihood of it birthing a homosexual offspring.[37]

Researchers found that disabling the fucose mutarotase (FucM) gene in laboratory mice which influences the levels of estrogen to which the brain is exposed caused the female mice to behave as if they were male as they grew up. "The mutant female mouse underwent a slightly altered developmental programme in the brain to resemble the male brain in terms of sexual preference" said Professor Chankyu Park of the Korea Advanced Institute of Science and Technology in Daejon, South Korea, who led the research. His most recent findings have been published in the BMC Genetics journal on July 7, 2010.[40][41] Another study found that by manipulating a gene in fruit flies (Drosophila), homosexual behavior appeared to have been induced. However, in addition to homosexual behavior, several abnormal behaviors were also exhibited apparently due to this mutation.[42]

In March 2011, research showed that serotonin is involved in the mechanism of sexual orientation of mice.[43][44] A study conducted on fruit flies found that inhibiting the dopamine neurotransmitter inhibited lab-induced homosexual behavior.[45]

An estimated one-quarter of all black swans pairings are of males. They steal nests, or form temporary threesomes with females to obtain eggs, driving away the female after she lays the eggs. The males spent time in each other's society, guarded the common territory, performed greeting ceremonies before each other, and (in the reproductive period) pre-marital rituals, and if one of the birds tried to sit on the other, an intense fight began.[1][2] More of their cygnets survive to adulthood than those of different-sex pairs, possibly due to their superior ability to defend large portions of land. The same reasoning has been applied to male flamingo pairs raising chicks.[46][47]

Female albatross, on the north-western tip of the island of Oahu, Hawaii, form pairs for co-growing offspring. On the observed island, the number of females considerably exceeds the number of males (59% N=102/172), so 31% of females, after mating with males, create partnerships for hatching and feeding chicks. Compared to male-female couples female partnerships have a lower hatching rate (41% vs 87%) and lower overall reproductive success (31% vs. 67%).[48]

Research has shown that the environmental pollutant methylmercury can increase the prevalence of homosexual behavior in male American white ibis. The study involved exposing chicks in varying dosages to the chemical and measuring the degree of homosexual behavior in adulthood. The results discovered was that as the dosage was increased the likelihood of homosexual behavior also increased. The endocrine blocking feature of mercury has been suggested as a possible cause of sexual disruption in other bird species.[49][50]

Mallards form male-female pairs only until the female lays eggs, at which time the male leaves the female. Mallards have rates of male-male sexual activity that are unusually high for birds, in some cases, as high as 19% of all pairs in a population.[36][pageneeded] Kees Moeliker of the Natural History Museum Rotterdam has observed one male mallard engage in homosexual necrophilia.[51]

Penguins have been observed to engage in homosexual behaviour since at least as early as 1911. George Murray Levick, who documented this behaviour in Adlie penguins at Cape Adare, described it as "depraved". The report was considered too shocking for public release at the time, and was suppressed. The only copies that were made available privately to researchers were translated into Greek, to prevent this knowledge becoming more widely known. The report was unearthed only a century later, and published in Polar Record in June 2012.[52]

In early February 2004 the New York Times reported that Roy and Silo, a male pair of chinstrap penguins in the Central Park Zoo in New York City had successfully hatched and fostered a female chick from a fertile egg they had been given to incubate.[21] Other penguins in New York zoos have also been reported to have formed same-sex pairs.[53][54]

In Odense Zoo in Denmark, a pair of male king penguins adopted an egg that had been abandoned by a female, proceeding to incubate it and raise the chick.[55][56]Zoos in Japan and Germany have also documented homosexual male penguin couples.[33][34] The couples have been shown to build nests together and use a stone as a substitute for an egg. Researchers at Rikkyo University in Tokyo found 20 homosexual pairs at 16 major aquariums and zoos in Japan.

The Bremerhaven Zoo in Germany attempted to encourage reproduction of endangered Humboldt penguins by importing females from Sweden and separating three male pairs, but this was unsuccessful. The zoo's director said that the relationships were "too strong" between the homosexual pairs.[57] German gay groups protested at this attempt to break up the male-male pairs[58] but the zoo's director was reported as saying "We don't know whether the three male pairs are really homosexual or whether they have just bonded because of a shortage of females ... nobody here wants to forcibly separate homosexual couples."[59]

A pair of male Magellanic penguins who had shared a burrow for six years at the San Francisco Zoo and raised a surrogate chick, split when the male of a pair in the next burrow died and the female sought a new mate.[60]

Buddy and Pedro, a pair of male African penguins, were separated by the Toronto Zoo to mate with female penguins.[61][62] Buddy has since paired off with a female.[62]

Suki and Chupchikoni are two female African penguins that pair bonded at the Ramat Gan Safari in Israel. Chupchikoni was assumed to be male until her blood was tested.[63]

In 2014 Jumbs and Hurricane, two Humboldt penguins at Wingham Wildlife Park became the center of international media attention as two male penguins who had pair bonded a number of years earlier and then successfully hatched and reared an egg given to them as surrogate parents after the mother abandoned it halfway through incubation.[64]

In 1998 two male griffon vultures named Dashik and Yehuda, at the Jerusalem Biblical Zoo, engaged in "open and energetic sex" and built a nest. The keepers provided the couple with an artificial egg, which the two parents took turns incubating; and 45 days later, the zoo replaced the egg with a baby vulture. The two male vultures raised the chick together.[65] A few years later, however, Yehuda became interested in a female vulture that was brought into the aviary. Dashik became depressed, and was eventually moved to the zoological research garden at Tel Aviv University where he too set up a nest with a female vulture.[66]

Two male vultures at the Allwetter Zoo in Muenster built a nest together, although they were picked on and their nest materials were often stolen by other vultures. They were eventually separated to try to promote breeding by placing one of them with female vultures, despite the protests of German homosexual groups.[67]

Both male and female pigeons sometimes exhibit homosexual behavior. In addition to sexual behavior, same-sex pigeon pairs will build nests, and hens will lay (infertile) eggs and attempt to incubate them.[citation needed]

The Amazon river dolphin or boto has been reported to form up in bands of 35 individuals engaging in sexual activity. The groups usually comprise young males and sometimes one or two females. Sex is often performed in non-reproductive ways, using snout, flippers and genital rubbing, without regard to gender.[68] In captivity, they have been observed to sometimes perform homosexual and heterosexual penetration of the blowhole, a hole homologous with the nostril of other mammals, making this the only known example of nasal sex in the animal kingdom.[68][69] The males will sometimes also perform sex with males from the tucuxi species, a type of small porpoise.[68]

Courtship, mounting, and full anal penetration between bulls has been noted to occur among American bison. The Mandan nation Okipa festival concludes with a ceremonial enactment of this behavior, to "ensure the return of the buffalo in the coming season".[70] Also, mounting of one female by another (known as "bulling") is extremely common among cattle. The behaviour is hormone driven and synchronizes with the emergence of estrus (heat), particularly in the presence of a bull.

More than 20 species of bat have been documented to engage in homosexual behavior.[26][71] Bat species that have been observed engaging in homosexual behavior in the wild include:[26]

Bat species that have been observed engaging in homosexual behavior in captivity include the Comoro flying fox (Pteropus livingstonii), the Rodrigues flying fox (Pteropus rodricensis) and the common vampire bat (Desmodus rotundus).[26]

Homosexual behavior in bats has been categorized into 6 groups: mutual homosexual grooming and licking, homosexual masturbation, homosexual play, homosexual mounting, coercive sex, and cross-species homosexual sex.[26][71]

In the wild, the grey-headed flying fox (Pteropus poliocephalus) engages in allogrooming wherein one partner licks and gently bites the chest and wing membrane of the other partner. Both sexes display this form of mutual homosexual grooming and it is more common in males. Males often have erect penises while they are mutually grooming each other. Like opposite-sex grooming partners, same-sex grooming partners continuously utter a pre-copulation call, which is described as a "pulsed grating call," while engaged in this activity.[26][71]

In wild Bonin flying foxes (Pteropus pselaphon), males perform fellatio or 'male-male genital licking' on other males. Malemale genital licking events occur repeatedly several times in the same pair, and reciprocal genital licking also occurs. The male-male genital licking in these bats is considered a sexual behavior. Allogrooming in Bonin flying foxes has never been observed, hence the male-male genital licking in this species does not seem to be a by-product of allogrooming, but rather a behavior of directly licking the male genital area, independent of allogrooming.[71] In captivity, same-sex genital licking has been observed among males of the Comoro flying fox (Pteropus livingstonii) as well as among males of the common vampire bat (Desmodus rotundus).[26][71]

In wild Indian flying foxes (Pteropus giganteus), males often mount one another, with erections and thrusting, while play-wrestling.[26] Males of the long-fingered bat (Myotis capaccinii) have been observed in the same position of male-female mounting, with one gripping the back of the others fur. A similar behavior was also observed in the common bent-wing bat (Miniopterus schreibersii).[26]

In wild little brown bats (Myotis lucifugus), males often mount other males (and females) during late autumn and winter, when many of the mounted individuals are torpid.[26] 35% of matings during this period are homosexual.[72] These coercive copulations usually include ejaculation and the mounted bat often makes a typical copulation call consisting of a long squawk.[26] Similarly, in hibernacula of the common noctule (Nyctalus noctula), active males were observed to wake up from lethargy on a warm day and engage in mating with lethargic males and (active or lethargic) females. The lethargic males, like females, called out loudly and presented their buccal glands with opened mouth during copulation.[26]

Vesey-Fitzgerald (1949) observed homosexual behaviours in all 12 British bat species known at the time: Homosexuality is common in the spring in all species, and, since the males are in full possession of their powers, I suspect throughout the summer...I have even seen homosexuality between Natterer's and Daubenton's bats (Myotis nattereri and M. daubentonii)."[26]

Dolphins of several species engage in homosexual acts, though it is best studied in the bottlenose dolphins.[36][pageneeded] Sexual encounters between females take the shape of "beak-genital propulsion", where one female inserts her beak in the genital opening of the other while swimming gently forward.[73] Between males, homosexual behaviour includes rubbing of genitals against each other, which sometimes leads to the males swimming belly to belly, inserting the penis in the others genital slit and sometimes anus.[74]

Janet Mann, Georgetown University professor of biology and psychology, argues that the strong personal behavior among male dolphin calves is about bond formation and benefits the species in an evolutionary context.[75] She cites studies showing that these dolphins later in life as adults are in a sense bisexual, and the male bonds forged earlier in life work together for protection as well as locating females to reproduce with. Confrontations between flocks of bottlenose dolphins and the related species Atlantic spotted dolphin will sometimes lead to cross-species homosexual behaviour between the males rather than combat.[76]

African and Asian males will engage in same-sex bonding and mounting. Such encounters are often associated with affectionate interactions, such as kissing, trunk intertwining, and placing trunks in each other's mouths. Male elephants, who often live apart from the general herd, often form "companionships", consisting of an older individual and one or sometimes two younger males with sexual behavior being an important part of the social dynamic. Unlike heterosexual relations, which are always of a fleeting nature, the relationships between males may last for years. The encounters are analogous to heterosexual bouts, one male often extending his trunk along the other's back and pushing forward with his tusks to signify his intention to mount. Same-sex relations are common and frequent in both sexes, with Asiatic elephants in captivity devoting roughly 45% of sexual encounters to same-sex activity.[77]

Male giraffes have been observed to engage in remarkably high frequencies of homosexual behavior. After aggressive "necking", it is common for two male giraffes to caress and court each other, leading up to mounting and climax. Such interactions between males have been found to be more frequent than heterosexual coupling.[78] In one study, up to 94% of observed mounting incidents took place between two males. The proportion of same sex activities varied between 30 and 75%, and at any given time one in twenty males were engaged in non-combative necking behavior with another male. Only 1% of same-sex mounting incidents occurred between females.[79]

Olympic marmot (left) and Hoary marmot (right).

Homosexual behavior is quite common in wild marmots.[80] In Olympic marmots (Marmota olympus) and Hoary Marmots (Marmota caligata), females often mount other females as well as engage in other affectionate and sexual behaviors with females of the same species.[80] They display a high frequency of these behaviors especially when they are in heat.[80][81] A homosexual encounter often begins with a greeting interaction in which one female nuzzles her nose on the other females cheek or mouth, or both females touch noses or mouths. Additionally, a female may gently chew on the ear or neck of her partner, who responds by raising her tail. The first female may sniff the other's genital region or nuzzle that region with her mouth. She may then proceed to mount the other female, during which the mounting female gently grasps the mounted female's dorsal neck fur in her jaws while thrusting. The mounted female arches her back and holds her tail to one side to facilitate their sexual interaction.[80][82]

Both male and female lions have been seen to interact homosexually.[83][84] Male lions pair-bond for a number of days and initiate homosexual activity with affectionate nuzzling and caressing, leading to mounting and thrusting. About 8% of mountings have been observed to occur with other males. Pairings between females are held to be fairly common in captivity but have not been observed in the wild.

European polecats Mustela putorius were found to engage homosexually with non-sibling animals. Exclusive homosexuality with mounting and anal penetration in this solitary species serves no apparent adaptive function.[85][pageneeded]

Bonobos, which have a matriarchal society, unusual among apes, are a fully bisexual speciesboth males and females engage in heterosexual and homosexual behavior, being noted for femalefemale homosexuality in particular, including[86] between juveniles and adults. Roughly 60% of all bonobo sexual activity occurs between two or more females. While the homosexual bonding system in bonobos represents the highest frequency of homosexuality known in any primate species, homosexuality has been reported for all great apes (a group which includes humans), as well as a number of other primate species.[87][88][89][pageneeded][90][86][91][92][93][94]

Dutch primatologist Frans de Waal on observing and filming bonobos noted that there were two reasons to believe sexual activity is the bonobo's answer to avoiding conflict. Anything that arouses the interest of more than one bonobo at a time, not just food, tends to result in sexual contact. If two bonobos approach a cardboard box thrown into their enclosure, they will briefly mount each other before playing with the box. Such situations lead to squabbles in most other species. But bonobos are quite tolerant, perhaps because they use sex to divert attention and to defuse tension.

Bonobo sex often occurs in aggressive contexts totally unrelated to food. A jealous male might chase another away from a female, after which the two males reunite and engage in scrotal rubbing. Or after a female hits a juvenile, the latter's mother may lunge at the aggressor, an action that is immediately followed by genital rubbing between the two adults.[95]

With the Japanese macaque, also known as the "snow monkey", same-sex relations are frequent, though rates vary between troops. Females will form "consortships" characterized by affectionate social and sexual activities. In some troops up to one quarter of the females form such bonds, which vary in duration from a few days to a few weeks. Often, strong and lasting friendships result from such pairings. Males also have same-sex relations, typically with multiple partners of the same age. Affectionate and playful activities are associated with such relations.[96]

Homosexual behavior forms part of the natural repertoire of sexual or sociosexual behavior of orangutans. Male homosexual behavior occurs both in the wild and in captivity, and it occurs in both adolescent and mature individuals. Homosexual behavior in orangutans is not an artifact of captivity or contact with humans.[97]

Among monkeys[clarification needed], Lionel Tiger and Robin Fox conducted a study on how Depo-Provera contraceptives lead to decreased male attraction to females.[98]

Ovis aries has attracted much attention due to the fact that around 810% of rams have an exclusive homosexual orientation.[9][99][100][101][102] Furthermore, around 1822% of rams are bisexual.[100]

An October 2003 study by Dr. Charles E. Roselli et al. (Oregon Health and Science University) states that homosexuality in male sheep (found in 8% of rams) is associated with a region in the rams' brains which the authors call the "ovine Sexually Dimorphic Nucleus" (oSDN) which is half the size of the corresponding region in heterosexual male sheep.[35] Scientists found that, "The oSDN in rams that preferred females was significantly larger and contained more neurons than in male-oriented rams and ewes. In addition, the oSDN of the female-oriented rams expressed higher levels of aromatase, a substance that converts testosterone to estradiol, a form of estrogen which is believed to facilitate typical male sexual behaviors. Aromatase expression was no different between male-oriented rams and ewes."

"The dense cluster of neurons that comprise the oSDN express cytochrome P450 aromatase. Aromatase mRNA levels in the oSDN were significantly greater in female-oriented rams than in ewes, whereas male-oriented rams exhibited intermediate levels of expression." These results suggest that "... naturally occurring variations in sexual partner preferences may be related to differences in brain anatomy and its capacity for estrogen synthesis."[35] As noted before, given the potential unagressiveness of the male population in question, the differing aromatase levels may also have been evidence of aggression levels, not sexuality. It should also be noted that the results of this study have not been confirmed by other studies.

The Merck Manual of Veterinary Medicine appears to consider homosexuality among sheep as a routine occurrence and an issue to be dealt with as a problem of animal husbandry.[103]

Homosexual courtship and sexual activity routinely occur among rams of wild sheep species, such as Bighorn sheep (Ovis canadensis), Thinhorn sheep (Ovis dalli), mouflons and urials (Ovis orientalis).[104] Usually a higher ranking older male courts a younger male using a sequence of stylized movements. To initiate homosexual courtship, a courting male approaches the other male with his head and neck lowered and extended far forward in what is called the 'low-stretch' posture. He may combine this with the 'twist,' in which the courting male sharply rotates his head and points his muzzle toward the other male, often while flicking his tongue and making grumbling sounds. The courting male also often performs a 'foreleg kick,' in which he snaps his front leg up against the other males belly or between his hind legs. He also occasionally sniffs and nuzzles the other males genital area and may perform the flehmen response. Thinhorn rams additionally lick the penis of the male they are courting. In response, the male being courted may rub his cheeks and forehead on the courting males face, nibble and lick him, rub his horns on the courting males neck, chest, or shoulders, and develop an erection. Males of another wild sheep species, the Asiatic Mouflons, perform similar courtship behaviors towards fellow males.[104]

Sexual activity between wild males typically involves mounting and anal intercourse. In Thinhorn sheep, genital licking also occurs. During mounting, the larger male usually mounts the smaller male by rearing up on his hind legs and placing his front legs on his partners flanks. The mounting male usually has an erect penis and accomplishes full anal penetration while performing pelvic thrusts that may lead to ejaculation. The mounted male arches his back to facilitate the copulation. Homosexual courtship and sexual activity can also take place in groups composed of three to ten wild rams clustered together in a circle. These non-aggressive groups are called 'huddles' and involve rams rubbing, licking, nuzzling, horning, and mounting each other. Female Mountain sheep also engage in occasional courtship activities with one another and in sexual activities such as licking each others genitals and mounting.[104]

The family structure of the spotted hyena is matriarchal, and dominance relationships with strong sexual elements are routinely observed between related females. Due largely to the female spotted hyena's unique urogenital system, which looks more like a penis rather than a vagina, early naturalists thought hyenas were hermaphroditic males who commonly practiced homosexuality.[105][not in citation given] Early writings such as Ovid's Metamorphoses and the Physiologus suggested that the hyena continually changed its sex and nature from male to female and back again. In Paedagogus, Clement of Alexandria noted that the hyena (along with the hare) was "quite obsessed with sexual intercourse". Many Europeans associated the hyena with sexual deformity, prostitution, deviant sexual behavior, and even witchcraft.

The reality behind the confusing reports is the sexually aggressive behavior between the females, including mounting between females. Research has shown that "in contrast to most other female mammals, female Crocuta are male-like in appearance, larger than males, and substantially more aggressive,"[106] and they have "been masculinized without being defeminized".[105][not in citation given]

Study of this unique genitalia and aggressive behavior in the female hyena has led to the understanding that more aggressive females are better able to compete for resources, including food and mating partners.[105][107] Research has shown that "elevated levels of testosterone in utero"[108] contribute to extra aggressiveness; both males and females mount members of both the same and opposite sex,[108][109] who in turn are possibly acting more submissive because of lower levels of testosterone in utero.[106]

Parthenogenesis. Several species of whiptail lizard (especially in the genus Aspidoscelis) consist only of females that have the ability to reproduce through parthenogenesis.[110] Females engage in sexual behavior to stimulate ovulation, with their behavior following their hormonal cycles; during low levels of estrogen, these (female) lizards engage in "masculine" sexual roles. Those animals with currently high estrogen levels assume "feminine" sexual roles. Some parthenogenetic lizards that perform the courtship ritual have greater fertility than those kept in isolation due to an increase in hormones triggered by the sexual behaviors. So, even though asexual whiptail lizards populations lack males, sexual stimuli still increase reproductive success. From an evolutionary standpoint, these females are passing their full genetic code to all of their offspring (rather than the 50% of genes that would be passed in sexual reproduction). Certain species of gecko also reproduce by parthenogenesis.[111]

"True" homosexuality in lizards. Some species of sexually reproducing geckos have been found to display homosexual behavior, e.g the day geckos Phelsuma laticauda and Phelsuma cepediana.[112]

Jonathan, the world's oldest tortoise (an Aldabra giant tortoise), had been mating with another tortoise named Frederica since 1991. In 2017, it was discovered that Frederica was actually probably male all along, and was renamed Frederic.[113]

There is evidence of same-sex sexual behavior in at least 110 species of insects and arachnids.[114] Scharf et al. says: "Males are more frequently involved in same-sex sexual (SSS) behavior in the laboratory than in the field, and isolation, high density, and exposure to female pheromones increase its prevalence. SSS behavior is often shorter than the equivalent heterosexual behavior. Most cases can be explained via mistaken identification by the active (courting/mounting) male. Passive males often resist courting/mating attempts".[114]

Scharf et al. continues: "SSS behavior has been reported in most insect orders, and Bagemihl (1999) provides a list of ~100 species of insects demonstrating such behavior. Yet, this list lacks detailed descriptions, and a more comprehensive summary of its prevalence in invertebrates, as well as ethology, causes, implications, and evolution of this behavior, remains lacking".[114]

Male homosexuality has been inferred in several species of dragonflies (the order Odonata). The cloacal pinchers of male damselflies and dragonflies inflict characteristic head damage to females during sex. A survey of 11 species of damsel and dragonflies[115][116] has revealed such mating damages in 20 to 80% of the males too, indicating a fairly high occurrence of sexual coupling between males.

Male Drosophila melanogaster flies bearing two copies of a mutant allele in the fruitless gene court and attempt to mate exclusively with other males.[20] The genetic basis of animal homosexuality has been studied in the fly Drosophila melanogaster.[117] Here, multiple genes have been identified that can cause homosexual courtship and mating.[118] These genes are thought to control behavior through pheromones as well as altering the structure of the animal's brains.[119][120] These studies have also investigated the influence of environment on the likelihood of flies displaying homosexual behavior.[121][122]

Male bed bugs (Cimex lectularius) are sexually attracted to any newly fed individual and this results in homosexual mounting. This occurs in heterosexual mounting by the traumatic insemination in which the male pierces the female abdomen with his needle-like penis. In homosexual mating this risks abdominal injuries as males lack the female counteradaptive spermalege structure. Males produce alarm pheromones to reduce such homosexual mating.

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Homosexual behavior in animals - Wikipedia

Stallion – Wikipedia

A stallion is a male horse that has not been gelded (castrated).Stallions follow the conformation and phenotype of their breed, but within that standard, the presence of hormones such as testosterone may give stallions a thicker, "cresty" neck, as well as a somewhat more muscular physique as compared to female horses, known as mares, and castrated males, called geldings.

Temperament varies widely based on genetics, and training, but because of their instincts as herd animals, they may be prone to aggressive behavior, particularly toward other stallions, and thus require careful management by knowledgeable handlers. However, with proper training and management, stallions are effective equine athletes at the highest levels of many disciplines, including horse racing, horse shows, and international Olympic competition.

The term "stallion" dates from the era of Henry VII, who passed a number of laws relating to the breeding and export of horses in an attempt to improve the British stock, under which it was forbidden to allow uncastrated male horses to be turned out in fields or on the commons; they had to be "kept within bounds and tied in stalls." (The term "stallion" for an uncastrated male horse dates from this time; stallion = stalled one.)[1] "Stallion" is also used to refer to males of other equids, including zebras and donkeys.

Contrary to popular myths, many stallions do not live with a harem of mares. Nor, in natural settings, do they fight each other to the death in competition for mares. Being social animals, stallions who are not able to find or win a harem of mares usually band together in stallions-only "bachelor" groups which are composed of stallions of all ages. Even with a band of mares, the stallion is not the leader of a herd but defends and protects the herd from predators and other stallions. The leadership role in a herd is held by a mare, known colloquially as the "lead mare" or "boss mare." The mare determines the movement of the herd as it travels to obtain food, water, and shelter. She also determines the route the herd takes when fleeing from danger. When the herd is in motion, the dominant stallion herds the straggling members closer to the group and acts as a "rear guard" between the herd and a potential source of danger. When the herd is at rest, all members share the responsibility of keeping watch for danger. The stallion is usually on the edge of the group, to defend the herd if needed.

There is usually one dominant mature stallion for every mixed-sex herd of horses. The dominant stallion in the herd will tolerate both sexes of horses while young, but once they become sexually mature, often as yearlings or two-year-olds, the stallion will drive both colts and fillies from the herd. Colts may present competition for the stallion, but studies suggest that driving off young horses of both sexes may also be an instinctive behavior that minimizes the risk of inbreeding within the herd, as most young are the offspring of the dominant stallion in the group. In some cases, a single younger mature male may be tolerated on the fringes of the herd. One theory is that this young male is considered a potential successor, as in time the younger stallion will eventually drive out the older herd stallion.

Fillies usually soon join a different band with a dominant stallion different from the one that sired them. Colts or young stallions without mares of their own usually form small, all-male, "bachelor bands" in the wild. Living in a group gives these stallions the social and protective benefits of living in a herd. A bachelor herd may also contain older stallions who have lost their herd in a challenge.[2]

Other stallions may directly challenge a herd stallion, or may simply attempt to "steal" mares and form a new, smaller herd. In either case, if the two stallions meet, there rarely is a true fight; more often there will be bluffing behavior and the weaker horse will back off. Even if a fight for dominance occurs, rarely do opponents hurt each other in the wild because the weaker combatant has a chance to flee. Fights between stallions in captivity may result in serious injuries; fences and other forms of confinement make it more difficult for the losing animal to safely escape. In the wild, feral stallions have been known to steal or mate with domesticated mares.

The stallion's reproductive system is responsible for his sexual behavior and secondary sex characteristics (such as a large crest).The external genitalia comprise:

The internal genitalia comprise the accessory sex glands, which include the vesicular glands, the prostate gland and the bulbourethral glands. These contribute fluid to the semen at ejaculation, but are not strictly necessary for fertility.[3][9]

Domesticated stallions are trained and managed in a variety of ways, depending on the region of the world, the owner's philosophy, and the individual stallion's temperament. In all cases, however, stallions have an inborn tendency to attempt to dominate both other horses and human handlers, and will be affected to some degree by proximity to other horses, especially mares in heat. They must be trained to behave with respect toward humans at all times or else their natural aggressiveness, particularly a tendency to bite, may pose a danger of serious injury.[2]

For this reason, regardless of management style, stallions must be treated as individuals and should only be handled by people who are experienced with horses and thus recognize and correct inappropriate behavior before it becomes a danger.[10] While some breeds are of a more gentle temperament than others, and individual stallions may be well-behaved enough to even be handled by inexperienced people for short periods of time, common sense must always be used. Even the most gentle stallion has natural instincts that may overcome human training. As a general rule, children should not handle stallions, particularly in a breeding environment.

Management of stallions usually follows one of the following models: confinement or "isolation" management, where the stallion is kept alone, or in management systems variously called "natural", "herd", or "pasture" management where the stallion is allowed to be with other horses. In the "harem" model, the stallion is allowed to run loose with mares akin to that of a feral or semi-feral herd. In the"bachelor herd" model, stallions are kept in a male-only group of stallions, or, in some cases, with stallions and geldings. Sometime stallions may periodically be managed in multiple systems, depending on the season of the year.

The advantage of natural types of management is that the stallion is allowed to behave "like a horse" and may exhibit fewer stable vices. In a harem model, the mares may "cycle" or achieve estrus more readily. Proponents of natural management also assert that mares are more likely to "settle" (become pregnant) in a natural herd setting. Some stallion managers keep a stallion with a mare herd year-round, others will only turn a stallion out with mares during the breeding season.[11]

In some places, young domesticated stallions are allowed to live separately in a "bachelor herd" while growing up, kept out of sight, sound or smell of mares. A Swiss study demonstrated that even mature breeding stallions kept well away from other horses could live peacefully together in a herd setting if proper precautions were taken while the initial herd hierarchy was established.[12]

As an example, in the New Forest, England, breeding stallions run out on the open Forest for about two to three months each year with the mares and youngstock. On being taken off the Forest, many of them stay together in bachelor herds for most of the rest of the year.[13][14][15] New Forest stallions, when not in their breeding work, take part on the annual round-ups, working alongside mares and geldings, and compete successfully in many disciplines.[16][17]

There are drawbacks to natural management, however. One is that the breeding date, and hence foaling date, of any given mare will be uncertain. Another problem is the risk of injury to the stallion or mare in the process of natural breeding, or the risk of injury while a hierarchy is established within an all-male herd. Some stallions become very anxious or temperamental in a herd setting and may lose considerable weight, sometimes to the point of a health risk. Some may become highly protective of their mares and thus more aggressive and dangerous to handle. There is also a greater risk that the stallion may escape from a pasture or be stolen. Stallions may break down fences between adjoining fields to fight another stallion or mate with the "wrong" herd of mares, thus putting the pedigree of ensuing foals in question.[18]

The other general method of managing stallions is to confine them individually, sometimes in a small pen or corral with a tall fence, other times in a stable, or, in certain places, in a small field (or paddock) with a strong fence. The advantages to individual confinement include less of a risk of injury to the stallion or to other horses, controlled periods for breeding mares, greater certainty of what mares are bred when, less risk of escape or theft, and ease of access by humans. Some stallions are of such a temperament, or develop vicious behavior due to improper socialization or poor handling, that they must be confined and cannot be kept in a natural setting, either because they behave in a dangerous manner toward other horses, or because they are dangerous to humans when loose.

The drawbacks to confinement vary with the details of the actual method used, but stallions kept out of a herd setting require a careful balance of nutrition and exercise for optimal health and fertility. Lack of exercise can be a serious concern; stallions without sufficient exercise may not only become fat, which may reduce both health and fertility, but also may become aggressive or develop stable vices due to pent-up energy. Some stallions within sight or sound of other horses may become aggressive or noisy, calling or challenging other horses. This sometimes is addressed by keeping stallions in complete isolation from other animals.

However, complete isolation has significant drawbacks; stallions may develop additional behavior problems with aggression due to frustration and pent-up energy. As a general rule, a stallion that has been isolated from the time of weaning or sexual maturity will have a more difficult time adapting to a herd environment than one allowed to live close to other animals. However, as horses are instinctively social creatures, even stallions are believed to benefit from being allowed social interaction with other horses, though proper management and cautions are needed.[12]

Some managers attempt to compromise between the two methods by providing stallions daily turnout by themselves in a field where they can see, smell, and hear other horses. They may be stabled in a barn where there are bars or a grille between stalls where they can look out and see other animals. In some cases, a stallion may be kept with or next to a gelding or a nonhorse companion animal such as a goat, a gelded donkey, a cat, or other creature.

Properly trained stallions can live and work close to mares and to one another. Examples include the Lipizzan stallions of the Spanish Riding School in Vienna, Austria, where the entire group of stallions live part-time in a bachelor herd as young colts, then are stabled, train, perform, and travel worldwide as adults with few if any management problems. However, even stallions who are unfamiliar with each other can work safely in reasonable proximity if properly trained; the vast majority of Thoroughbred horses on the racetrack are stallions, as are many equine athletes in other forms of competition. Stallions are often shown together in the same ring at horse shows, particularly in halter classes where their conformation is evaluated. In horse show performance competition, stallions and mares often compete in the same arena with one another, particularly in Western and English "pleasure"-type classes where horses are worked as a group. Overall, stallions can be trained to keep focused on work and maybe brilliant performers if properly handled.[19]

A breeding stallion is more apt to present challenging behavior to a human handler than one who has not bred mares, and stallions may be more difficult to handle in spring and summer, during the breeding season, than during the fall and winter. However, some stallions are used for both equestrian uses and for breeding at the same general time of year. Though compromises may need to be made in expectations for both athletic performance and fertility rate, well-trained stallions with good temperaments can be taught that breeding behavior is only allowed in a certain area, or with certain cues, equipment, or with a particular handler.[20][21] However, some stallions lack the temperament to focus on work if also breeding mares in the same general time period, and therefore are taken out of competition either temporarily or permanently to be used for breeding. When permitted by a breed registry, use of artificial insemination is another technique that may reduce behavior problems in stallions.

Attitudes toward stallions vary between different parts of the world. In some parts of the world, the practice of gelding is not widespread and stallions are common. In other places, most males are gelded and only a few stallions are kept as breeding stock.Horse breeders who produce purebred bloodstock often recommend that no more than the top 10 percent of all males be allowed to reproduce, to continually improve a given breed of horse.

People sometimes have inaccurate beliefs about stallions, both positive and negative. Some beliefs are that stallions are always mean and vicious or uncontrollable, other beliefs are that misbehaving stallions should be allowed to misbehave because they are being "natural", "spirited" or "noble." In some cases, fed by movies and fictional depictions of horses in literature, some people believe a stallion can bond to a single human individual to the exclusion of all others. However, like many other misconceptions, there is only partial truth to these beliefs. Some, though not all stallions can be vicious or hard to handle, occasionally due to genetics, but usually due to improper training. Others are very well-trained and have excellent manners. Misbehaving stallions may look pretty or be exhibiting instinctive behavior, but it can still become dangerous if not corrected. Some stallions do behave better for some people than others, but that can be true of some mares and geldings, as well.

In some parts of Asia and the Middle East, the riding of stallions is widespread, especially among male riders. The gelding of stallions is unusual, viewed culturally as either unnecessary or unnatural. In areas where gelding is not widely practised, stallions are still not needed in numbers as great as mares, and so many will be culled, either sold for horsemeat or simply sold to traders who will take them outside the area. Of those that remain, many will not be used for breeding purposes.

In Europe, Australia, and the Americas, keeping stallions is less common, primarily confined to purebred animals that are usually trained and placed into competition to test their quality as future breeding stock. The majority of stallions are gelded at an early age and then trained for use as everyday working or riding animals.

If a stallion is not to be used for breeding, gelding the male horse will allow it to live full-time in a herd with both males and females, reduce aggressive or disruptive behavior, and allow the horse to be around other animals without being seriously distracted.[22] If a horse is not to be used for breeding, it can be gelded prior to reaching sexual maturity. A horse gelded young may grow taller[22] and behave better if this is done.[23] Older stallions that are sterile or otherwise no longer used for breeding may also be gelded and will exhibit calmer behavior, even if previously used for breeding. However, they are more likely to continue stallion-like behaviors than horses gelded at a younger age, especially if they have been used as a breeding stallion. Modern surgical techniques allow castration to be performed on a horse of almost any age with relatively few risks.[24]

In most cases, particularly in modern industrialized cultures, a male horse that is not of sufficient quality to be used for breeding will have a happier life without having to deal with the instinctive, hormone-driven behaviors that come with being left intact. Geldings are safer to handle and present fewer management problems.[23] They are also more widely accepted. Many boarding stables will refuse clients with stallions or charge considerably more money to keep them. Some types of equestrian activity, such as events involving children, or clubs that sponsor purely recreational events such as trail riding, may not permit stallions to participate.[citation needed]

However, just as some pet owners may have conflicting emotions about neutering a male dog or cat, some stallion owners may be unsure about gelding a stallion. One branch of the animal rights community maintains that castration is mutilation and damaging to the animal's psyche.[25]

A ridgling or "rig" is a cryptorchid, a stallion which has one or both testicles undescended. If both testicles are not descended, the horse may appear to be a gelding, but will still behave like a stallion. A gelding that displays stallion-like behaviors is sometimes called a "false rig".[26] In many cases, ridglings are infertile, or have fertility levels that are significantly reduced. The condition is most easily corrected by gelding the horse. A more complex and costly surgical procedure can sometimes correct the condition and restore the animal's fertility, though it is only cost-effective for a horse that has very high potential as a breeding stallion. This surgery generally removes the non-descended testicle, leaving the descended testicle, and creating a horse known as a monorchid stallion. Keeping cryptorchids or surgically-created monorchids as breeding stallions is controversial, as the condition is at least partially genetic and some handlers claim that cryptorchids tend to have greater levels of behavioral problems than normal stallions.[27][28]

Term for a male horse that has not been castrated

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Stallion - Wikipedia

Understanding Genetics – genetics.thetech.org

-A curious adult from CaliforniaAugust 6, 2004What a fun question! This sort of thing has been bothering me too lately. The usual statistic is that all people are 99.9% the same. But is that true for men and women?And what about our similarity to other animals? We are really only about 80% the same as a mouse at the genetic level so men and women are clearly more similar to each other than to mice. But what about chimpanzees? If people really are 98.7% the same as a chimpanzee, are male chimpanzees closer genetically to men than men are to women? As you know, men have an X and a Y chromosome and women have two X chromosomes. So besides the usual 0.1% (or 3.2 million base pair) difference between people, men and women differ by the presence of the Y chromosome.The Y chromosome is a tiny thing; it is about 59 million base pairs long and has only 78 genes. If we look at base pairs, the difference between men and women would be 59 million divided by 3.2 billion or about 1.8%. This translates to men and women being 98.2% the same.Men and women are actually a bit more similar as the Y chromosome has about 5% of its DNA sequences in common with the X chromosome. This would change the number to 98.4% the same.If the 98.7% number for chimp-human similarity is right, then by this measure, men and women are less alike than are female chimps and women. (More recent data suggests that chimps may be 95% instead of 98.7% the same, but this is still up in the air.) Now if we look at the gene level instead of at the base pair level, men and women become much more similar. If we assume 30,000 total genes, then men and women are about 99.7% the same instead of 98.4%. (I haven't been able to find a good number for how many genes chimpanzees and humans share.)So is the bottom line that men and male chimps have more in common than men and women? Of course not. If we take a closer look, we see some of the dangers of looking at raw percentages instead of individual changes.Another way to think about this is the 55 million or so differences between men and women are all concentrated on one chromosome and 78 genes. For chimps, the 42-150 million differences are spread out all over the chromosomes over many, many more genes.In other words, while the quantity of changes may be the same, the quality is different. Even though we share most of our genes with a chimpanzee, lots of the chimp's genes have changed in ways not seen in people. These changes make a chimp a chimp and a human a human.Some of the products of these changed genes in a chimp now do different things, or do things differently, do them in different places, do them more strongly or weakly, or even do nothing at all. It only takes a single DNA change to make a gene stop working and there are millions and millions of differences between you and a chimp. What all of this means is that in essence, chimps have many more "different" genes than the 78 different ones between men and women even though the % difference at the DNA level may be comparable. So, even if it may not seem like it sometimes, your brother has more in common with you than with a chimp.

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Understanding Genetics - genetics.thetech.org

WHO Classification of Tumours of the Urinary System and …

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Main Inheritance Patterns | Genes in Life

Genetictraitscan be passed from parent to child in different ways. As you will see, people can carry agenebut not be affected directly by it themselves. These patterns help to explain why a condition can seem to skip a generation or be more common in boys than in girls. Making a family health portrait, as described inHow Do I Collect My Family History?, can help to uncover these patterns.

Ourgenesare grouped into collections calledchromosomes. Most people have 46 chromosomes, in 23 pairs. One of the pairs is the sex chromosomes, called X and Y. Your sex chromosomes carry the genes that make you male or female. Women have two X chromosomes, and men have an X and a Y. The rest of your chromosomes are calledautosomalchromosomes. Let's see what happens when you have a gene that does not work the way it is supposed to on these chromosomes.

Autosomal Inheritance Patterns

Autosomal dominant

Autosomal dominant means that only one copy of the gene that does not work correctly is needed for someone to have the condition.

If one parent has an autosomal dominant condition, they have one functional copyof the gene and one copy that does not work properly. If the other parent has two copies of the gene that work correctly:

Autosomal dominant conditions, such as Huntingtons disease, affect males and females equally.

Autosomal recessive means that a person needs two copies of a gene that do not work properly to have the condition. In this pattern, people with one working copy of the gene and one copy of the gene that does not function correctly are called carriers. Carriers do not have any signs or symptoms of the condition, but they can still pass on the gene that does not function properly to their children. Usually, parents of children with anautosomal recessivecondition are carriers.

If both parents are carriers of a condition:

Autosomal recessive conditions, such as cystic fibrosis, affect males and females equally.

Your sex chromosomes carry the genes that make you a male or female. A female has two X chromosomes. A male has oneX chromosomeand oneY chromosome. If a gene for a condition is carried on the sex chromosomes, we say it is X-linked. X-linked patterns are not as simple as autosomal patterns, because they show up differently in males and females.

X-linked dominantinheritanceoccurs when a gene that does not work correctly on a single X-chromosome results in a condition. Conditions caused by X-linked dominance are rare, and the same condition can vary considerably in severity, especially among women.

The odds of passing down a condition that is X-linked dominant are different depending on whether the mother or father has the gene that does not function properly and on the sex of the child.

If a father has the condition:

If a mother has one working copy of the gene and one copy of the gene that does not work correctly:

Males are often more seriously affected than females by disorders inherited through X-linked dominance. Sometimes, even if a female inherits the gene change on one of her X chromosomes, she will not show symptoms or her symptoms will be less severe. It is thought that if a female has a working copy of the gene on one X-chromosome in addition to the altered copy on the other X-chromosome, the effects of the condition may be dampened. This has led some scientists to suggest that X-linked inheritance should not be described in terms of dominant and recessive, but rather simply be explained as X-linked inheritance.

Incontinentia pigmentiis an X-linked dominantdisorderthat affects multiple systems, but especially the skin.

X-linked recessive means that if there is one working copy of the gene, a person will not have the condition. The gene for these conditions is on the X chromosome. X-linked recessive conditions affect males more often than females. If a male has a copy of the gene that does not function the way it should on his only X chromosome, then he will be affected by the condition.

Some forms of hemophilia are X-linked recessive conditions.

If a father has an X-linked recessive condition:

If a female has two copies of the gene that do not function correctly, then she will be affected by the condition. If she has a working copy on one X chromosome and a copy of the gene that does not work the way it should on her other X chromosome, then she is called a carrier. Carriers are not affected by the condition, but they can still pass the gene that does not work correctly on to their children.

If a mother has an X-linked recessive condition, then she has two copies of the gene that do not function properly:

If a mother is a carrier of an X-linked recessive condition, she has one functional copy of the gene and one copy that does not function correctly:

If the mother is a carrier and the father has the condition, then there is a 1 in 2 chance (50%) that a daughter would be affected. She would always get the gene that does not work properly from her father, but she might get a working gene from her mother.

Most of our genes are stored in our chromosomes, which sit in each cells headquartersthe nucleus. We also have some genes in small structures in the cell called mitochondria. Mitochondria are sometimes called the power plants of the cell: they work on molecules to make them ready to give us the energy we need for our body functions. The mitochondrial genes always pass from the mother to the child. Fathers get their mitochondrial genes from their mothers, and do not pass them to their children.

Mitochondrial inheritance, also called maternal inheritance, refers to genes in the mitochondria. Although these conditions affect both males and females, only mothers pass mitochondria on to their children.

Diabetes mellitus and deafness, a rare form of diabetes, follows the mitochondrial inheritance pattern.

Check outGenetics Home Referencefor more about genetic conditions and inheritance.

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Main Inheritance Patterns | Genes in Life

Gay genetics | Science Focus

WANTED! Gay Men with a Gay Brother, reads the banner. Its held aloft by Dr Alan Sanders and a group of colleagues from NorthShore University near Chicago who are attending a gay pride festival. Theyre recruiting volunteers for a groundbreaking study that sets out to answer fundamental questions about who we are.

Were trying to locate genes that may influence variation in male sexual orientation, Sanders says. Volunteers from over 700 families responded. Researchers asked them questions about their sexuality, the size and structure of their families, and took DNA samples. Sanders is now analysing that data and the results could tell us once and for all whether theres such a thing as a gay gene.

The people participating in our study are interested in contributing to this kind of scientific knowledge and want to understand at least part of how they came to be the way they are, Sanders says.

The search for gay genes goes back to 1993, when a US team led by Dr Dean Hamer described a region of DNA located on the X chromosome called Xq28. The region also goes by another name: GAY-1, a genetic marker linked to male homosexuality.

The discovery caused Hamer to be attacked from all sides. Conservative, right-wing people hated it because they felt that it was saying that being gay is like being black, that it was in-born, that it would somehow excuse gay people or give them more rights, says Hamer. On the other hand, gay people hated it too because, at that time, there were fears that the discovery would be misused to abort gay babies and wipe gay people off the face of the Earth.

Although these fears remain, in recent years the search for gay genes has become more accepted by the gay community, in no small part because a biological explanation wouldundermine arguments that being gay is a social or lifestyle choice. Conservative attitudes remain unchanged, however. They continue to be vehemently opposed to any notion that homosexuality is something natural, says Hamer.

Despite their objections, theres a lot of evidence that homosexuality has a biological basis. While there hasnt been much research on lesbians, there has been on gay men. For instance, identical twin brothers (siblings derived from the same fertilised egg) are more likely to both be gay than fraternal twins (twins that develop from separate eggs). The fact that identical twins have the same DNA and fraternal twins share 50 per cent suggests that male homosexuality is hereditary.

It was scrutinising family trees to see how homosexuality is inherited that led Hamer to the discovery of Xq28. Now chief of the gene structure and regulation section at the US National Cancer Institute, his study revealed a curious pattern: gay men tended to have more gay uncles and gay male cousins on their mothers side of the family than on their fathers.

For geneticists thats fascinating because it suggests it could be due to X chromosome linkage those types of traits tend to run on the female side for males, says Hamer. This is because males inherit their X chromosome from their mother.

To track down the DNA region linked to the gay trait, Hamer used a technique called linkage mapping, an approach that lets geneticists find a gene even when they dont know what it does or where its located. Linkage mapping works because close relatives like brothers share not only a particular trait, such as homosexuality, but also the genes underlying the trait. When comparing bits of DNA from two brothers, the sequences will, on average, be the same 50 per cent of the time. So, if you study many pairs of gay brothers and find a DNA region thats the same in more than 50 per cent of cases, its likely to be linked to homosexuality. In this case, Hamer compared the X chromosomes from 40 pairs of gay brothers, and Xq28 stood out.

Inheriting the gay version of Xq28 wont necessarily make you homosexual. Our studies showed that it significantly increased the odds of being gay, but it was not determinative, says Hamer. Many people who are gay dont have any history of homosexuality in their families. He points out that some heterosexual men in his 1993 study also had the so-called gay gene. A subsequent study in 1999 failed to replicate Hamers results and other researchers are sceptical that Xq28 is linked to homosexuality at all.

Many scientists believe that exposure to hormones during pregnancy heavily influences sexuality. Hormones are chemical messengers, released by certain cells to affect the growth and development of other cells in the body. During pre-natal development, for example, the sex organs in a foetus can recognise testosterone, which will switch on genes to make it male.

Aside from a few superficial differences (among them penis and ring-finger length both longer in homosexuals), gay and straight mens bodies appear the same. The exception is homosexual mens brains, which show remarkable similarities to the brains of heterosexual women, suggesting that sexual orientation depends on the effect hormones have on the developing brain.

But these two factors only go so far in explaining how homosexuality develops. People assume that all of the biological influence on sexual orientation is either genes or hormones, says sexologist Ray Blanchard from the University of Toronto. They might account for the lions share of variance in sexual orientation, but it looks like theres some other bit that requires a third biological mechanism.

In 1996 Blanchard and Professor Tony Bogaert revealed a peculiar phenomenon: the more older brothers a boy has, the greater their chances of being homosexual. This fraternal birth order effect meant that each subsequent brother increases the odds of being gay by 33 per cent. An only child has a two per cent chance, but with 10 brothers the odds are over 20 per cent. But why the increasing odds? Blanchard believes its related to how a mothers body protects itself when pregnant with a son.

Theres only one system in the mother that would have the memory to know how many male foetuses shes previously carried: the immune system, says Professor Blanchard. According to his theory, a mothers immune system keeps track of the number of sons shes already had, producing antibodies to protect her against male-specific proteins entering her bloodstream, which often occurs during childbirth. As the mothers level of immunisation increases with each son, so too do the chances of variation from typical sexual orientation as, in theory, the mothers antibodies could cross the placenta and neutralise proteins that her son needs for normal sexual development.

Many of these male-specific proteins are found on the Y chromosome, DNA thats foreign to females. A lot of male-specific proteins are preferentially expressed in the testes and have a crucial role in sperm development, says Blanchard. Some are expressed in the foetal brain for reasons that no-one has established, but you wouldnt expect them to be expressed without a reason.

Blanchard believes that homosexuality is 100 per cent biological, and estimates that the fraternal birth order effect accounts for 15-30 per cent of gay men in the population. So what explains the rest?

Professor Andrea Camperio Ciani at the University of Padova in Italy has tested various hypotheses by studying 100 families of gay men. Not only did he replicate Blanchards birth order effect, he also detected inheritance of homosexuality on the mothers side, supporting Hamers idea of a gay gene on chromosome X. The maternal inheritance effect seems most important too.

Genetics explains 20-25 per cent for the moment, says Camperio Ciani. The rest is unknown. A part is environment; a part can be other genetic elements that we cannot perceive with our study. In principle, the genetic component might even be the Xq28 region.

Regardless of which regions of DNA are linked to homosexuality, the very existence of gay genes creates a Darwinian paradox. How would genes that cause homosexuality pass from one generation to the next, given that gay people reproduce less than heterosexuals? Natural selection opposes anything that might cause even a small reduction in the number of offspring you produce, so a gay trait would soon disappear from the gene pool. If you carry a trait that reduces your fecundity [the number of offspring you produce] by 10 per cent, in seven to eight generations your trait and all your descendents disappear, says Camperio Ciani.

The paradox was finally resolved by his 15-year-old daughter. After Camperio Ciani described the observed patterns in pedigrees of homosexuality the effects of maternal inheritance and birth order his daughter suggested that he re-check his data to see if the female relatives of gay men had more children on the mothers side. When Camperio Ciani went back to the lab, thats exactly what he found. Mothers and aunts on the maternal line of homosexuals had around one-fifth to one-fourth more kids than the heterosexual comparison, and also than the paternal line.

He thinks that the evolution of homosexuality is driven by a process called sexually antagonistic selection. Its where a genetic factor confers an advantage when expressed in one sex, but incurs an evolutionary cost in the other. In this instance, the gay genes dont exist to make men homosexual, instead theyre a consequence of fertility factors that help women reproduce.

Nipples are another example of a sexually antagonistic trait: theyre needed for feeding babies, but developing nipples in men is a waste of the bodys resources and allow errors leading to breast cancer.

Even if Camperio Cianis fecundity factors are the same as Hamers gay genes, it doesnt tell us what the specific genes actually do. Hamer speculates the genes might boost the size or connections from parts of the brain used in reproduction such as the hypothalamus to make people more libidinous.

Alan Sanderss study at NorthShore University could finally reveal the identity and function of gay genes. Sanders, director of the Behavior Genetics Unit, is comparing DNA from gay brothers to find shared genes that underlie sexual orientation. Hes initially using linkage mapping to find candidate regions. The large sample size over 700 families provides huge statistical power for detecting regions significantly linked to homosexuality. Sanders will then use sequences from databases like the Human Genome Project to pinpoint which genes are in these regions.

So what happens if gay genes are found? While they may confirm the idea that homosexuality has a biological basis, many people fear that the results could be used to discriminate against gay people. It is a valid concern, says Sanders. People we talked to at gay pride festivals have designer-baby kind of worries a genetic test employed in a pre-natal way, or for employment and insurance discrimination, maybe in the military too. Its not just an issue in sexual orientation, but intelligence or disease screening .

A test for gay genes also has a flipside: homosexual couples might exploit reproductive technology to have gay kids. This has been a huge debate in other areas, like deaf parents wanting to have deaf children, says Hamer, who has fathered a daughter with a woman from a lesbian couple. One of them said, If I had my choice, Id select the sexual orientation of my child. But this is all theoretical for now, as its not actually happening yet.

Genes that influence our sexual orientation further fuel the debate over what makes us who we are. For Hamer at least, sexual orientation is determined at birth. Its mostly biological, he says. The way a person acts is altered by culture, society and individual choice, but thats a different issue than the underlying deep-seated orientation.

Link:
Gay genetics | Science Focus

How Telehealth and Generic Drugs Are Allowing Companies To Treat Men’s Most Embarrassing Health Issues

When it comes to men and their health, the idea that men don’t care about their health comes from the alarming rate at which they don’t go to the doctor. Men care about their health, but many common sexual health issues lead to embarrassment and, usually, a lack of proactivity. Today, companies are forming to challenge and inspire self-care in men when it comes to their most common – and most embarrassing – health issues.

 

Hair loss, erectile dysfunction, and premature ejaculation are all very common health issues that plague men, a lot of men. According to the American Hair Loss Association, 25 percent of men with male pattern baldness begin losing their hair before they turn 21 years old. The Cleveland Clinic reports that 52 percent of men experience erectile dysfunction. The Mayo Clinic shares that as many as 1 in 3 men experience premature ejaculation at some point.

 

But why aren’t men going to their doctor’s office to talk about these issues more?

Hair, Sexual Wellness, and Self-Esteem

The answer is pretty simple: these issues are deeply rooted in the idea of masculinity and self-esteem, especially for younger men.

 

Andrew Dudum, founder of the new online men’s wellness brand Hims, is using this idea to fuel his new startup. Dudum recently spoke to Business Insider and stated, “between hair, sexual wellness, and skin, that makes up, from our testing, upwards of 85% what contributes to your self-esteem."

 

Hims mission is to normalize the information and conversation about these issues, while also offering a convenient solution to the issue – allowing men to order generic prescription products that treat these common health issues online without having to see a doctor in person.

H2: Telehealth and Expiring Patents

Hims isn’t the only company seizing this opportunity to change men’s health and, essentially, change the way men take control of their health and self-esteem. Other companies like Roman aim at men and erectile dysfunction directly, while a similar brand called Lemonaid offers treatment for men’s health, birth control pills for women, and more general health issues like UTIs and sinus infections.

 

These new companies are able to positively impact people’s health due to changes in telehealth laws. In the past, health insurance companies resisted paying for or offering reimbursements for telehealth services received because an in-person visit is not required. Today, roughly 80 percent of the U.S. is able to receive coverage and reimbursements for telehealth services. It’s possible for people to receive a prescription by filling out an online survey that provides similar information that an in-person doctor’s visit would offer.

 

Another opportunity is presenting itself this December when Teva Pharmaceuticals begins selling a generic version of Viagra. Pfizer, maker of Viagra, has a generic drug competition patent expiring in 2020 and sold a license to Teva to begin production of a generic form of the leading erectile dysfunction drug and selling it in 2017. A generic version means a cheaper price tag for men and allows companies like Hims to begin offering the generic version in their product kit for about the cost of visiting your doctor, with the added benefit of not having to speak about your common health issues in person.

 

Currently, Hims only offers hair loss products, with their complete hair kit offering prescription finasteride, the generic version of Merck’s once-exclusive name-brand hair loss drug Propecia. Other products in the kit include a DHT shampoo, minoxidil drops — two over-the-counter treatments that are found in Rogaine — and Biotin vitamin supplements. For $44, men can get the power of prescription drugs and common over-the-counter treatments from their phone, all without ever facing a doctor, a pharmacist, or even someone at a checkout counter.

Online Wellness Hubs

Hims is an example of what is sure to be a growing market for online health and wellness hubs. For Hims customers, Dudum wants to serve and help men through all stages of their life and their health challenges. In an interview with TechCrunch, Dudum states, “Maybe you come for hair loss products initially, but you come back for sexual wellness products, then cholesterol wellness products. We want to grow with you as different challenges arise.”

 

Hims’ mission of creating an empowered health culture and inspire proactive and preventative self-care can hopefully start to inspire self-care in men. The idea of telehealth and self-care is an idea that will persist in these new online wellness hubs and is one that men, and certainly their partners, can get behind.

Genetics | Female Cannabis Seeds

Gibberellic Acid

Sooner or later every grower is going to want to produce marijuana seeds. Developing a new stable strain is beyond the scope of this discussion and requires the ability to grow hundreds or even thousands of breeding plants. However, just about any grower can manage to preserve some genetics by growing f2 seeds where they have crossed a male and female of the same strain, or can produce a simple cross which would be referred to as strain1xstrain2 for instance white widow crossed with ak-47 would be referred to as a WW x AK-47. You can produce some excellent seed and excellent marijuana this way.

To Feminise or not to Feminise

There are numerous myths surrounding feminized seeds. Feminizing seeds is a bit more work than simply crossing two plants naturally. However it will save you a lot of time in the end. If you make fem seeds properly then there is no increased chance of hermaphrodites and all seeds will be female. This means no wasted time and effort growing males and it means that all your viable seeds produce useful plants, since roughly half of normal seeds are male this effectively doubles the number of seeds you have.

Other times you will have no choice but to produce feminized seed because it will be a female plants genetics that you want to preserve and you wont have any males. Perhaps you received these genetics via clone or didnt keep males.

The new thing on the market for commercial Cannabis cultivation are Autoflowering feminized strains. By crossing of the Cannabisruderalis with Sativa and Indica strains many cultivators have created interesting hybrids which boast benefits from both sides of these families.

Although Sensi Seeds already created the Ruderalis Indica and the Ruderalis Skunk crossing, the first variety to be marketed specifically as Autoflowering cannabis seed was the Lowryder #1. This hybrid was a crossing between a Ruderalis, a Williams Wonder and a Northern Lights #2. This strain was marketed by The Joint Doctor and was honestly speaking not very impressive. The genetics of the ruderalis was still highly present which caused for a very low yield and little psychoactive effect.

Despite these first disappointing results for the grower and user, the interest of the cannabis community was most definitely caught. After the Lowryder #1 the Lowryder #2 was introduced by The Joint Doctor. See also the article:What are autoflowering cannabis seeds about auto-flowering seeds.

Auto-flowering cannabis and the easily distributed seed have opened a whole new market in the world of the online grow-shop, making it easy for home growers with shortage of space to grow rewarding cannabis plants in many different varieties.

Selecting Suitable Parents

There are a number of important characteristics when selecting parents. First are you making fem seeds? If you are then both parents will be female. This makes things easier. If not then the best you can do is select a male with characteristics in common with the females you hope to achieve from the seed.

Obviously potency, yield, and psychoactive effects are critical to the selection process. But some other important traits are size, odor, taste, resistance to mold and contaminants, early finishing and consistency.

Collecting and Storing PollenIn order to collect pollen you simply put down newspaper around the base of the plant. The pollen will fall from the plant onto the newspaper. You can then put this newspaper into a plastic bag and store it in the refrigerator or freeze it. Pollen will keep for a few months in the refrigerator and can be used on the next crop. The freezer will extend that to up to six months but gives the pollen a lower chance of viability that increases with time.

Pollinating a Plant

To pollinate a plant you can brush the pollen on a flower with a cotton swab or you can take the plastic bag and wrap the flower inside it and shake. In this way you can selectively pollinate plants and even individual buds and branches.

Male Isolation

A male plant or a plant with male flowers will pollinate your entire crop rendering it seedy. You probably dont want THAT many seeds so how can you avoid it? Moving the male to another room might work but if that other room shares an air path via ducting or air conditioning then pollen may still find its way. One technique is to construct a male isolation chamber.

A male isolation chamber is simply a transparent container such as a large plastic storage tub turned on its side (available at your local megamart). Get a good sized PC fan that can be powered with pretty much any 12v wall adapter, by splicing together the + (yellow or red on fan, usually dotted on power adapter) and the wires (black on fan, usually dotted power adapter) just twist with the like wire on the other device and then seal up the connection with electric tape. Then take a filtrate filter and cut out squares that fit the back of the pc fan so that the fan pulls (rather than pushes) air through the filter. Tape several layers of filter to the back of the pc fan so all the air goes through the filter. Now cut a large hole in the top of the plastic container and mount the pc fan over top of it so it pulls air out the box. You can use silicon sealant, latex, whatever youve got that gives a good tight seal.

This can be used as is, or you can cut a small intake in the bottom to improve airflow. Pollen wont be able to escape the intake as long as the fan is moving but you might put filter paper over the intake to protect against fan failures. You can also use grommets to seal holes and run tubing into the chamber in order to water hydroponically from a reservoir outside the chamber. Otherwise you will need to remove the whole chamber to a safe location in order to water the plant or maintain a reservoir kept inside the chamber.

Making Feminised Seed

To make feminized seed you must induce male flowers in a female plant. There is all sorts of information on the Internet about doing this with light stress (light interruptions during flowering) and other forms of stress. The best of the stress techniques is to simply keep the plant in the flowering stage well past ripeness and it will produce a flower.

Stress techniques will work but whatever genetic weakness caused the plants to produce a male flower under stress will be carried on to the seeds. This means the resulting seeds have a known tendency to produce hermaphrodites. Fortunately, environmental stress is not the only way to produce male flowers in a female plant.

The ideal way to produce feminized seed through hormonal alteration of the plant. By adding or inhibiting plant hormones you can cause the plant to produce male flowers. Because you did not select a plant that produces male flowers under stress there is no genetic predisposition to hermaphroditism in the seed vs plants bred between a male and female parent. There are actually a few ways to do this, the easiest I will list here.

Colloidal Silver (CS)

This is the least expensive and most privacy conscious way to produce fem seed. CS has gotten a bad name because there is so much bad information spread around about its production and concentrations. It doesnt help that there are those who believe in drinking low concentration colloidal silver for good health and there is information mixed in about how to produce that low concentration food grade product. Follow the information here and you will consistently produce effective CS and know how to apply it to get consistent results.

Simply construct a generator using a 9-12v power supply (DC output, if it says AC then its no good) that can deliver at least 250ma (most wall wart type power supplies work, batteries are not recommended since their output varies over time). The supply will have a positive and negative lead, attach silver to each lead (contrary to Internet rumors, you arent drinking this is cheap 925 silver is more than pure enough) you can expose the leads by clipping off the round plug at the end and splitting the wires, one will be positive and the other negative just like any old battery. Submerge both leads about 2-3 inches apart in a glass of distilled water (roughly 8oz). Let this run for 8-24hrs (until the liquid reads 12-15ppm) and when you return the liquid will be a purple or silver hue and there may be some precipitate on the bottom.

This liquid is called colloidal silver. It is nothing more or less than fine particles of silver suspended in water so it is a completely natural solution and is safe to handle without any special precautions. The silver inhibits female flowering hormones in cannabis and so the result is that male flowering hormone dominates and male flowers are produced.

To use the silver, spray on a plant or branch three days prior to switching the lights to 12/12 and continue spraying every three days until you see the first male flowers. Repeated applications after the first flowers appear may result in more male flowers and therefore more pollen. As the plant matures it will produce pollen that can be collected and used to pollinate any female flower (including flowers on the same plant).Silver Thiosulfate (STS)

Only mentioned for completeness. Silver Thiosulfate is more difficult to acquire and works on the same principle as CS. Its application is similar to CS and achieves the same results.

Gibberellic Acid (GA3)

This is probably the most popular way to produce feminized seed. GA3 can be purchased readily in powdered form, a quick search reveals numerous sources on e-bay for as little as $15. Simply add to water to reach 100ppm concentration and spray the plant daily for 10 days during flowering and male flowers will be produced.

Article: Marijuana Cultivation/Producing Seeds http://en.wikibooks.org/wiki/Marijuana_Cultivation/Producing_Seeds

Tags: auto-flowering, Autoflowering, Breeding, Colloidal Silver, Cross, Crossing, F2, Feminized, Feminized Seeds, Feminizing Seeds, Flowers, Genetics, Gibberellic Acid, Hermaphrodites, Hybrid, Parents, Pollen, Pollinate, Pollination, Potency, Produce Marijuana Seeds, Producing Feminized Seeds, Psychoactive Effects, Seeds, Silver Thiosulfate, Spraying Spray, Yield

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Genetics | Female Cannabis Seeds

Sandwalk: The Genetics of Eye Color

The genetics of blood type is a relatively simple case of one locus Mendelian geneticsalbeit with three alleles segregating instead of the usual two (Genetics of ABO Blood Types).

Eye color is more complicated because there's more than one locus that contributes to the color of your eyes. In this posting I'll describe the basic genetics of eye color based on two different loci. This is a standard explanation of eye color but, as we'll see later on, it doesn't explain the whole story. Let's just think of it as a convenient way to introduce the concept of independent segregation at two loci. Variation in eye color is only significant in people of European descent.

At one locus (site=gene) there are two different alleles segregating: the B allele confers brown eye color and the recessive b allele gives rise to blue eye color. At the other locus (gene) there are also two alleles: G for green or hazel eyes and g for lighter colored eyes.

The B allele will always make brown eyes regardless of what allele is present at the other locus. In other words, B is dominant over G. In order to have true blue eyes your genotype must be bbgg. If you are homozygous for the B alleles, your eyes will be darker than if you are heterozygous and if you are homozygous for the G allele, in the absence of B, then your eyes will be darker (more hazel) that if you have one one G allele.

Here's the Punnett Square matrix for a cross between two parents who are heterozygous at both alleles. This covers all the possibilities. In two-factor crosses we need to distinguish between the alleles at each locus so I've inserted a backslash (/) between the two genes to make the distinction clear. The alleles at each locus are on separate chromosomes so they segregate independently.*

As with the ABO blood groups, the possibilities along the left-hand side and at the top represent the genotypes of sperm and eggs. Each of these gamete cells will carry a single copy of the Bb alleles on one chromosome and a single copy of the Gg alleles on another chromosome.

Since there are four possible genotypes at each locus, there are sixteen possible combinations of alleles at the two loci combined. All possibilities are equally probable. The tricky part is determining the phenotype (eye color) for each of the possibilities.

According to the standard explanation, the BBGG genotype will usually result in very dark brown eyes and the bbgg genotype will usually result in very blue-gray eyes. See the examples in the eye chart at the lower-right and upper-left respectively. The combination bbGG will give rise to very green/hazel eyes. The exact color can vary so that sometimes bbGG individuals may have brown eyes and sometimes their eyes may look quite blue. (Again, this is according to the simple two-factor model.)

The relationship between genotype and phenotype is called penetrance. If the genotype always predicts the exact phenotpye then the penetrance is high. In the case of eye color we see incomplete penetrance because eye color can vary considerably for a given genotype. There are two main causes of incomplete penetrance; genetic and environmental. Both of them are playing a role in eye color. There are other genes that influence the phenotype and the final color also depends on the environment. (Eye color can change during your lifetime.)

One of the most puzzling aspects of eye color genetics is accounting for the birth of brown-eyed children to blue-eyed parents. This is a real phenomenon and not just a case of mistaken fatherhood. Based on the simple two-factor model, we can guess that the parents in this case are probably bbGg with a shift toward the lighter side of a light hazel eye color. The child is bbGG where the presence of two G alleles will confer a brown eye color under some circumstances.

*If the two genes were on the same chromosome this assumption might be invalid because the two alleles on the same chromosome (e.g., B + g) would tend to segregate together. Linked genes don't obey Mendel's Laws and this is called linkage disequilibrium.

Continued here:
Sandwalk: The Genetics of Eye Color

Budgie Parakeet Colors, Varieties, Mutations, Genetics

Budgie parakeets come in so many colors and mutations they remind me of jellybeans! These birds are part of our family flock.

Original Australian wild type green budgerigar parakeet

In the wild, Budgie Parakeets are green with yellow, with black stripes and markings, and dark blue-green-black flight and tail feathers. Captive breeding programs, however, have produced Budgies in almost every color of the rainbow, except red and pink. They are so colorful, they remind me of jellybeans!

All captive budgerigars are divided into two basic series of colors: white-based (includes skyblue, cobalt, mauve, gray, violet, and white) and yellow-based (includes light-green, dark-green, gray-green, olive, and yellow). Green (yellow base) is dominant and blue (white base) is recessive.There are at least 32 primary mutations in the budgerigar, enabling hundreds of possible secondary mutations and color varieties!

One of my all time personal favorite mutation combinations is pictured below I call it a Rainbow Spangle. Toto, a budgie raised by us, is a yellow-face type 2 sky-blue opaline spangle.

A combination of several mutations, I call this a Rainbow Spangle.

Green (yellow base) is dominant and blue (white base) is recessive.

There are 3 color variations for both the white base colorand the yellow base color. In the yellow base color, the dark factor genes make these color variations:

Yellow Base Color:0 dark factors = light green1 dark factors = dark green2 dark factors = olive

Mutations like Lutinos and Double-Factor Spangles still have dark factors but they are not seen visually.

Lutino

Light-Green (additional mutations present: Opaline, Spangle)

Dark-Green

Dark Factor budgie parakeet breeding punnett square

Blue (white base) is recessive to green (yellow base).

There are 3 color variations for both the white (blue) series and the yellow (green) series birds. In the white series, the dark factor genes make these color variations:

White (blue) series:0 dark factors = skyblue1 dark factors = cobalt2 dark factors = mauve

Albinos and Double-Factor Spangles still have dark factors but they are not seen visually.

Albino

Skyblue (other mutation present: Cinnamon-Wing)

Cobalt(other mutation present:Yellowface type 1)

The violet factor affects both white-based (blue) and yellow-based (green) colors.

Violet (other mutation present: Sky-blue, Greywing)

Violet (other mutations present: Sky-blue, Opaline, Spangle)

Violet (other mutations present: Cobalt)

Violet Factor budgie parakeet breeding punnett square

The gray factor affects both white-based (blue) and yellow-based (green) colors.

Gray normal English x American budgie

Gray yellowface spangle budgie parakeet

Gray-green opaline baby English Budgie

Gray factor budgie parakeet breeding punnett square

In addition to a dark factor, budgies may also have a degree of dilution. There are four types of dilution: Greywing, Full-Body-Color Greywing, Clearwing, and Dilute.

Dilute blue opaline American parakeet

When a budgie has two of the recessive Dilute genes, its markings and color are about 70% washed out when compared to a normal.

Greywing blue American Parakeet

Greywing light-green American parakeet

A homozygous Greywing (or a Greywing budgie with the recessive Dilute gene) has gray wing markings and a 50% diluted body color.

Full-Body-Color Greywing light green American parakeet

When a budgie has both the Greywing and Clearwing gene, it is a Full-Body-Color Greywing with grey wing markings and bright body color.

Clearwing dark green American parakeet

A homozygous Clearwing (or a Clearwing budgie with the recessive Dilute gene) has less pigment in the wings, causing very light markings, and more pigment in the body feathers, causing a bright body color.

Normal = dominantGreywing = recessive, co-dominant with clearwingClearwing = recessive, co-dominant with greywingDilute= recessive

normal + normal = normalnormal + greywing = normal split for greywingnormal + clearwing = normal split for clearwingnormal + dilute = normal split for dilutegreywing + greywing = greywinggreywing + clearwing = full body color greywinggreywing + dilute = greywing split for diluteclearwing + clearwing = clearwingclearwing + dilute = clearwing split for dilutedilute + dilute = dilute

Two full body color greywings =50% full body color greywing25% greywing25% clearwing

Dilute budgie parakeet breeding punnet square

Lutino American parakeet (solid yellow with red/pink eyes)

Albino American parakeet (solid white with red/pink eyes)

The ino gene removes all the melanin (the substance that creates all the dark colors) removed, so a blue series budgie becomes white (Albino) and a green series one become yellow (Lutino). The gene also removes the dark shade from the skin and beak leaving them with pink legs and an orange beak. The dark color of the eye is also gone leaving a red eye with a white iris ring, and the cheek patches are silvery white. It removes the blue shade from the cocks cere too so hell have a pink/purple colored cere; the hens cere is the usual white to brown shade. Because usually only the white and yellow colors are left, an ino can hide the fact that it also has other varieties present genetically. The only varieties that show are the yellow faces or golden faces and they are only obvious on an albino budgie.

The ino gene is sex-linked and recesssive:

ino x ino =100% ino

ino cock x normal hen =50% normal split for ino cocks50% ino hens

normal cock x ino hen =50% normal split for ino cocks50% normal hens

normal split for ino cock x normal hen =25% normal cocks25% normal split for ino cocks25% ino hens25% normal hens

Albino / Lutino / Ino budgie parakeet breeding punnett square

Yellowface type 1 blue English budgie

Yellow face gray dominant pied English budgie

Yellowface budgies are in between yellow-based budgies and white-based budgies and the genetics are complicated. There are different degrees of the level of yellow pigment but it is less than the yellow-based variety. The double factor birds contain less yellow than single factor birds. The Yellowface mutation is possible in all of the blue series birds, including Albinos, Dark-Eyed Clears, Grays, Violets and in all their three depths of shade (ie. Skyblue, Cobalt, Mauve). Green series birds can mask a Yellowface character, and they can carry both Yellowface and Blue splits at the same time. Visually, there are two types of Yellowface: Type 1 and Type 2:

Yellowface type 1 skyblue single-factor violet clearflight pied opaline American parakeet

In Type 1, the yellow is confined to the mask feathers, plus maybe the peripheral tail feathers, only. The body feathers are normally colored.

Yellowface type 2 skyblue Greywing American Parakeet. The Yellowface type 2 mutation bleeds down into the blue body color, creating a seafoam-green effect.

Yellow face type 2 American parakeet. With the YF 2 mutation, the yellow spreads into the blue body color to create turquoise.

Type 2 Yellowface budgies have yellow in the mask feathers and tail, just like the Type 1. However, after the first molt at around 3 months of age, the yellow diffuses into the body color and creates a new color, depending on the original color. The single factor (SF) Yellowface 2 Skyblue variety is like a normal Light Green but has a very bright body color midway between blue and green a shade often called sea-green or turquoise. The body feathers of the SF Yellowface 2 Cobalt are bottle-green and in the SF Yellowface 2 Mauve they are a mixture of mauve and olive. The double factor (DF) Yellowface 2 Skyblue variety is very similar to the Yellowface 1 Skyblue, but the yellow pigmentation is brighter, and tends to leak into the body feathers to a greater extent.

In combination with the Blue, Opaline and Clearwing mutations, the single factor (SF) Yellowface 2 mutation produces the variety called Rainbow.

The yellowface type 2 gene is dominant to the yellowface type 1, meaning that it is visually expressed and the type 1 is masked in a genotypically type 1 x type 2 bird. When two yellowface type 1 skyblues are paired together, half the chicks will be yellowface type 1 skyblues and half will be normal skyblues in appearance. But half of these apparent skyblues will be double factor (DF) yellowface 1s. Here are the breeding expectations using punnett squares:

Yellowface budgie parakeet breeding punnett square

Cinnamon-Wing gray-green English Budgie baby

Cinnamon-wing sky-blue English budgie hen

All the markings which appear black or dark gray in the Normal appear brown in the Cinnamon. The Cinnamon markings on cocks tend to be darker than on hens. The long tail feathers are lighter than Normals. The body color and cheek patches are much paler, being about half the depth of color of the Normal. The feathers of Cinnamons appear tighter than Normals, giving a silky appearance. The eyes of the newly-hatched Cinnamon are not black like the eyes of Normals, but deep plum-colored. This color can be seen through the skin before the eyes open. A few days after the eyes open, the eye darkens and is then barely distinguishable from the that of a Normal chick, but by this time the difference in down color is visible: Normal chicks have gray down, but Cinnamon (and Opaline and Ino) chicks have white. The skin of Cinnamon chicks is also redder than Normals, and this persists into adulthood: the feet of Cinnamons are always pink rather than bluey-gray. The beak tends to be more orange in color.

In birds, the cock has two X chromosomes and the hen has one X and one Y chromosome. So in hens whichever allele is present on the single X chromosome is fully expressed in the phenotype. Hens cannot be split for Cinnamon (or any other sex-linked mutation). In cocks, because Cinnamon is recessive, the Cinnamon allele must be present on both X chromosomes (homozygous) to be expressed in the phenotype. Cocks which are heterozygous for Cinnamon are identical to the corresponding Normal. Such birds are said to be split for Cinnamon. The Cinnamon with Ino can create the Lacewing variety.

Cinnamon is a sex-linked recessive gene:

cinnamon x cinnamon =100% cinnamon

cinnamon cock x normal hen =50% normal split for cinnamon cocks50% cinnamon hens

normal cock x cinnamon hen =50% normal split for cinnamon cocks50% normal hens

normal split for cinnamon cock x normal hen =25% normal cocks25% normal split for cinnamon cocks25% cinnamon hens25% normal hens

normal split for cinnamon cock x cinnamon hen =25% normal cocks25% normal split for cinnamon cocks25% cinnamon hens25% normal hens

Cinnamon-wing budgie parakeet breeding punnett square

Opaline parakeet on the right, normal on the left.

The striping pattern on the head feathers is reversed so that there are thicker white areas and thinner black stripes. Another feature of this mutation is that the body feather color runs through the stripes on the back of the neck and down through the wing feathers. Opaline budgies tails are characteristically patterned with light and colored areas running down the tail feather. Most Opalines show a brighter body color than the corresponding non-Opaline, particularly in nest feather and in the rump area. The Opaline (and the Cinnamon) can be identified at a very early age because the color of the down feathers of the young nestling are white instead of the usual gray.

Opaline is a sex-linked recessive gene:

opaline x opaline =100% opaline

opaline cock x normal hen =50% normal split for opaline cocks50% opaline hens

normal cock x opaline hen =50% normal split for opaline cocks50% normal hens

normal split for opaline cock x normal hen =25% normal cocks25% normal split for opaline cocks25% opaline hens25% normal hens

normal split for opaline cock x opaline hen =25% normal cocks25% normal split for opaline cocks25% opaline hens25% normal hens

Single Factor Spangle violet opaline American parakeet x English budgie cross

Double Factor Spangle English budgie

SINGLE Factor Spangle: The markings on the wings, the throat spots and the tail feathers are altered on the single factor Spangle. The feathers have a white or yellow edge, then a thin black pencil line, then the center of the feather is yellow or white. The throat spots are often all or partly missing but if present look like targets, with a yellow or white center. The long tail feathers can be like the wing feathers with a thin line near the edge, or they may be plain white, yellow or solid dark blue as in a normal.

DOUBLE Factor Spangle: Pure white or yellow bird, though sometimes with a slight suffusion of body color.

Both types of Spangle have normal dark eyes with a white iris ring and normal ceres. Their feet and legs can be gray or fleshy pink. They can have either violet or silvery white cheek patches (or a mixture of both).

Spangle Breeding Outcomes:

Spangle is an incomplete dominant gene. This means it has three forms: the non-spangle, the single factor spangle and the double factor spangle. Spangle genetics sometimes do not act as expected.

normal x single factor spangle =50% normal50% single factor spangle

normal x double factor spangle =100% single factor spangle

single factor spangle x single factor spangle =25% normal50% single factor spangle25% double factor spangle

single factor spangle x double factor spangle =50% single factor spangle50% double factor spangle

double factor spangle x double factor spangle =100% double factor spangle

Spangle budgie parakeet breeding punnett square

All pied budgerigars are characterized by having irregular patches of completely clear feathers appearing anywhere in the body, head or wings. These clear feathers are pure white in blue-series birds and yellow in birds of the green series. Such patches are completely devoid of black melanin pigment. The remainder of the body is colored normally.

Dominant Pied (single factor) yellow face type 2 skyblue English budgie

Dominant pied (single factor) skyblue American parakeet

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Budgie Parakeet Colors, Varieties, Mutations, Genetics

How animal genes go into battle to dominate their offspring – Gears Of Biz

Authors

Director of the Ecology Institute, Universidad Nacional Autnoma de Mxico (UNAM)

Professor of Evolutionary Biology and Speciation, University of St Andrews

University of St Andrews

The burdens of becoming parents are often shared unequally between male and female animals. This is particularly true of species that give birth to live young, where male duties such as defending the breeding territory and building dens or nests rarely compare with the ordeals of pregnancy and labour.

You might have thought that animals just accept this imbalance and get on with it. But actually, they compete over how much each parent contributes. This isnt like the competition to win a mate, with locking horns or displays of plumage. Instead this remarkable battle takes place at the level of the genes.

It now appears it may have evolved very early in animal evolution, perhaps among the first child-bearing animals. What is more, it may even help to explain why animals diversified into different lineages.

One arena in which this battle plays out is over the size of offspring. In principle its in both a mothers and fathers interests to produce bigger newborns, since they are more likely to prevail in the struggle for food and survival.

Yet live-bearing females are more likely to die giving birth to larger offspring or become unable to reproduce again. Their mates neednt care unless they are likely to sire more broods together, as with humans and certain gibbons, wolves and mice. Otherwise, the males only concern is that their mate invests as much as possible in the offspring they produce together.

This common conflict of interests manifests itself in various ways in nature. Males often desert pregnant females from birds to humans, for example thereby leaving them with the burden of bringing up the young. More rarely, in some normally biparental species females desert males. We see this in some beetles, for example.

The genetic battle mentioned previously is another manifestation of this conflict. The males of many species can manipulate the genes that they pass on to their offspring so that they induce extra growth at the expense of the mother. As with desertion, this effectively hands the female a greater share of the child-bearing burden than is in her interests.

It works as follows. When an embryo grows inside its mother, it consumes resources from her, signalling its metabolic needs along the way. These signals are influenced by certain hormones which either come from the growth genes of the mother or father. The males manipulate the females to deliver more resources by increasing the extent to which these hormones are produced through a chemical modification of their growth genes during sperm formation.

Females have evolved mechanisms to resist this. They can, for instance, pass on to their offspring what is known as a silenced copy of their own growth gene. This can counterbalance the male genes influence by making the embryo grow less than it otherwise would.

This battle is far less prevalent in truly monogamous species, including humans. This goes back to the fact that it becomes less genetically necessary where the two parents have a common interest in the female producing more offspring in future.

British microbiologist David Haig first proposed in 2003 that this battle was more likely in organisms where one sex disproportionately contributes to the offspring, such as live-bearing species, particularly polygamous ones. This was used to explain the puzzling size of the offspring of crosses between oldfield mice and deer mice.

Separately, these species produce similar sized offspring. Yet crosses between male deer mice and female oldfield mice produce offspring that are larger, while the offspring from female deer mice and oldfield males are smaller. Oldfield mice are monogamous while deer mice are polyandrous, meaning one female mates with several males.

Mimicking nature by artificially manipulating a growth gene called igf2, researchers showed that these smaller and larger offspring were due to genetics. In further support of the theory, placental mammals and marsupials including kangaroos and opossums have since been found to have signs of female resistance to such male manipulation.

How early did this mechanism evolve? Researchers have previously suggested it arose in live-born mammals, and would therefore be absent in egg-laying mammals such as the platypus and other vertibrates.

But that raises questions about all the reptiles, amphibians and fish which produce live young, since the same genetic manipulation would equally be in their males interests. To see if it was present, we looked at a Mexican fish called the amarillo or dark-edged splitfin (see lead image).

Along with co-researchers Yolitzi Saldvar and Jean Philippe Vielle Calzada, we crossed males and females from two distant populations of these fish, since they would not have evolved mechanisms which cancel one another out in the way that a single population is likely to have. Sure enough, the size of the embryos was influenced by the specific combination of father and mother. We found signs of male manipulation and probable resistance from the females.

Though based on a small sample size, this suggests that these mechanisms evolved much earlier than previously believed: fish split from other vertebrates some 200m years before live-bearing mammals appeared, dating back about 370m years in total. Whether it comes from a single evolution or from several in different lineages, we cannot yet tell.

One consequence of these genetic battles is the effect on reproductive compatibility within a species. The genetic mutations aimed at manipulating offspring that take place among males and females within a certain group of a species are like a sort of arms race. The genes continually adapt and counter-adapt to one another to try and further their reproductive interests.

If they then mate with an animal from a different group of the same species, their genetic mutations can have made them sufficiently unmatched over time that they are unable to reproduce thus they are now two species. If this started happening much earlier in evolution than was previously thought, it is likely to have influenced how different groups of live-born animals diverged, including lizards, sharks and mammals. From little acorns, these are the kinds of big oak trees that can grow.

This article was originally published on The Conversation. Read the original article.

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How animal genes go into battle to dominate their offspring - Gears Of Biz

The Genetics of Male Infertility | The Turek Clinics

High technology approaches to fertility, including ICSI, are really a two edged sword: they allow us to treat severe male infertility, but they may alter natural selection in that decisions regarding sperm and eggs are made in the laboratory and not by nature.

Dr. Paul Turek

Among the 15% of couples who experience infertility, about 40% of the time the infertility is due to male factors. About half of male infertility cases are due to defined reasons, including varicocele, infection, hormone imbalances, exposures such as drugs or medications, x-rays, tobacco use and hot tubs, blockage of the reproductive tract ducts, and previous surgery that has left scarring. Another cause of male infertility that has been underestimated in the past, but is now gaining in importance is genetic infertility. The reason for its increased importance is that our knowledge about genetics is growing so quickly. Men who may have had unexplained infertility in the past may now be diagnosed with genetic causes of infertility through recently available testing. In fact, this field is progressing so quickly that genetic infertility has already become one of the most commonly diagnosed reasons for male infertility.

Developed in the early 1990s, assisted reproduction in the form of IVF and ICSI (intracytoplasmic sperm injection) is a revolutionary laboratory technique in which a single sperm is placed directly inside an egg for fertilization. This technique has opened the door to fertility for men who formerly had few available treatment options, as it allows men who were previously considered severely infertile or sterile the possibility of fatherhood. However, with ICSI sperm are chosen by laboratory technicians and not by nature and because of this, it is not clear what barriers to natural selection are altered. Thus, along with this technology comes the possibility of passing on to a child certain genetic issues that may have caused the fathers infertility, or even more severe conditions. Another reason to know whether male

Infertility is genetic or not is because classic treatments such as varicocele repair or medications given to improve male infertility. In fact, Dr Turek was one of the first to publish on this issue, showing that varicocele repair was not effective in improving fertility in men with genetic infertility. Because he recognized these issues early on, Dr. Turek, while at UCSF in 1997, founded the first formal genetic counseling and testing program for infertility in the U.S. Called the Program in the Genetics of Infertility (PROGENI), Dr. Tureks program has helped over 2000 patients at risk for genetic infertility to navigate the decision-making waters that surround this condition.

Men with infertility should be seen by a urologist for a thorough medical history, physical examination, and appropriate medical testing. If genetic infertility is a possibility, then a genetic counselor can help couples understand the possible reasons, offer appropriate genetic testing, and discuss the complex emotional and medical implications of the test results. The approach taken early on by Dr. Turek is outlined in Figure 1. Just like the medical diagnosis from a urologist or fertility specialist, information about family history plays a critical role in genetic risk assessment. This approach to genetic evaluation, termed non-prescriptive, has been the corner- stone of Dr. Tureks critically acclaimed clinical program that now has over a dozen publications contributing to our current knowledge in the field. It is important to note that a lack of family history of infertility or other medical problems does not eliminate or reduce the risk of genetic infertility. In fact, a family history review will often be unremarkable. However, family history can provide crucial supporting in- formation toward making a genetic diagnosis (such as a family history of recurrent miscarriages or babies born with problems). Dr. Turek has published that having a genetic counselor obtain family history information is much more accurate than simply giving patients a written questionnaire to fill out and bring to their visit. A genetic counselor can also discuss appropriate genetic testing options and review the test results in patients in a meaningful way.

When speaking to Dr. Tureks genetic counselor about genetic testing, keep in mind that he or she will not tell you what to do. Genetic counselors are trained to provide information, address questions and concerns, and support you in the decision making process. A genetic counselor does not assume which decisions are most appropriate for you.

Among the various infertility diagnoses that men have, some are more commonly associated with genetic causes. Diagnoses that can have genetic causes include men nonobstructive azoospermia (no sperm count), oligospermia (low sperm count), and congenital absence of the vas deferens. A list of some of the best- described causes of genetic male infertility and their frequencies and associated conditions are listed in Table 1.

Nonobstructive azoospermia is defined as zero sperm count in the ejaculate due to an underlying sperm production problem within the testicles. This is quite dif- ferent from obstructive azoospermia in which sperm production within the testes is normal, but there is a blockage in the reproductive tract ducts that prevents thesperm from leavingthe body. There can be changes in the levels of reproductive hormones, such as follicle stimulating hormone (FSH), observed withnonobstructiveazoospermia. Most commonly, the FSH is elevated in this condition, which is an appropriate and safe hormone responseofthe pituitary gland to states of low or no sperm production. This diagnosis is associated with a 15%chance forhaving chromosome abnormalities(Figure 2) and a 13% chance for having gene regions missing on the Y chromosome (termed Y chromosome microdeletions, Figure3). To detect these changes, blood tests are typically offered to men with nonobstructive azoospermia.

Oligospermia that places men at risk for genetic infertility occurs when the ejaculate contains a sperm concentration of

Congenital absence of the vas deferens is characterized by the malformation or absence of the ducts that allow sperm to pass from the testicles into the ejaculate and out of the body during ejaculation. The duct that is affected in this condition is the vas deferens. This is the same duct that is treated during a vasectomy, a procedure for men who want birth control. Men with this condi tion are essentially born with a natural vasectomy. This congenital condition is associated with mutations and/or variations in the genes for cystic fibrosis (the CFTR gene) in 70-80% men if the vas deferens is absent on both sides, but less than this if the duct is missing on only one side. For most men with this condition with a mutation in the cystic fibrosis gene, the missing vas deferens is the only problem that results from this genetic change and they do not have the full spectrum of symptoms associated with cystic fibrosis, the most common genetic disease in the U.S. and generally lethal in early adulthood.

A less common reason for men to have a zero sperm count (azoospermia) than nonobstructive azoospermia is obstructive azoospermia. In essence, this is an unexplained zero sperm count due to a blockage of the reproductive tract ducts leading from the testicle to the ejaculate. Blockages are most commonly found in the epididymis but can also be located in the vas deferens or ejaculatory ducts. Most cases of obstructive azoospermia are amendable to surgical repair and naturally fertility is common. However, a high proportion of these men (47%) have mutations in the cystic fibrosis gene (CFTR) or harbor variations in the CFTR gene, termed 5T alleles. As such, genetic counseling and testing is also important in these patients.

These conditions represent only the most common genetic conditions encountered when evaluating men for genetic infertility. For this reason, consider reading Dr. Turekspublished paper that discusses most of the currently understood syndromes and conditions that are associated with infertility. It is also important to remember that if all genetic test results are normal, there is still a possibility that the infertility has a genetic cause. However, in many cases, medical science is currently unable to offer testing to detect it.

If a man has a chromosome abnormality identified as the cause of infertility, then depending on the chromosome abnormality detected, there may be a higher risk for children to be born with birth defects or mental impairment. This occurs as a result of a child inheriting from the father an imbalance in chromosome material. A genetic counselor can provide more detailed information about such potential risks, and offer other resources for individuals who have been diagnosed with a chromosome abnormality. There may be support organizations available to help men with genetic diagnoses and their partners cope with the impact of this information. Some couples find it helpful to talk to others in similar circumstances.

If a man is diagnosed with a Y chromosome deletion, then he will pass on that Y chromosome deletion to any son he conceives. To his daughters, he will pass on his X chromosome, instead of the Y chromosome. It is assumed that any son inheriting a Y chromosome deletion from his father will also have infertility. It is unclear whether the type and severity of the infertility will be different from the fathers. So far, there have only been a few reports of sons born to fathers with Y chromosome deletions after conception by assisted reproduction. As expected, there has not been an increase in the rate of birth defects or other problems for these boys, although this group is still small in number, and too young to have fertility evalua- tions.

Transmission of CFTR mutations in cases of infertility due to congenital absence of the vas deferens is somewhat more complex than either Y microdeletions or a chromosome abnormality. This is because there are over 1400 described muta- tions in the CFTR gene and the impact of mutations differs depending on which one is present. In general, the partner of an affected man should be tested as well, so that the residual risk of a child having either congenital absence of the vas deferens or full-blown cystic fibrosis can be estimated.

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The Genetics of Male Infertility | The Turek Clinics

New ways to target low sperm count? – Genetic Literacy Project

August 30, 2017 | Case Western Reserve School of Medicine

[Ahmad Khalil, Assistant Professor of Genetics and Genome Sciences at Case Western Reserve University School of Medicine] and colleagues have been working to understand genetic mechanisms behind male infertility.

His work focuses on long strands of genetic material with elusive functions. The strands, called long non-coding RNAs or lncRNAs dont seem to encode proteins, but have been implicated in everything from cancer to brain function. Many are located in the testes, suggesting they could also play a role in fertility.

A team of seven researchers, led by Khalil, collected and measured lncRNA levels during the process of cellular differentiation that leads to sperm production [in mice]. They found that specific lncRNAs are associated with each stage of sperm development.

We have demonstrated for the first time that new types of genes, lncRNAs, are important for male fertility, Khalil said. This is a step closer to uncovering new genetic causes of infertility.

Our hope is that lncRNAs can be used in future RNA-based therapeutic approaches, Khalil said.

The GLP aggregated and excerpted this blog/article to reflect the diversity of news, opinion, and analysis. Read full, original post: Long, mysterious strip of RNA contribute to low sperm count

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New ways to target low sperm count? - Genetic Literacy Project

Fruit fly protein dual duties may make it model for studies of protein function in context – Phys.Org

Clamp (glowing green) is found all over these fly chromosomes, but it's particularly concentrated at the histone locus (red) at the bottom center. Credit: Rieder, et. al.

An essential fruit fly protein called CLAMP may help biologists answer the key question of how the same protein can manage to coordinate two completely different processes on distinct chromosomes in the same cell.

New research on a crucial protein in fruit flies provides a clear model for a fundamental question in biology that's significant for drug development in particular: What influences the exact same protein to coordinate a vital molecular process on one chromosome but an entirely different one on another chromosome?

The new study concerns the recently discovered protein CLAMP. Previously, scientists at Brown University had identified CLAMP as the linchpin in the process by which cells in males doubly express their single X chromosome to achieve genetic parity with females, a process necessary for male existence and survival. Now, in a study published in the journal Genes and Development, the researchers have identified another role for CLAMP that is equally essential to males and females alikethe protein is responsible for coordinating the process by which the DNA in newly replicating cells of an embryo becomes properly wound up and structured.

"It's really exciting because now we have these two separate chromosomes on which CLAMP does vital jobs," said senior author Erica Larschan. "That sets us up for a compare-and-contrast strategy where we can understand how one protein can function differently in context-specific ways."

That matters, added co-lead author Leila Rieder, a postdoctoral researcher at Brown, because in order for clinical interventions that target key proteins to do more good than harm, they need to be tailored to a specific context. It may be tempting to block or amplify a gene or protein to treat a disease, but without confining the intervention to that one process, it could upset the entirely healthy actions of the same gene or protein in an unrelated process. That could produce potentially devastating side effects.

"One of the biggest fears about using genetics in people is that there are off-target effects," Rieder said. "You don't know when you manipulate a gene if it's going to have a single effect or if it's going to have many effects. We don't understand all the roles that that one manipulation is going to have."

The confirmation of a second life-giving role for CLAMP, Rieder and Larschan said, provides a perfect example of a protein that is essential in two completely different ways in the convenient research model of the fruit fly.

CLAMP goes GAGA

CLAMP binds to DNA all over the fly genome, but it kicks into consequential action when it finds a long series of repeats of the nucleotides GA. In the new study, the scientists found long GA repeats and CLAMP on chromosome 2L at the "histone locus," where a cluster of genes produce the proteins around which DNA gets wound up to fit inside the nucleus. In many organisms, humans included, cells assemble the same cadre of proteins around which they wrap their DNA. Approximately a yard of DNA is present in every microscopic cell, so it is essential that it be tightly packed but still accessible for regulation immediately in a newly fertilized egg.

In a series of experiments, a team at Brown, the University of North Carolina and Massachusetts General Hospital found that in fruit flies, CLAMP is the protein that launches the process of gene regulation that produces histones by recruiting other known regulators. It is among the very first proteins on the scene of the histone locus in a newly fertilized egg and opens up the histone locus for expression by the cell, they found. Experiments in which the team interfered with CLAMP led almost universally to fly eggs failing to hatch.

Foiling CLAMP proved to be so lethal, in fact, that studying its function at all required an experimental ploy that would allow the scientists to manipulate CLAMP while keeping the flies alive. To understand, for example, how CLAMP lures the other histone-related proteins to the histone locus, the Brown team worked with the University of North Carolina collaborators, including co-lead author Kaitlin Koreski, to generate CLAMP mimics that wouldn't interfere with natural CLAMP's DNA binding, but could still attract the other key regulatory proteins that control histone gene regulation.

Same protein, different functions

Larschan and Rieder's new understanding of CLAMP's function at the histone locus now matches their understanding of its function on the X chromosome. But they said they don't yet know exactly what differs about the context of those two chromosomes such that CLAMP, with the same molecular anatomy and bound to the same GA repeats, manages to recruit two completely different groups of proteins to perform separate gene expression tasks.

That's the next step in their research.

"It sets up a paradigm for the future," Larschan said. "There are very few casesthat's what I'm always surprised about when I read the literaturewhere there are such specific roles at different sites for a single protein. It's a really strong model."

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More information: Leila E. Rieder et al, Histone locus regulation by the Drosophila dosage compensation adaptor protein CLAMP, Genes & Development (2017). DOI: 10.1101/gad.300855.117

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Fruit fly protein dual duties may make it model for studies of protein function in context - Phys.Org

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