“About half of the human genome is made up of retrotransposons,” said Professor of Biology Vera Gorbunova. “By better understanding why these genomic parasites become active, we hope to better understand and perhaps delay the aging process in humans.”
Retrotransposons usually remain inactive throughout the entire life, but once they become active, they can “jump around” through the genome, causing trouble in one or more areas of the body. Sirt6 keeps this expansion at bay. But what happens when you get older?
In order to further test this idea, they artificially caused damage in the cells of younger mice. They then found that “stressed cells”, with more damage to the DNA also have more retrotransposons. Then, they also introduced Sirt6 protein in the mice, and found that the “jumping genes” disappeared.
"This suggests that supplying more Sirt6 protein might protect older cells from aging,” said Gorbunova. “The idea would be to increase the Sirt6 pool so that enough proteins are available for both DNA repair and for keeping the retrotransposons inactive.”
Source:health.howstuffworks.com;