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某些线虫线粒体突变体寿命延长的原因是激活了一种替代的能量产生途径。

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

机构信息

Department of Medical Genetics, Faculty of Medicine, The University of British Columbia, Vancouver, BC, Canada.

出版信息

Mech Ageing Dev. 2011 Oct;132(10):515-8. doi: 10.1016/j.mad.2011.08.004. Epub 2011 Aug 22.

Abstract

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.

摘要

秀丽隐杆线虫的 misc-1 基因编码一种在线粒体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 介导的乙醛酸支路,这是一种线粒体以外的能量产生途径。我们表明,gei-7 是 clk-1 线粒体突变体长寿所必需的。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。

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