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A mutation in a mitochondrial dehydrogenase/reductase gene causes an increased sensitivity to oxidative stress and mitochondrial defects in the nematode Caenorhabditis elegans
Author(s) -
Fujii Michihiko,
Yasuda Kayo,
Hartman Phil S.,
Ayusawa Dai,
Ishii Naoaki
Publication year - 2011
Publication title -
genes to cells
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.912
H-Index - 115
eISSN - 1365-2443
pISSN - 1356-9597
DOI - 10.1111/j.1365-2443.2011.01547.x
Subject(s) - biology , caenorhabditis elegans , mutant , mitochondrion , reactive oxygen species , mitochondrial dna , oxidative stress , gene , mutation , respiratory chain , mitochondrial respiratory chain , genetics , microbiology and biotechnology , biochemistry
rad‐8 is an interesting mutant that shows increased sensitivities to UV radiation and reactive oxygen species in the nematode Caenorhabditis elegans . In this study, we have characterized rad‐8 and have found that rad‐8 showed several phenotypes of mitochondrial dysfunction such as a decreased activity of the respiratory chain, increased generation of superoxide anions, increased oxidative damage, increased apoptosis, and abnormal mitochondrial structure. Our genetic analysis has also indicated that rad‐8 has a causative mutation in the F56H1.6 gene, which encodes a mitochondrial dehydrogenase/reductase. The functional role of RAD‐8 may be evolutionarily conserved because expression of the putative human homologue RTN4IP/NIMP in rad‐8 rescued the increased sensitivity to oxygen in rad‐8 . These results suggest that RAD‐8 plays an important role in oxygen metabolism in mitochondria in higher eukaryotes.