Involvement of G2-dependent DNA double-strand break repair in the formation of ultraviolet light B-induced chromosomal aberrations.
Wortmannin, an inhibitor of DNA double-strand break (DSB) repair added 19 h before harvest enhanced the incidence of ultraviolet light B (UVB)-induced chromatid aberrations in Chinese hamster V79 cells. Posttreatment with wortmannin for last 3 h of culture also enhanced the yield of breakage-type chromatid aberrations and suppressed the yield of exchange-type chromatid aberrations almost completely. Thus, the inhibition of DSB repair in the G2 phase stimulated the breakage-type aberration formation, while suppressing the exchange-type aberration formation. We propose the model of UVB-induced chromatid-type aberration formation which might be fully related to G2-dependent DSB repair pathway.
Department of Radiation Biology, B4, Faculty of Medicine, Osaka University, 2-2, Yamada-oka, Suita, Osaka 565-0871, Japan. ishii@radbio.med.osaka-u.ac.jp
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D000730:Androstadienes / Q000494:pharmacology; D000818:Animals; D002460:Cell Line; D002842:Chromatids / Q000235:genetics; D002869:Chromosome Aberrations / Q000235:genetics*; D006224:Cricetinae; D003412:Cricetulus; D004247:DNA / Q000235:genetics; D004260:DNA Repair / Q000235:genetics*; D016195:G2 Phase / Q000235:genetics*; D014466:Ultraviolet Rays; D000077191:Wortmannin
D000730:Androstadienes; D004247:DNA; D000077191:Wortmannin