Worm Breeder's Gazette 16(3): 30 (June 1, 2000)
These abstracts should not be cited in bibliographies. Material contained herein should be treated as personal communication and should be cited as such only with the consent of the author.
| 1 | Dept of Biology, Texas Christian University, Fort Worth, Texas 76129 |
| 2 | Tokai University of Medicine Isehara, Kanagawa 259-1193, Japan |
| 3 | Department of Anestesiology, Case Western university, Cleveland, Ohio 44106 |
Both gas-1 and mev-1 encode subunits of key respiratory enzymes (Kayser et al., 1999; Ishii et al., 1998); however, mutations in these two genes were isolated based upon their abilities to confer hypersensitivity to two seemingly unrelated agents. Specifically, mev-1(kn1) is hypersensitive to oxidative damage, presented in the form of either methyl viologen (paraquat) or hyperoxia. Conversely, gas-1(fc21) is hypersensitive to volatile anesthetics such as halothane. We now report that gas-1 is hypersensitive to oxidative stress but mev-1 is not hypersensitive to volatile anaestetics.
As with mev-1, a mutation in gas-1 resulted in hypersensitivity to the superoxide anion-generating chemical paraquat. gas-1 was more hypersenstive at 20C than 15C, which was not surprising given that gas-1 is difficult to even propagate at 25oC. As with mev-1, the gas-1 mutation also rendered animals hypersensitive to hyperoxia. In addition, the life spans of both gas-1 and mev-1 mutants were significantly shortened by elevated oxygen concentrations. It was determined previously that mev-1 animals were hypermutable to oxygen (Ponder, Hartman and Ishii, unpublished data). Conversely, gas-1 was only weakly hypermutable if at all. Finally, kn1 mutation in mev-1 did not confer hypersensitivity to the volatile anaestetic halothane.
In summary, these two genes encode subunits in two key mitochondrial complexes I (gas-1) and II (mev-1). Mutations in these genes confer an overlapping but distinct set of phenotypes. We are currently attempting to elucidate the bases of these similarities and differences.
Kayser, EB, Morgan, PG, Sedensky, MM. 1999. GAS-1: A Mitochondrial Protein Controls Sensitivity to Volatile Anesthetics in the Nematode Caenorhabditis elegans, Anastesiol. 45, 545.
Ishii, N, Fujii, M, Hartman, P.S., Tsuda, M., Yasuda, K., Senoo-Matsuda, N., Yanase, S, Ayusawa, D., Suzuki, K. 1998. A mutation in succinate dehydrogenase cytochrome b causes oxidative stress and ageing in nematodes, Nature 394, 694.