Insulin-like signaling determines survival during stress via posttranscriptional mechanisms in C. elegans.
Insulin-like signaling determines survival during stress via posttranscriptional mechanisms in C. elegans.
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DOI：
10.1016/j.cmet.2010.08.004
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发表时间：
2010-09-08
期刊：
影响因子：
29
通讯作者：
Lithgow GJ
中科院分区：
文献类型：
--
作者：
McColl G;Rogers AN;Alavez S;Hubbard AE;Melov S;Link CD;Bush AI;Kapahi P;Lithgow GJ
胰岛素样信号通路(ILS)调节新陈代谢，并被认为可以调节线虫的成虫寿命。改变的应激反应和对各种压力源的抵抗力也与ILS的变化有关，并有助于延长寿命。转录因子DAF-16和HSF-1是长寿表型的关键效应因子。我们证明，由于ILS降低而导致的内在耐热性增加，并不依赖于应激诱导的转录反应，而是需要活性蛋白质翻译。翻译图谱实验揭示了在热休克过程中以DAF-16依赖的方式对改变的ILS做出反应而转录后调控的基因。此外，ILS对耐热性的影响还需要一些新的蛋白质。我们认为，降低ILS会导致代谢和生理变化。DAF-16诱导的这些变化是在急性应激下的翻译反应调节生存的前提下进行的。
The insulin-like signaling (ILS) pathway regulates metabolism and is known to modulate adult lifespan 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 post-transcriptionally 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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影响因子：
7.8
作者：
Fisher, AL;Lithgow, GJ
通讯作者：
Lithgow, GJ
影响因子：
7.8
作者：
McElwee, J;Bubb, K;Thomas, JH
通讯作者：
Thomas, JH
影响因子：
56.9
作者：
JOHNSON, TE
通讯作者：
JOHNSON, TE
DOI：
10.1111/j.2517-6161.1995.tb02031.x
发表时间：
1995-01-01
影响因子：
5.8
作者：
BENJAMINI, Y;HOCHBERG, Y
通讯作者：
HOCHBERG, Y
影响因子：
13.3
作者：
Florez-McClure, Maria L.;Hohsfield, Lindsay A.;Link, Christopher D.
通讯作者：
Link, Christopher D.