Repair analysis of mitomycin C-induced DNA crosslinking in ribosomal RNA genes in lymphoblastoid cells from Fanconi's anemia patients.
The repair of mitomycin C (MMC)-induced DNA crosslinking was analyzed by denaturation-renaturation gel electrophoresis in ribosomal RNA genes in lymphoblastoid cell lines from 4 patients with Fanconi's anemia (FA). In comparison to normal lymphoblastoid cell lines, 2 lines of FA cells belonging to complementation group A clearly exhibited higher sensitivity to MMC and an almost identical deficiency in the removal of DNA crosslinking. A complementation group B cell line, HSC 62, exhibited a lower sensitivity than group A cells and a lesser deficiency in crosslink repair. Another 'non-A' group cell line, HSC 230, reproducibly exhibited even higher sensitivity to MMC than group A cells. The results on MMC crosslinkage removal at the molecular level correlated well with cell survival. The observed subtle differences of repair among the 4 FA cell lines might represent possible genetic differences in the respective FA complementation groups.
Matsumoto
A
A
Department of Biological Sciences, Stanford University, CA 94305-5020.
Vos
J M
JM
Hanawalt
P C
PC
D000741:Anemia, Aplastic / Q000235:genetics*; D002470:Cell Survival / Q000187:drug effects; D002478:Cells, Cultured; D003432:Cross-Linking Reagents; D004249:DNA Damage; D004260:DNA Repair; D004275:DNA, Ribosomal / Q000235:genetics*; D005199:Fanconi Anemia / Q000235:genetics*; D006801:Humans; D066298:In Vitro Techniques; D008214:Lymphocytes; D016685:Mitomycin; D008937:Mitomycins / Q000633:toxicity*; D012335:RNA, Ribosomal / Q000235:genetics
D003432:Cross-Linking Reagents; D004275:DNA, Ribosomal; D008937:Mitomycins; D012335:RNA, Ribosomal; D016685:Mitomycin