The muscles of a 19-month-old mutant look like those of a 35-month-old wild-type animal.

Scientists have hypothesized that aneuploidy could be a driving factor in aging. On page 529, Baker et al. report evidence to the contrary.

Using a mutation series in the BubR1 mitotic checkpoint protein, the researchers previously showed that as the amount of functional protein decreased, aneuploidy increased, as did the rate of aging. To determine whether the correlation was causal, Baker et al. now compared the BubR1 mutants to mice carrying mutations in two other mitotic checkpoint genes, Bub3 and Rae1. The double mutant animals had significantly more aneuploidy than did the BubR1 mice. However, the double mutants reached old age at 18 to 24 months, which is about four months earlier than wild-type controls, whereas the BubR1 animals were completely aged at just five months.

There was a correlation...

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