Increased longevity of some C. elegans mitochondrial mutants explained by activation of an alternative energy-producing pathway
Increased longevity of some C. elegans mitochondrial mutants explained by activation of an alternative energy-producing pathway
复制标题
DOI：
10.1016/j.mad.2011.08.004
复制
发表时间：
2011-10-01
影响因子：
5.3
通讯作者：
Riddle, Donald L.
中科院分区：
文献类型：
--
作者：
Gallo, Marco;Park, Donha;Riddle, Donald L.
秀丽隐杆线虫misc-1基因编码在氧化应激反应中起作用的线粒体载体。敲除突变体没有寿命表型，也不能上调gei-7介导的乙醛酸分流，这是一种线粒体外的能量产生途径。我们发现gei-7是线粒体突变体clk-1长寿所必需的。我们的数据表明，只有上调gei-7的线粒体突变体才能实现长寿。2011爱思唯尔爱尔兰有限公司版权所有。
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.