Researchers at the University of Rochester, however, have uncovered more evidence that the key to longevity resides instead in a gene.
In a new paper published in the journal Cell, the researchers -- including Vera Gorbunova and Andrei Seluanov, professors of biology; Dirk Bohmann, professor of biomedical genetics; and their team of students and postdoctoral researchers -- found that the gene sirtuin 6 (SIRT6) is responsible for more efficient DNA repair in species with longer lifespans. The research illuminates new targets for anti-aging interventions and could help prevent age-related diseases.
Humans - Mammals - DNA - Breaks - Gene
As humans and other mammals grow older, their DNA is increasingly prone to breaks, which can lead to gene rearrangements and mutations -- hallmarks of cancer and aging. For that reason, researchers have long hypothesized that DNA repair plays an important role in determining an organism's lifespan. While behaviors like smoking can exacerbate double-strand breaks (DSBs) in DNA, the breaks themselves are unavoidable. "They are always going to be there, even if you're super healthy," says Bohmann. "One of the main causes of DSBs is oxidative damage and, since we need oxygen to breathe, the breaks are inevitable."
Organisms like mice have a smaller chance of accumulating double-strand breaks in their comparatively short lives, versus organisms with longer lifespans, Bohmann says. "But, if you want to live for 50 years or so, there's more of a need to put a system into place to fix these breaks."
SIRT6 - Longevity - Gene - Role - Proteins
SIRT6 is often called the "longevity gene" because of its important role in organizing proteins and recruiting enzymes that repair broken DNA; additionally, mice without the gene age prematurely, while mice with extra copies live longer. The researchers hypothesized that if more efficient DNA repair is required for a longer lifespan, organisms with longer lifespans may have evolved more efficient DNA repair regulators. Is SIRT6 activity therefore...
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