The scid mutation in mice causes defects in the repair system for both double-strand DNA breaks and DNA cross-links.
The sensitivity of scid fibroblasts established from C.B17-scid/scid fetuses to the DNA-damaging agents bleomycin, neocarzinostatin, mechlorethamine, mitomycin C, methyl methanesulfonate, and ultraviolet light, all of which induce different types of DNA damage, was examined. Scid fibroblasts were 2.8-, 3.7-, and 3.0-fold more sensitive to bleomycin, neocarzinostatin, and mechlorethamine, respectively, than wild-type fibroblasts derived from C.B17-+/+ fetuses. These findings indicate that the scid mutation in mice causes defects in repairing both double-strand DNA breaks and DNA cross-links.
Tanaka
T
T
Department of Medicine III, Osaka University Medical School, Japan.
Yamagami
T
T
Oka
Y
Y
Nomura
T
T
Sugiyama
H
H
D000818:Animals; D001761:Bleomycin / Q000633:toxicity; D002460:Cell Line; D002470:Cell Survival / Q000187:drug effects; D004249:DNA Damage; D004260:DNA Repair; D005260:Female; D008297:Male; D008466:Mechlorethamine / Q000633:toxicity; D051379:Mice; D016513:Mice, SCID / Q000235:genetics*; D009154:Mutation; D011247:Pregnancy; D009353:Zinostatin / Q000633:toxicity
D001761:Bleomycin; D008466:Mechlorethamine; D009353:Zinostatin