Animal species that more slowly accumulate mutations in the DNA of their non-sexual cells also have a longer life. Which would partly explain why the risk of cancer does not increase with longevity.
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This is a new step in the long track of the causes of biological aging. New, but not so new: L Study published on April 13 in the journal Nature , in reality, comes to validate “a hypothesis issued in 1952 by a future Nobel Prize, Peter Medawar [1915-1987], but so far impossible to demonstrate: idea that aging would result, at least, of an inevitable accumulation of mutations in the genome of our cells, is Hugo Aguilaniu, a geneticist, director of the Serrapilheira Institute, a Brazilian non-profit foundation. And this accumulation would eventually by inducing a critical state for the operation of these cells. “
The immense rise of sequencing capabilities has changed the game. Thanks to what British researchers have been able to prove the reality of this phenomenon. Coordinated by the Wellcome Sanger Institute (United Kingdom), they counted the alterations of DNA in cells of sixteen mammalian species, covering a wide range of lifetimes and body sizes: cat, dog, horse, cow , rabbit, ferret, mouse, rat, rat-tau, giraffe, marsouin, lion, tiger, leemur with ringed tail, colobe black and white and human species. For five of them, several individuals (56 in total) of different ages were analyzed.
Result: The species that live longer acquire more slowly mutations into the DNA of their somatic cells (nonsense) than those living less long. This observation partly explains the famous “paradox of Peto”, the name of the British epidemiologist Richard Peto who stated in 1977. A whale or an elephant, for example, possess much more cells and live much longer than ‘a mouse. The probability that one of their cells undergoes mutations – resulting in its uncontrolled proliferation – is therefore higher. Similarly, these mastodontes should have an increased risk of cancer. But this is not the case.
Differences very marked
But how to estimate the pace at which these mutations accumulate in the cells of each species? Hard to follow an individual all his life! The researchers therefore analyzed the genome of a particular type of cells, conducive to this examination: the cells that line the tiny folds of the inner wall of the colon, or “intestinal crypts”. All cells of the same crypt – laser micro-cutable – derive from the same ancestral strain cell and linearly accumulate mutations with age. In these cells, most of theself, most mutations are caused by endogenous natural processes – common to other tissues – rather than exposure to environmental toxes. He was then sufficient to divide the number of mutations measured by the age of the individual studied to obtain the transfer rates of each species over the years.
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