C. elegans SIR-2.1 interacts with 14-3-3 proteins to activate DAF-16 and extend life span

被引：307

作者：

Berdichevsky, Ala

Viswanathan, Mohan

Horvitz, H. Robert

Guarente, Leonard

机构：

[1] MIT, Dept Biol, Cambridge, MA 02139 USA

[2] MIT, Howard Hughes Med Inst, Cambridge, MA 02139 USA

来源：

CELL | 2006年 / 125卷 / 06期

基金：

美国国家卫生研究院;

关键词：

D O I：

10.1016/j.cell.2006.04.036

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

The longevity of Caenorhabditis elegans is promoted by extra copies of the sir-2.1 gene in a manner dependent on the forkhead transcription factor DAF-16. We identify two C. elegans 14-3-3 proteins as SIR-2.1 binding partners and show that 14-3-3 genes are required for the life-span extension conferred by extra copies of sir-2.1. 14-3-3 proteins are also required for SIR-2.1-induced transcriptional activation of DAF-16 and stress resistance. Following heat stress, SIR-2.1 can bind DAF-16 in a 14-3-3-dependent manner. Ely contrast, low insulin-like signaling does not promote SIR-2.1/DAF-16 interaction, and sir-2.1 and the 14-3-3 genes are not required for the regulation of life span by the insulin-like signaling pathway. We propose the existence of a stress-dependent pathway in which SIR-2.1 and 14-3-3 act in parallel to the insulin-like pathway to activate DAF16 and extend life span.

引用

收藏

页码：1165 / 1177

页数：13

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