Increased spontaneous DNA damage in Cu/Zn superoxide dismutase (SOD1) deficient Drosophila.
The superoxide dismutases (SODs) protect oxygen-using cells against reactive oxygen species, the potentially toxic by-products of respiration, oxidative metabolism, and radiation. We have previously shown that genetic disruption of CuZn SOD (SOD1) in Drosophila imparts a recessive phenotype of reduced lifespan, infertility, and hypersensitivity to oxidative stress. We now show that the absence of SOD1 increases spontaneous genomic damage. The increase in spontaneous mutation rate occurs in SOD1-null mutants in somatic cells as well as in the germ line. Further, we show that specific DNA repair-defective mutations, which are easily tolerated in SOD1(+) flies, lead to high mortality when introduced into the SOD1-null homozygous mutant background.
Woodruff
R C
RC
Department of Biological Sciences, Bowling Green State University, Bowling Green, OH 43403, USA. rwoodru@bgnet.bgsu.edu
Phillips
J P
JP
Hilliker
A J
AJ
D000818:Animals; D002470:Cell Survival; D003433:Crosses, Genetic; D004249:DNA Damage; D004260:DNA Repair; D004331:Drosophila melanogaster / Q000235:genetics*; D005260:Female; D016678:Genome; D005838:Genotype; D006720:Homozygote; D008297:Male; D009154:Mutation; D018384:Oxidative Stress; D010100:Oxygen / Q000378:metabolism; D010641:Phenotype; D017382:Reactive Oxygen Species; D013482:Superoxide Dismutase / Q000235:genetics* / Q000502:physiology; D000072105:Superoxide Dismutase-1
D017382:Reactive Oxygen Species; D013482:Superoxide Dismutase; D000072105:Superoxide Dismutase-1; D010100:Oxygen