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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.


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Journal ArticleDOI
TL;DR: Data from yeast and Drosophila point to the likelihood that changes in expression of genes located in heterochromatin could contribute to the developmental deficits in Cornelia de Lange (CdLS).
Abstract: The sister chromatid cohesion apparatus mediates physical pairing of duplicated chromosomes. This pairing is essential for appropriate distribution of chromosomes into the daughter cells upon cell division. Recent evidence shows that the cohesion apparatus, which is a significant structural component of chromosomes during interphase, also affects gene expression and development. The Cornelia de Lange (CdLS) and Roberts/SC phocomelia (RBS/SC) genetic syndromes in humans are caused by mutations affecting components of the cohesion apparatus. Studies in Drosophila suggest that effects on gene expression are most likely responsible for developmental alterations in CdLS. Effects on chromatid cohesion are apparent in RBS/SC syndrome, but data from yeast and Drosophila point to the likelihood that changes in expression of genes located in heterochromatin could contribute to the developmental deficits.

154 citations

Journal ArticleDOI
TL;DR: The distribution of DNA migration among cells, a function of dose, revealed that the majority of exposed cells expressed more DNA damage than cells from control cultures and that with increasing length ofDNA migration the variability in migration among Cells increased as well.
Abstract: Sodium arsenite (NaAsO2) and cadmium sulphate (CdSO4) were tested for their ability to induce genotoxic effects in the single cell gel (SCG) assay and the sister chromatid exchange (SCE) test in human blood cultures in vitro Both metals induced DNA damage in white blood cells that was expressed and detected as DNA migration in the SCG assay Dose dependent effects were seen for cadmium in concentrations from 5 × 10−4-5 × 10−3 M and for arsenic in concentrations from 2 × 10−4-15 × 10−3 M The distribution of DNA migration among cells, a function of dose, revealed that the majority of exposed cells expressed more DNA damage than cells from control cultures and that with increasing length of DNA migration the variability in migration among cells increased as well Treatment of cells for 2 hr or 24 hr beginning 48 hr after the start of the blood cultures did not increase the SCE frequency in the case of cadmium but caused a small but significant SCE induction with arsenic at the highest concentration The metal concentrations which could be investigated in the SCE test were much lower due to a strong toxic effect Metal concentrations which were toxic in the SCE test were without visible effect in the SCG assay Thus the two endpoints for the determination of genotoxic effects in vitro differed markedly with respect to the detection of genotoxicity induced by metals These differences and the biological significance of the findings are discussed © 1994 Wiley-Liss, Inc

150 citations

Journal ArticleDOI
TL;DR: In conclusion, lindane was genotoxic in cells of the gastric and nasal mucosa in vitro and also in vivo following appropriate routes of application (oral and inhalational exposure) and this compound was assessed for its potential to induce sister chromatid exchanges in vivo in the bone marrow of Chinese hamsters.

150 citations

Journal ArticleDOI
TL;DR: No correlation was found between the frequencies of SCE and aberrations, but two chemicals, which are mutagenic in microorganisms but whose carcinogenicity is poorly documented, increased the frequency of S CE.
Abstract: Several chemical carcinogens and noncarcinogens were tested for their ability to induce sister chromatid exchanges (SCE) and structural chromosome aberrations in cultured V79-4 Chinese hamster cells. All of the direct-acting carcinogens induced a large increase in SCE frequency. Two chemicals, which are mutagenic in microorganisms but whose carcinogenicity is poorly documented, also increased the frequency of SCE. Carcinogenic polycyclic hydrocarbons caused an increased incidence of SCE only when a metabolizing feeder layer was used, whereas no increase was observed with noncarcinogenic polycyclic hydrocarbons. The other noncarcinogens also did not influence the SCE frequency. Although some chemicals increased the frequency of structural chromosome aberrations, no correlation was found between the frequencies of SCE and aberrations.

149 citations

Journal ArticleDOI
01 Apr 1976-Nature
TL;DR: Differential staining of sister chromatids can be demonstrated with Hoechst 33258 fluorochrome and with Giemsa after special pretreatment, even if 5-bromodeoxyuridine is present during the first S phase only.
Abstract: DIFFERENTIAL staining of sister chromatids can be demonstrated with Hoechst 33258 fluorochrome1 and with Giemsa after special pretreatment2, even if 5-bromodeoxyuridine (BUdR) is present during the first S phase only3. These techniques permit the use of the phenomenon of the sister chromatid exchange (SCE). The average spontaneous rate of 10–14 SCEs per metaphase seems to be fairly constant in all cultures from several species4,5. A variety of mutagenic factors (that is, ultraviolet light and alkylating agents) produce very high frequencies of SCE even at concentrations far below the level necessary for the induction of chromosomal breakage, whereas others, like X rays or certain chemicals, hardly influence the rate of SCE6. Because of the high turnover of BrdU in the liver and the physiologically available thymidine, differential chromatid staining has so far only been produced in in vitro systems (cell cultures) and in the chicken embryo.

149 citations


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Performance
Metrics
No. of papers in the topic in previous years
YearPapers
20238
202222
20215
202011
201914
201811