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1 is a major determinant of ILS effects on thermotolerance and is as important as?DAF-16 in modulating thermotolerance. However, C08H9.1(RNAi) had no effect on wild-type thermotolerance ( Figure?7F), consistent with our observation that, in wild-type, this transcript is not induced under heat stress, and the ribosomal loading of C08H9.1 mRNA does not appear to be changed ( Figure?7B and 7C). C08H9.1(RNAi) also had no effect on daf-16(m26);daf-2(e1370) thermotolerance ( Figure?S5A), consistent with C08H9.1 effects being dependent on DAF-16. Chronic knockdown of C08H9.1 via RNAi over the entire lifetime had no measurable effect on wild-type longevity. However, a modest but significant suppression of longevity (?19% reduction in median life span, p ALG1 findings support an association between longevity and cellular stress response, including HSP expression, in C. elegans. The heat find more shock response (HSR) is a conserved and regulated genetic response to diverse environmental and physiological stressors that results in the rapid induction of genes encoding molecular chaperones (including HSPs) and additional proteins that protect and assist in recovery from the cellular damage associated with expression and accumulation of misfolded protein. The HSR and HSP induction have long dominated the stress literature as having critical roles in cellular protection against heat shock and other cytotoxic stressors ( Morimoto, 2008). In the nematode model, overexpression of HSF-1 extends life span (Hsu et?al., 2003), and both lowered-ILS and dietary restriction effect on longevity are dependent on HSF-1 (Morley and Morimoto, 2004?and?Steinkraus et?al., 2008). These observations provide support for the hypothesis that the rate of aging may be modulated by the ability of cells/tissues/organisms to withstand the effects of stress by maintaining protein homeostasis and hence normal function. Here, we have presented results consistent find protocol with a conceptual framework to further understand how whole organisms tolerate extreme heat stress and how ILS modulates this resistance. These results challenge the notion that transcriptional regulation of HSP genes is a preeminent mechanism of survival during acute heat shock. Although HSPs contribute to acquired thermotolerance, their stress induction appears not to be essential for?wild-type or ILS-mediated intrinsic thermotolerance in C.?elegans. ILS mutants do have altered stress-induced expression of HSP, but this may not be the primary reason underlying their increased resistance to acute heat stress. In wild-type, survival to a lethal 35��C heat shock is not altered when, prior to the stress, either transcription or translation is inhibited.
