Abstract
A key prediction of the somatic mutation theory of aging is that there is an invariant relationship between life span and the number of random mutations. A number of studies at a number of gene loci have shown that somatic mutations of a variety of types accumulate with age. Dietary restriction, which prolongs life span, results in slowed accumulation of HPRT mutants in mice. Conversely, senescence‐accelerated mice, which have been bred to have a shortened life span, show accelerated accumulation of somatic mutations.

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