Increased spontaneous DNA damage in Cu/Zn superoxide dismutase (SOD1) deficient Drosophila.

Abstract:

: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.

journal_name

Genome

journal_title

Genome

authors

Woodruff RC,Phillips JP,Hilliker AJ

doi

10.1139/g04-083

subject

Has Abstract

pub_date

2004-12-01 00:00:00

pages

1029-35

issue

6

eissn

0831-2796

issn

1480-3321

pii

g04-083

journal_volume

47

pub_type

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