SCE and DNA methylation.
The interrelationship between sister chromatid exchange (SCE) formation and DNA methylation was studied in Chinese hamster V79 and Indian muntjac cells. A DNA methylation inhibitor, 5-azacytidine (5AzaC), induced SCEs only when it had been present in cells for at least 2 rounds of DNA replication. This result suggests that SCEs are formed during replication of hemimethylated or demethylated DNA possessing 5AzaC, and that hypomethylated sites may become fully methylated after they pass 1 cell division. It also appears that hypomethylated DNA is not more sensitive to ultraviolet light (UV) or 3-aminobenzamide (3AMB) than normal chromosomes, but sensitized to mitomycin C (MMC) for the induction of SCEs. An analysis of sites of SCEs induced by 5AzaC within Indian muntjac chromosomes showed that the SCE frequency was enhanced at the 5 methylcytosine-rich regions where spontaneous SCEs were intensively suppressed. The SCE mechanism at the junction between contiguous replicons with different replication timing was discussed.
D044503:5-Methylcytosine; D000818:Animals; D001374:Azacitidine / Q000494:pharmacology; D001549:Benzamides / Q000494:pharmacology; D002460:Cell Line; D006224:Cricetinae; D003412:Cricetulus; D003596:Cytosine / Q000031:analogs & derivatives / Q000032:analysis; D004247:DNA / Q000378:metabolism*; D004261:DNA Replication; D003670:Deer; D005260:Female; D005347:Fibroblasts / Q000648:ultrastructure; D008297:Male; D008745:Methylation; D016685:Mitomycin; D008937:Mitomycins / Q000494:pharmacology; D008957:Models, Genetic; D012854:Sister Chromatid Exchange / Q000187:drug effects
D001549:Benzamides; D008937:Mitomycins; D016685:Mitomycin; D044503:5-Methylcytosine; D003596:Cytosine; C025160:3-aminobenzamide; D004247:DNA; D001374:Azacitidine