Quiet Little Traitors; August 2012; Scientific American Magazine; by David Stipp; 6 Page(s)
In 1999 JAN M. VAN deursen and his colleagues at the Mayo Clinic in Rochester, Minn., wanted to see whether mangled chromosomes cause cancer. So they engineered mice deficient in a protein that helps to maintain chromosomal integrity. The rodents' coils of DNA were duly deranged. Surprisingly, though, the animals were not particularly tumor-prone. Instead they developed a strange grab bag of ills, including cataracts, dwindling muscles, rapid thinning of fat under the skin and progressive spinal curvature, that made them look like one-humped camels. They also tended to die young.
Van Deursen had no idea why those particular abnormalities showed up. Then, in 2002, he spotted a report on mice afflicted by accelerated aging and was struck by photographs showing that their backs became humped as they aged. Suddenly, it hit him: his camel-backed mice, too, were aging unusually fast. Probing deeper, the Mayo team discovered that cells in a number of the rodents' tissues had prematurely slid into a state called cellular senescence, in which cells permanently lose the ability to divide and become aberrant in other ways. Such failure of cell division would explain the bone, muscle, eye and skin abnormalities observed by van Deursen's group.