Live Fast, Die Early

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Science  10 Nov 2006:
Vol. 314, Issue 5801, pp. 895
DOI: 10.1126/science.314.5801.895c

How an organism repairs damage to its DNA has important implications for disease and, potentially, for aging, as the latter is correlated with increasing DNA damage. Double-stranded breaks (DSBs) in DNA are particularly noxious, and cells have evolved several ways to cope: Homologous recombination (HR) uses the sequences of a homologous chromosome to patch the damaged site, which minimizes the chance of mutation, whereas nonhomologous end joining (NHEJ) is faster but may introduce small additions or deletions.

Preston et al. have looked at the way germ cells in male Drosophila deal with DSB damage over the lifetime of the individual. They find that the importance of the various pathways changes substantially, with young (1-week-old) males showing a low level (∼15%) of repair via HR, which increases to 60% in 6-week-old flies. On the other hand, flies that died or became infertile after only 4 weeks had a tendency to show increasing NHEJ-based repair of the DSB with age. The authors speculate that young flies might benefit from rapid gamete development and production (and thus being first to mate), and therefore evolution favors the rapidity of NHEJ repairs, which outweighs the mutational burden. Older flies, having outlived most of the competition, might find themselves in an environment where the frequency of mating is low and speed is no longer a critical factor. — GR

Curr. Biol. 16, 2009 (2006).

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