The genomes of organisms from humans to corn are replete with "parasitic" strands of DNA that, when not suppressed, copy themselves and spread throughout the genome, potentially affecting health. Earlier this year, Brown University researchers found that these "retrotransposable elements" (RTEs) were increasingly able to break free of the genome's control in cultures of human cells. Now, the researchers have shown that RTEs are increasingly able to break free and copy themselves in the tissues of mice as the animals aged. In further experiments, the biologists showed that this activity was readily apparent in cancerous tumors, but that it also could be reduced by restricting calories. "As mice age, we are seeing deregulation of these elements and they begin to be expressed and increase in copy number in the genome," said Dr. Jill Kreiling, a research assistant professor at Brown, and leader of the study published online on December 7, 2013 in an open-access article in the journal Aging. "This may be a very important mechanism in leading to genome instability. A lot of the chronic diseases associated with aging, such as cancer, have been associated with genome instability." Whether the proliferation of RTEs is exclusively a bad thing remains a hot question among scientists, but what they do know is that the genome tries to control RTEs by wrapping them up in a tightly wound configuration called heterochromatin. In their experiments, Dr. Kreiling and co-corresponding author Professor John Sedivy found that overall, the genomes of several mouse tissues become more heterochromatic with age. But they also found, paradoxically, that some regions where RTEs are concentrated became - loosened up instead , particularly after mice reached the 2-year mark (equivalent to about the 70-year mark for a person).
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