Chromosome aberration formation and sister chromatid exchange in relation to DNA repair in human cells.
Apparent association between the ability to induce chromosome aberrations and sister chromatid exchanges and mutagenic-carcinogenic potential found in a variety of physical and chemical agents has led us to speculate that these cytogenetic changes might be reflection of DNA damage and repair and might provide induces of mutagenic changes. However, the mechanisms of their formation and their relation to DNA repair as well as the mechanism of their linking to mutation are by no means well understood. Studies in some human genetic mutant cells defective in their ability to repair DNA damage indicate, as a testable proposition, that sister chromatid exchanges and chromosome aberrations are cytological manifestations of replication-mediated dual-step repair pathways that are in operation to tolerate DNA damage when damage-bearing DNA enters and passes through semiconservative replication. The observations are also in line with idea that the majority of sister chromatid exchanges can arise when damage DNA attempts replication possibly by a process relating with the replicative bypass repair mechanisms such as those proposed by Fujiwara and Tatsumi [34] and Higgins et al. [54], while chromosome aberration formation and some fraction of sister chromatid exchanges are related with the post-replication repair processes which attempt to rescue damaged template post-replicationally by de novo synthesis or recombination type repair systems. The former sister chromatid exchange-relating process seems to link mutation to less extent, if any, than the latter process, which is caffeine sensitive and likely to be error-prone.
D001260:Ataxia Telangiectasia / Q000235:genetics; D002273:Carcinogens / Q000494:pharmacology; D002869:Chromosome Aberrations; D002875:Chromosomes / Q000187:drug effects / Q000528:radiation effects; D003434:Crossing Over, Genetic; D004247:DNA / Q000378:metabolism / Q000528:radiation effects; D004260:DNA Repair; D005199:Fanconi Anemia / Q000235:genetics; D005720:Gamma Rays; D006801:Humans; D008540:Meiosis; D008957:Models, Genetic; D009153:Mutagens / Q000494:pharmacology; D009154:Mutation; D010859:Pigmentation Disorders / Q000235:genetics; D012854:Sister Chromatid Exchange; D014983:Xeroderma Pigmentosum / Q000235:genetics
D002273:Carcinogens; D009153:Mutagens; D004247:DNA