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Sci. Signal., 24 February 2009
Vol. 2, Issue 59, p. ec78
[DOI: 10.1126/scisignal.259ec78]

EDITORS' CHOICE

Cell Biology Caloric Intake and Stress Relief?

L. Bryan Ray

Science, Science Signaling, AAAS, Washington, DC 20005, USA

What biochemical mechanisms link an organism’s caloric intake with the mechanisms that help protect cellular proteins during stress? The NAD-dependent deacetylase SIRT1 contributes to the life-span–extending effects of low caloric intake by altering gene transcription. The transcription factor heat shock factor 1 (HSF1) also has a role in this process, acting to enhance transcription of genes encoding protein-protective chaperone proteins. Westerheide et al. (see the Perspective by Saunders and Verdin) showed that SIRT1 may acetylate HSF1 directly, thus enhancing its activation of transcription of target genes. Furthermore, overexpression of SIRT1 in cultured cells helped the cells to survive exposure to heat stress.

S. D. Westerheide, J. Anckar, S. M. Stevens Jr., L. Sistonen, R. I. Morimoto, Stress-inducible regulation of heat shock factor 1 by the deacetylase SIRT1. Science 323, 1063–1066 (2009). [Abstract] [Full Text]

L. R. Saunders, E. Verdin, Stress response and aging. Science 323, 1021–1022 (2009). [Summary] [Full Text]

Citation: L. B. Ray, Caloric Intake and Stress Relief? Sci. Signal. 2, ec78 (2009).

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