Effect of oxidative stress on translocation of DAF-16 in oxygen-sensitive mutants, mev-1 and gas-1 of Caenorhabditis elegans
Mutations in the mev-1 and gas-1 genes of the nematode Caenorhabditis elegans render animals hypersensitive to oxygen and paraquat, and lead to premature aging. We show that both mutants overproduce superoxide anion in isolated sub-mitochondrial particles, which probably explains their hypersensitiv...
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Published in | Mechanisms of ageing and development Vol. 126; no. 6; pp. 637 - 641 |
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Main Authors | , , , , , |
Format | Journal Article |
Language | English |
Published |
Shannon
Elsevier Ireland Ltd
01.06.2005
Elsevier Science |
Subjects | |
Online Access | Get full text |
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Summary: | Mutations in the
mev-1 and
gas-1 genes of the nematode
Caenorhabditis elegans render animals hypersensitive to oxygen and paraquat, and lead to premature aging. We show that both mutants overproduce superoxide anion in isolated sub-mitochondrial particles, which probably explains their hypersensitivity to oxidative stress. The
daf-16 gene encodes a fork-head transcription factor that is negatively regulated by an insulin-signaling pathway. In wild-type animals, the DAF-16 protein normally resides in the cytoplasm and only becomes translocated to nuclei upon activating stimuli such as oxidative stress. Conversely, DAF-16 resides constitutively in the nuclei of
mev-1 and
gas-1 mutants even under normal growth conditions. Supplementation of the antioxidant coenzyme Q
10 reversed this nuclear translocation of DAF-16. Since both
gas-1 and
mev-1 encode subunits of electron transport chain complexes, these data illustrate how mitochondrial perturbations can impact signal transduction pathways. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0047-6374 1872-6216 |
DOI: | 10.1016/j.mad.2004.11.011 |