The cell-non-autonomous nature of electron transport chain-mediated longevity.
The cell-non-autonomous nature of electron transport chain-mediated longevity.
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DOI：
10.1016/j.cell.2010.12.016
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发表时间：
2011-01-07
期刊：
影响因子：
64.5
通讯作者：
Dillin A
中科院分区：
文献类型：
--
作者：
Durieux J;Wolff S;Dillin A
C.线虫的衰老可以通过线粒体功能的降低而增加;然而，单个不同组织中线粒体的改变在多大程度上可能影响整个生物体的衰老仍然是未知的。我们通过询问对ETC功能的操纵是否可以以细胞非自主的方式调节衰老来解决这个问题。我们报告说，关键组织中线粒体功能的改变对于建立和维持促长寿线索是必不可少的。我们发现，线粒体应激反应的调节是电子传递链（ETC）长寿途径的基本和特定的遗传要求。引人注目的是，我们发现，在一个组织中的线粒体扰动的感知和作用的线粒体应激反应途径在远端组织。这些结果表明，线粒体可以建立和延续整个生物体的衰老速度独立于细胞自主功能。
The life span of C. elegans can be increased via reduced function of the mitochondria; however, the extent to which mitochondrial alteration in a single, distinct tissue may influence aging in the whole organism remains unknown. We addressed this question by asking whether manipulations to ETC function can modulate aging in a cell non-autonomous fashion. We report that the alteration of mitochondrial function in key tissues is essential for establishing and maintaining a pro-longevity cue. We find that regulators of mitochondrial stress responses are essential and specific genetic requirements for the electron transport chain (ETC) longevity pathway. Strikingly, we find that mitochondrial perturbation in one tissue is perceived and acted upon by the mitochondrial stress response pathway in a distal tissue. These results suggest that mitochondria may establish and perpetuate the rate of aging for the whole organism independent of cell-autonomous functions.
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