Stuart K. Kim*
The mysteries of what causes aging and how to extend life span are being tackled by applying evolving technologies to model organisms. The tiny roundworm Caenorhabditis elegans has been a powerhouse in this arena. A key breakthrough occurred in 1993, when worms with a mutation in the daf-2 gene were observed to lead active and healthy lives twice as long as that of normal worms (1). Since then, the quest to determine what makes these worms live so long has spurred powerful "top-down" genomics or proteomic approaches in wide and unbiased screens of daf-2 mutants. On page 660 in this issue, Dong et al. (2) use mass spectrometry to identify quantitative differences in protein levels in daf-2 versus wild-type worms. The changes in protein abundance not only identify potential longevity factors, but also indicate that daf-2 may regulate a network of signaling pathways that both increase and decrease life span.
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