Reducing Myc gene activity extends healthy lifespan in mice

Posted: January 23, 2015 at 12:42 am

Mice with one rather than the normal two copies of the gene Myc (also found in humans) lived 15 percent longer and had considerably healthier lives than normal mice, according to a new Brown University-led study in Cell.

A team of scientists based at Brown University has found that reducing expression of a fundamentally important gene called Myc significantly increased the healthy lifespan of laboratory mice, the first such finding regarding this gene in a mammalian species.

Myc is found in the genomes of all animals, ranging from ancestral single-celled organisms to humans. It is a major topic of biomedical research and has been shown to be a central regulator of cell proliferation, growth, and death. It is of such widespread and fundamental importance that animals cannot live without it. But in humans and mice, too much expression of the protein that Myc encodes has been closely linked to cancer, making it a well-known but elusive target of drug developers.

In a new study in the journal Cell, the scientists report that when they bred laboratory mice to have only one copy of the gene, instead of the normal two, thus reducing the expression of the encoded protein, those mice lived 15 percent longer on average -- 20 percent longer for females and 10 percent longer among males -- than normal mice. Moreover, the experimental mice showed many signs of better health into old age.

The experimental -- "heterozygous" -- mice grew to be about 15 percent smaller than the normal mice (a probable disadvantage in the wild) but that was the only discernable downside found to date for lacking a second copy of the gene, said senior author John Sedivy, the Hermon C. Bumpus Professor of Biology and professor of medical science at Brown.

"The animals are definitely aging slower," he said. "They are maintaining the function of their organs and tissues for longer periods of time."

Physiological differences

That assessment is based on detailed studies of the physiology -- down to the molecular level -- of the heterozygous and normal mice. The researchers conducted these experiments to try to understand the longevity difference between the two groups.

Co-lead author Jeffrey Hoffman, a medical and doctoral student, led the studies of the health of the mice, including various bodily systems. In many cases they were just like their normal counterparts. They reproduced just as well, for example.

"These mice are incredibly normal, yet they are really long-lived," Sedivy said. "The reason why we were struck by that is because in many other longevity models like caloric restriction or treatment with rapamycin, the animals live longer but they also have some health issues."

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Reducing Myc gene activity extends healthy lifespan in mice

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