Sister chromatid exchange

About: Sister chromatid exchange is a research topic. Over the lifetime, 3187 publications have been published within this topic receiving 90029 citations. The topic is also known as: replication-born DSB repair by SCE & GO:1990414.

Sister Chromatid Exchange

Abstract: EARLY RESULTS 1 83 Sister Chromatid Exchange in Meiosis 1 83 Sister Chromatid Exchange in Somatic Cells 1 84 Isolabeling 1 86 Sister Chromatid Exchanges-Spontaneous or Induced? 1 86 RESULTS FROM NEW METHODS FOR DETECTING SISTER CHROMA TID EXCHANGES 1 86 Reasons for Differential Staining 1 87 Harlequin Chromosomes and Chromosome Structure 1 89 Multiple sister chromatid exchanges 1 90 Autoradiographic image spread 1 90 Labeling for more than one replication cycle 1 90 The Question 0/ Spontaneous Levels 0/ Sister Chromatid Exchanges 1 9 1 Location 0/ Sister Chromosome Exchanges in the Chromosome 1 93 Sister Chromatid Exchanges and Human Genetic Diseases 1 93 Sister Chromatid Exchanges as Indicators 0/ Mutagenic Carcinogens 1 94 Lesions Responsible for Sister Chromatid Exchange Formation 1 96 CONCLUSION 1 97

Chromosome Instability and Defective Recombinational Repair in Knockout Mutants of the Five Rad51 Paralogs

Abstract: The Rad51 protein, a eukaryotic homologue of Escherichia coli RecA, plays a central role in both mitotic and meiotic homologous DNA recombination (HR) in Saccharomyces cerevisiae and is essential for the proliferation of vertebrate cells. Five vertebrate genes, RAD51B, -C, and -D and XRCC2 and -3, are implicated in HR on the basis of their sequence similarity to Rad51 (Rad51 paralogs). We generated mutants deficient in each of these proteins in the chicken B-lymphocyte DT40 cell line and report here the comparison of four new mutants and their complemented derivatives with our previously reported rad51b mutant. The Rad51 paralog mutations all impair HR, as measured by targeted integration and sister chromatid exchange. Remarkably, the mutant cell lines all exhibit very similar phenotypes: spontaneous chromosomal aberrations, high sensitivity to killing by cross-linking agents (mitomycin C and cisplatin), mild sensitivity to gamma rays, and significantly attenuated Rad51 focus formation during recombinational repair after exposure to gamma rays. Moreover, all mutants show partial correction of resistance to DNA damage by overexpression of human Rad51. We conclude that the Rad51 paralogs participate in repair as a functional unit that facilitates the action of Rad51 in HR.

Cancer Risk in Humans Predicted by Increased Levels of Chromosomal Aberrations in Lymphocytes: Nordic Study Group on the Health Risk of Chromosome Damage

Abstract: Cytogenetic assays in peripheral blood lymphocytes (PBL) have been used extensively to survey the exposure of humans to genotoxic agents. The conceptual basis for this has been the hypothesis that the extent of genetic damage in PBL reflects critical events for carcinogenic processes in target tissues. Until now, no follow-up studies have been performed to assess the predictive value of these methods for subsequent cancer risk. In an ongoing Nordic cohort study of cancer incidence, 3182 subjects were examined between 1970 and 1988 for chromosomal aberrations (CA), sister chromatid exchange or micronuclei in PBL. In order to standardize for the interlaboratory variation, the results were trichotomized for each laboratory into three strata: low (1-33 percentile), medium (34-66 percentile), or high (67-100 percentile). In this second follow-up, a total of 85 cancers were diagnosed during the observation period (1970-1991). There was no significant trend in the standardized incidence ratio with the frequencies of sister chromatid exchange or micronuclei, but the data for these parameters are still too limited to allow firm conclusions. There was a statistically significant linear trend (P = 0.0009) in CA strata with regard to subsequent cancer risk. The point estimates of the standardized incidence ratio in the three CA strata were 0.9, 0.7, and 2.1, respectively. Thus, an increased level of chromosome breakage appears to be a relevant biomarker of future cancer risk.

Sister chromatids are preferred over homologs as substrates for recombinational repair in Saccharomyces cerevisiae.

Abstract: A diploid Saccharomyces cerevisiae strain was constructed in which the products of both homolog recombination and unequal sister chromatid recombination events could be selected. This strain was synchronized in G1 or in G2, irradiated with X-rays to induce DNA damage, and monitored for levels of recombination. Cells irradiated in G1 were found to repair recombinogenic damage primarily by homolog recombination, whereas those irradiated in G2 repaired such damage preferentially by sister chromatid recombination. We found, as have others, that G1 diploids were much more sensitive to the lethal effects of X-ray damage than were G2 diploids, especially at higher doses of irradiation. The following possible explanations for this observation were tested: G2 cells have more potential templates for repair than G1 cells; G2 cells are protected by the RAD9-mediated delay in G2 following DNA damage; sister chromatids may share more homology than homologous chromosomes. All these possibilities were ruled out by appropriate tests. We propose that, due to a special relationship they share, sister chromatids are not only preferred over homologous chromatids as substrates for recombinational repair, but have the capacity to repair more DNA damage than do homologs.

Sister chromatid exchange as an indicator of mutagenesis

Abstract: SISTER chromatid exchange (SCE), that is, the reciprocal interchange of DNA between chromatids, is easily visualised in metaphase chromosomes1,2 and has been applied to study chromosome structure3,4, chromosome damage5, and instability and DNA repair deficiency syndromes6–9. Since SCEs can be induced by subtoxic doses of carcinogens and mutagens5,10–13, their analysis offers the possibility of a rapid, sensitive and quantitative assay for genetic damage. We have begun to examine the relation between SCEs and mutations in Chinese hamster ovary (CHO) cells by quantifying the induction of SCEs in parallel with the induction of mutations producing 8-azaguanine resistance, that is, mutations predominately at the hypoxanthine phosphoribosyltransferase, hprt, locus. Since the conversion of a chemically induced DNA lesion to a SCE or mutation may depend on the nature of that lesion, we tested four chemicals that differ in their interaction with DNA—ethyl methanesulphonate (EMS; O6: N7 guanyl alkylation ratio14 of 0.03), N-ethyl-N-nitrosourea (ENU; O6: N7 guanyl alkylation ratio15 of about 0.35), the crosslinking agent mitomycin C (MMC)16 and the intercalator proflavine sulphate (PRO)17. Our results indicate a linear relation between induced SCEs and mutations. The relative efficiency, however, is different for each chemical.