Increased longevity of some C. elegans mitochondrial mutants explained by activation of an alternative energy-producing pathway

被引：25

作者：

Gallo, Marco ^{[1
,2
]}

Park, Donha ^{[2
]}

Riddle, Donald L. ^{[1
,2
]}

机构：

[1] Univ British Columbia, Dept Med Genet, Fac Med, Vancouver, BC V6T 1Z4, Canada

[2] Univ British Columbia, Michael Smith Labs, Vancouver, BC V6T 1Z4, Canada

来源：

MECHANISMS OF AGEING AND DEVELOPMENT | 2011年 / 132卷 / 10期

基金：

加拿大健康研究院; 加拿大自然科学与工程研究理事会;

关键词：

C; elegans; Mitochondria; Glyoxylate shunt; Oxidative stress response; Aging; CAENORHABDITIS-ELEGANS; LIFE-SPAN; ELECTRON-TRANSPORT; OXIDATIVE STRESS; DAF-16; GENE; DYSFUNCTION; METABOLISM; MODULATION; EXPRESSION;

D O I：

10.1016/j.mad.2011.08.004

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

The Caenorhabditis elegans misc-1 gene encodes a mitochondrial carrier with a role in oxidative stress response. The knock-out mutant has no lifespan phenotype and fails to upregulate the gei-7-mediated glyoxylate shunt, an extra-mitochondrial pathway of energy production. We show that gei-7 is required for the longevity of the mitochondrial mutant clk-1. Our data suggest that only mitochondrial mutants that upregulate gei-7 can achieve longevity. (C) 2011 Elsevier Ireland Ltd. All rights reserved.

引用

页码：515 / 518

页数：4

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