Glutathione S-transferase mediates an ageing response to mitochondrial dysfunction.

Glutathione S-transferase mediates an ageing response to mitochondrial dysfunction.
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DOI:
10.1016/j.mad.2015.12.001
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发表时间:
2016-01
影响因子:
5.3
通讯作者:
Morgan, Philip G.
Morgan, Philip G.
中科院分区:
医学3区
文献类型:
--
作者:
Dancy, Beverley M.;Brockway, Nicole;Ramadasan-Nair, Renjini;Yang, Yoing;Sedensky, Margaret M.;Morgan, Philip G.

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To understand primary mitochondrial disease, we utilized a complex I-deficient Caenorhabditis elegans mutant, gas-1. These animals strongly upregulate the expression of gst-14 (encoding a glutathione S-transferase). Knockdown of gst-14 dramatically extends the lifespan of gas-1 and increases hydroxynonenal (HNE) modified mitochondrial proteins without improving complex I function. We observed no change in reactive oxygen species levels as measured by Mitosox staining, consistent with a potential role of GST-14 in HNE clearance. The upregulation of gst-14 in gas-1 animals is specific to the pharynx. These data suggest that an HNE-mediated response in the pharynx could be beneficial for lifespan extension in the context of complex I dysfunction in C. elegans. Thus, whereas HNE is typically considered damaging, our work is consistent with recent reports of its role in signaling, and that in this case, the signal is pro-longevity in a model of mitochondrial dysfunction.
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