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- W2898184417 abstract "Interventions that promote healthy aging are typically associated with increased stress resistance. Paradoxically, reducing the activity of core biological processes such as mitochondrial or insulin metabolism promotes the expression of adaptive responses, which in turn increase animal longevity and resistance to stress. In this study, we investigated the relation between the extended Caenorhabditis elegans lifespan elicited by reduction in mitochondrial functionality and resistance to genotoxic stress. We find that reducing mitochondrial activity during development confers germline resistance to DNA damage-induced cell cycle arrest and apoptosis in a cell-non-autonomous manner. We identified the C. elegans homologs of the BRCA1/BARD1 tumor suppressor genes, brc-1/brd-1, as mediators of the anti-apoptotic effect but dispensable for lifespan extension upon mitochondrial stress. Unexpectedly, while reduced mitochondrial activity only in the soma was not sufficient to promote longevity, its reduction only in the germline or in germline-less strains still prolonged lifespan. Thus, in animals with partial reduction in mitochondrial functionality, the mechanisms activated during development to safeguard the germline against genotoxic stress are uncoupled from those required for somatic robustness and animal longevity." @default.
- W2898184417 created "2018-11-02" @default.
- W2898184417 creator A5005787961 @default.
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- W2898184417 creator A5024682015 @default.
- W2898184417 creator A5030035319 @default.
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- W2898184417 creator A5067687587 @default.
- W2898184417 creator A5077552949 @default.
- W2898184417 creator A5088031684 @default.
- W2898184417 date "2018-10-26" @default.
- W2898184417 modified "2023-10-12" @default.
- W2898184417 title "<scp>BRCA</scp>1 and<scp>BARD</scp>1 mediate apoptotic resistance but not longevity upon mitochondrial stress in<i>Caenorhabditis elegans</i>" @default.
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