Having the Nerve to Go On

Science's STKE  10 Oct 2000:
Vol. 2000, Issue 53, pp. tw9
DOI: 10.1126/stke.2000.53.tw9

In the nematode Caenorhabditis elegans, mutations that disrupt the signaling pathway of the insulin-like receptor daf-2 dramatically extend the animals' life-span and cause the accumulation of large amounts of fat. By selectively expressing normal versions of the mutated insulin-like receptors only in certain tissues, Wolkow et al. pinpoint the nervous system as responsible for this pathway's effect on life-span and the muscles, as the site that controls the metabolic alterations. The authors suggest that defects in the daf-2 pathway allow overexpression of free-radical scavenging enzymes, which protects neurons from oxidative damage and allows them to secrete life-prolonging neuroendocrine signals.

Wolkow, C.A., Kimura, K.D., Lee, M.-S., and Ruvkun, G. (2000) Regulation of C. elegans life-span by insulinlike signaling in the nervous system. Science 290: 147-150. [Abstract] [Full Text]