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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
Leigh Henderson1, R.J. Cole1, Jane Cole1, Helen Cole1, Z. Aghamohammadi1, T. Regan1 
TL;DR: The effectiveness of 3 compounds, procarbazine, mitomycin C and cyclophosphamide as inducers of sister-chromatid exchanges (SCEs) in granulocyte-macrophage progenitor cells, in foetal liver and bone marrow from pregnant mice at day 17 of gestation were determined.
Abstract: The effectiveness of 3 compounds, procarbazine, mitomycin C and cyclophosphamide as inducers of sister-chromatid exchanges (SCEs) in granulocyte-macrophage progenitor cells, in foetal liver and bone marrow from pregnant mice at day 17 of gestation were determined Cyclophosphamide and procarbazine induced similar SCE frquencies in maternal and foetal cells Mitomycin C was slightly less effective in foetal liver than in maternal bone marrow In contrast to the results of SCE induction, cyclophosphamide produced more micronucleated polychromatic erythrocytes in foetal liver than in bone marrow The SCE results for mitomycin C and procarbazine are compared with results obtained previously for micronuclei induction in 15-day pregnant animals

25 citations

Journal ArticleDOI
TL;DR: It is concluded that caffeine does not inhibit SCE formation, and the caffeine-mediated apparent decrease of SCE induction after UV or triaziquone exposure is due to a selective destruction of those metaphases otherwise exhibiting a high number of S CE.
Abstract: Studies are reported that are designed to analyze the mechanism by which caffeine reduces the induction of SCE by UV light or alkylating agents. The substantial points are (1) caffeine does not inhibit SCE formation, and (2) the caffeine-mediated apparent decrease of SCE induction after UV or triaziquone exposure is due to a selective destruction of those metaphases otherwise exhibiting a high number of SCE. These findings and their relavance to the ascertainment of the SCE-forming process are discussed.

25 citations

Journal ArticleDOI
TL;DR: It is shown for the first time that inactive centromeres are composed of heterochromatin, as defined by the presence of heter Cochromatin protein HP1Hsα, and it is shown that both the inner centromere protein (INCENP) and its binding partner Aurora-B/AIM-1 kinase can also be detected at the inactive Centromere.
Abstract: Inactive centromeres of stable dicentric chromosomes provide a unique opportunity to examine the resolution of sister chromatid cohesion in mitosis. Here we show for the first time that inactive centromeres are composed of heterochromatin, as defined by the presence of heterochromatin protein HP1(Hs alpha). We then show that both the inner centromere protein (INCENP) and its binding partner Aurora-B/AIM-1 kinase can also be detected at the inactive centromere. Thus, targeting of the chromosomal passengers is not dependent upon the presence of an active centromere/kinetochore. Furthermore, we show that the association of INCENP with the inactive centromere correlates strictly with the state of cohesion between sister chromatids: loss of cohesion is accompanied by loss of detectable INCENP. These results are consistent with recent suggestions that one function of the chromosomal passenger proteins may be to regulate sister chromatid separation in mitosis.

25 citations

Journal ArticleDOI
TL;DR: A unique function of BCCIP is suggested, not only in repair of DNA damage, but also in resolving stalled replication forks and prevention of replication stress.
Abstract: BCCIP is a BRCA2- and CDKN1A(p21)-interacting protein that has been implicated in the maintenance of genomic integrity. To understand the in vivo functions of BCCIP, we generated a conditional BCCIP knockdown transgenic mouse model using Cre-LoxP mediated RNA interference. The BCCIP knockdown embryos displayed impaired cellular proliferation and apoptosis at day E7.5. Consistent with these results, the in vitro proliferation of blastocysts and mouse embryonic fibroblasts (MEFs) of BCCIP knockdown mice were impaired considerably. The BCCIP deficient mouse embryos die before E11.5 day. Deletion of the p53 gene could not rescue the embryonic lethality due to BCCIP deficiency, but partially rescues the growth delay of mouse embryonic fibroblasts in vitro. To further understand the cause of development and proliferation defects in BCCIP-deficient mice, MEFs were subjected to chromosome stability analysis. The BCCIP-deficient MEFs displayed significant spontaneous chromosome structural alterations associated with replication stress, including a 3.5-fold induction of chromatid breaks. Remarkably, the BCCIP-deficient MEFs had a ∼20-fold increase in sister chromatid union (SCU), yet the induction of sister chromatid exchanges (SCE) was modestly at 1.5 fold. SCU is a unique type of chromatid aberration that may give rise to chromatin bridges between daughter nuclei in anaphase. In addition, the BCCIP-deficient MEFs have reduced repair of irradiation-induced DNA damage and reductions of Rad51 protein and nuclear foci. Our data suggest a unique function of BCCIP, not only in repair of DNA damage, but also in resolving stalled replication forks and prevention of replication stress. In addition, BCCIP deficiency causes excessive spontaneous chromatin bridges via the formation of SCU, which can subsequently impair chromosome segregations in mitosis and cell division.

24 citations


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