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Gene Review

mev-1  -  Protein MEV-1

Caenorhabditis elegans

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Disease relevance of mev-1


High impact information on mev-1


Chemical compound and disease context of mev-1


Biological context of mev-1


Anatomical context of mev-1

  • Here we report important biochemical changes in mev-1 animals that serve to explain their abnormalities under normoxic conditions: (i) an overproduction of superoxide anion from mitochondria; and (ii) a reciprocal reduction in glutathione content even under atmospheric oxygen [3].
  • To extend these data, a transgenic mouse cell line was constructed with a homologous mutation to mev-1 [9].

Associations of mev-1 with chemical compounds

  • A methyl viologen (paraquat)-sensitive mutant, mev-1 (LG III), in Caenorhabditis elegans was about 4 times more sensitive to methyl viologen than the wild type [10].
  • We also show that CoQ(10) but not Vitamin E reduced superoxide anion levels in wild type and mev-1 [11].

Physical interactions of mev-1

  • In the nematode Caenorhabditis elegans, mutations have been previously isolated that affect the activities of Complex I (gas-1) and Complex II (mev-1), two of the five membrane-bound complexes that control electron flow in mitochondrial respiration [12].

Other interactions of mev-1

  • The feeding method was employed to deliver dsRNA from the fourth subunit (ceSDHA) to wild-type, mev-1 (mutated in ceSDHC of complex II), and gas-1 animals (mutated in a complex I gene) [13].
  • Lifespans of gas-1 and mev-1 were decreased compared with N2, while that of clk-1 was increased [14].
  • We also demonstrate synthetic genetic interaction between frh-1 and mev-1, the gene encoding the succinate dehydrogenase cytochrome b subunit of complex II in mitochondria, suggesting a possible role of the C. elegans frataxin in the electron transport chain; thus, the respiratory chain might be involved in the pathogenesis of the disease [15].


  1. Effect of oxidative stress on translocation of DAF-16 in oxygen-sensitive mutants, mev-1 and gas-1 of Caenorhabditis elegans. Kondo, M., Senoo-Matsuda, N., Yanase, S., Ishii, T., Hartman, P.S., Ishii, N. Mech. Ageing Dev. (2005) [Pubmed]
  2. The ubiquinone-binding site of the Saccharomyces cerevisiae succinate-ubiquinone oxidoreductase is a source of superoxide. Guo, J., Lemire, B.D. J. Biol. Chem. (2003) [Pubmed]
  3. A defect in the cytochrome b large subunit in complex II causes both superoxide anion overproduction and abnormal energy metabolism in Caenorhabditis elegans. Senoo-Matsuda, N., Yasuda, K., Tsuda, M., Ohkubo, T., Yoshimura, S., Nakazawa, H., Hartman, P.S., Ishii, N. J. Biol. Chem. (2001) [Pubmed]
  4. Mitochondrial oxidative stress can lead to nuclear hypermutability. Hartman, P., Ponder, R., Lo, H.H., Ishii, N. Mech. Ageing Dev. (2004) [Pubmed]
  5. A mutation in succinate dehydrogenase cytochrome b causes oxidative stress and ageing in nematodes. Ishii, N., Fujii, M., Hartman, P.S., Tsuda, M., Yasuda, K., Senoo-Matsuda, N., Yanase, S., Ayusawa, D., Suzuki, K. Nature (1998) [Pubmed]
  6. A complex II defect affects mitochondrial structure, leading to ced-3- and ced-4-dependent apoptosis and aging. Senoo-Matsuda, N., Hartman, P.S., Akatsuka, A., Yoshimura, S., Ishii, N. J. Biol. Chem. (2003) [Pubmed]
  7. Oxidative stress and aging in Caenorhabditis elegans. Ishii, N. Free Radic. Res. (2000) [Pubmed]
  8. Adaptive responses to oxidative damage in three mutants of Caenorhabditis elegans (age-1, mev-1 and daf-16) that affect life span. Yanase, S., Yasuda, K., Ishii, N. Mech. Ageing Dev. (2002) [Pubmed]
  9. The role of the electron transport gene SDHC on lifespan and cancer. Ishii, N., Ishii, T., Hartman, P.S. Exp. Gerontol. (2006) [Pubmed]
  10. A methyl viologen-sensitive mutant of the nematode Caenorhabditis elegans. Ishii, N., Takahashi, K., Tomita, S., Keino, T., Honda, S., Yoshino, K., Suzuki, K. Mutat. Res. (1990) [Pubmed]
  11. Coenzyme Q10 can prolong C. elegans lifespan by lowering oxidative stress. Ishii, N., Senoo-Matsuda, N., Miyake, K., Yasuda, K., Ishii, T., Hartman, P.S., Furukawa, S. Mech. Ageing Dev. (2004) [Pubmed]
  12. Mitochondrial mutations differentially affect aging, mutability and anesthetic sensitivity in Caenorhabditis elegans. Hartman, P.S., Ishii, N., Kayser, E.B., Morgan, P.G., Sedensky, M.M. Mech. Ageing Dev. (2001) [Pubmed]
  13. Complex II inactivation is lethal in the nematode Caenorhabditis elegans. Ichimiya, H., Huet, R.G., Hartman, P., Amino, H., Kita, K., Ishii, N. Mitochondrion (2002) [Pubmed]
  14. The effects of complex I function and oxidative damage on lifespan and anesthetic sensitivity in Caenorhabditis elegans. Kayser, E.B., Sedensky, M.M., Morgan, P.G. Mech. Ageing Dev. (2004) [Pubmed]
  15. Reduction of Caenorhabditis elegans frataxin increases sensitivity to oxidative stress, reduces lifespan, and causes lethality in a mitochondrial complex II mutant. Vázquez-Manrique, R.P., González-Cabo, P., Ros, S., Aziz, H., Baylis, H.A., Palau, F. FASEB J. (2006) [Pubmed]
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