Large DNA deletions in mitochondria -- the energy-producing units of the cell -- are associated with premature ageing in mice, according to a study published online in Nature Genetics.
A widely debated mitochondrial theory of ageing proposes that the lifelong accumulation of mitochondrial DNA mutations contributes to the decline of tissue function observed in ageing. Lawrence Loeb and colleagues studied so-called 'mitochondrial mutator' mice, which have a greater mutation burden than normal mice. They previously reported that single base-pair mutations in mitochondrial DNA are not associated with accelerated ageing; however, they now show that these prematurely aged mice have abundant large deletions in mitochondrial DNA, suggesting an important role for these lesions in the ageing process. The effect of these deletions on mitochondrial function is different from tissue to tissue, which suggests that tissues are differentially susceptible to the effects of mitochondrial mutations. Author contact: Lawrence Loeb (University of Washington, Seattle, WA, USA)
E-mail: laloeb@u.washington.edu Marc Vermulst (University of Washington Medical School, Seattle, WA, USA)
E-mail: mave@u.washington.edu Abstract available online. (C) Nature Genetics press release.
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