Journal
CELL METABOLISM
Volume 12, Issue 3, Pages 260-272Publisher
CELL PRESS
DOI: 10.1016/j.cmet.2010.08.004
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Funding
- NIH National Center for Research Resources (NCRR)
- Glenn Foundation for Medical Research/American Federation for Aging Research
- NIH [AG21069, AG22868, AG029631-01A1, ES016655]
- Larry L. Hillblom Foundation
- Nathan Shock Center [AG025798]
- Glenn foundation for Medical Research
- [UL1 RR024917]
- [AG032113]
- [AG031337]
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The insulin-like signaling (ILS) pathway regulates metabolism and is known to modulate adult life span in C. elegans. Altered stress responses and resistance to a wide range of stressors are also associated with changes in ILS and contribute to enhanced longevity. The transcription factors DAF-16 and HSF-1 are key effectors of the longevity phenotype. We demonstrate that increased intrinsic thermotolerance, due to lower ILS, is not dependent on stress-induced transcriptional responses but instead requires active protein translation. Translation profiling experiments reveal genes that are posttranscriptionally regulated in response to altered ILS during heat shock in a DAF-16-dependent manner. Furthermore, several novel proteins are specifically required for ILS effects on thermotolerance. We propose that lowered ILS results in metabolic and physiological changes. These DAF-16-induced changes precondition a translational response under acute stress to modulate survival.
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