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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 Article
TL;DR: The sister chromatid exchange assay has predictive value as a clinical assay for drugs for which a strong correlation between cell kill and induction of SCEs has been established, and the range of chemosensitivities of cell subpopulations can be identified easily.
Abstract: The sister chromatid exchange (SCE) assay has been used to predict the chemosensitivity to 1,3-bis(2-chloroethyl)-1-nitrosourea of various neoplastic cell subpopulations in eight cell lines derived from human brain tumors. Because the SCE assay is based on analysis of individual cells, data obtained can be plotted as frequency histograms of SCEs per chromosome, and the range of chemosensitivities of cell subpopulations can be identified easily. Results suggest that the SCE assay has predictive value as a clinical assay for drugs for which a strong correlation between cell kill and induction of SCEs has been established.

67 citations

Journal ArticleDOI
TL;DR: It is shown that mutation of potential cyclin-dependent kinase 1 (Cdk1) phosphorylation sites leaves sororin stranded on chromosomes and bound to cohesin throughout mitosis, suggesting that phosphorin causes its release from chromatin in mitosis and increases cohesion between sister chromatids.
Abstract: Tumor cells are commonly aneuploid, a condition contributing to cancer progression and drug resistance. Understanding how chromatids are linked and separated at the appropriate time will help uncover the basis of aneuploidy and will shed light on the behavior of tumor cells. Cohesion of sister chromatids is maintained by the multi-protein complex cohesin, consisting of Smc1, Smc3, Scc1 and Scc3. Sororin associates with the cohesin complex and regulates the segregation of sister chromatids. Sororin is phosphorylated in mitosis; however, the role of this modification is unclear. Here we show that mutation of potential cyclin-dependent kinase 1 (Cdk1) phosphorylation sites leaves sororin stranded on chromosomes and bound to cohesin throughout mitosis. Sororin can be precipitated from cell lysates with DNA–cellulose, and only the hypophosphorylated form of sororin shows this association. These results suggest that phosphorylation of sororin causes its release from chromatin in mitosis. Also, the hypophosphorylated form of sororin increases cohesion between sister chromatids, suggesting that phosphorylation of sororin by Cdk1 influences sister chromatid cohesion. Finally, phosphorylation-deficient sororin can alleviate the mitotic block that occurs upon knockdown of endogenous sororin. This mitotic block is abolished by ZM447439, an Aurora kinase inhibitor, suggesting that prematurely separated sister chromatids activate the spindle assembly checkpoint through an Aurora kinase-dependent pathway.

67 citations

Journal ArticleDOI
TL;DR: It is concluded that iron overload is able to induce genetic damage in intact cells provided that iron is present in a bioavailable form.
Abstract: Ferric nitrilotriacetate (Fe-NTA) and ferric citrate (Fe-citrate) were used to study the cellular damage mediated by iron overload with respect to cytotoxicity, lipid peroxidation, DNA strand breaks and sister chromatid exchanges (SCE) At non-toxic concentrations, Fe-NTA induced lipid peroxidation, DNA strand breaks and SCE in a dose- and time-dependent manner Comparing the time courses of the different events, the increase in lipid peroxidation seems to be associated with the generation of DNA strand breaks, since both types of cellular damage were observed after 1-3 h of incubation In contrast, the induction of SCE was low after 24 h and increased after 48 and 72 h treatment, indicating the requirement of other types of DNA damage Fe-citrate was inactive in the induction of lipid peroxidation and SCE, and no significant number of DNA strand breaks were generated, as determined by the alkaline unwinding method Our results suggest that the induction of lipid peroxidation and DNA strand breaks by iron overload depend on special features of the iron complex applied, while the chromosomal and genetic effects require site specific DNA damage dependent on intracellular iron metabolism It is concluded that iron overload is able to induce genetic damage in intact cells provided that iron is present in a bioavailable form

67 citations

Book ChapterDOI
TL;DR: The two most important areas of the applications of BrdU differential staining techniques are the utilization of sister chromatid exchanges (SCEs) as an indication of DNA damage and repair and the employment of BISACK for examining cellular replication.
Abstract: Publisher Summary The chapter discusses the methodology for Bromodeoxyuridine (BrdU) differential staining, both in vitro as well as in vivo, and an examination of the many applications of this technique The chapter focuses on the BrdU labeling of mammalian chromosomes in vivo They involve multiple subcutaneous injections, multiple intraperitoneal injections, or continuous intravenous infusion of BrdU Examination of the concentrations of BrdU used in vitro for differential chromatid staining reveals extreme variation, even for the same cellular system The chapter discusses the two most important areas of the applications of BrdU differential staining techniques are the utilization of sister chromatid exchanges (SCEs) as an indication of DNA damage and repair and the employment of BISACK for examining cellular replication SCE analysis potentially detects an agent, which may not be mutagenic for bacterial systems and yet be mutagenic, and perhaps even carcinogenic, for human cells SCE analyses have been employed to examine various human genetic disorders The system for analyzing cell replication kinetics (BISACK), permit new insight into the nature of replicating cell populations both in vivo and in vitro

67 citations

Journal ArticleDOI
Mei Leng1, Doug W. Chan, Hao Luo, Cihui Zhu, Jun Qin, Yi Wang 
TL;DR: It is proposed that MPS1-dependent BLM phosphorylation is important for ensuring accurate chromosome segregation, and its deregulation may contribute to cancer.
Abstract: Spindle assembly checkpoint (SAC) ensures bipolar attachment of chromosomes to the mitotic spindle and is essential for faithful chromosome segregation, thereby preventing chromosome instability (CIN). Genetic evidence suggests a causal link between compromised SAC, CIN, and cancer. Bloom syndrome (BS) is a genetic disorder that predisposes affected individuals to cancer. BS cells exhibit elevated rates of sister chromatid exchange, chromosome breaks, and CIN. The BS gene product, BLM, is a member of the RecQ helicases that are required for maintenance of genome stability. The BLM helicase interacts with proteins involved in DNA replication, recombination, and repair and is required for the repair of stalled-replication forks and in the DNA damage response. Here we present biochemical evidence to suggest a role of BLM phosphorylation during mitosis in maintaining chromosome stability. BLM is associated with the SAC kinase MPS1 and is phosphorylated at S144 in a MPS1-dependent manner. Phosphorylated BLM interacts with polo-like kinase 1, a mitotic kinase that binds to phospho-serine/threonine through its polo-box domain (PBD). Furthermore, BS cells expressing BLM-S144A show normal levels of sister chromatid exchange but fail to maintain the mitotic arrest when SAC is activated and exhibit a broad distribution of chromosome numbers. We propose that MPS1-dependent BLM phosphorylation is important for ensuring accurate chromosome segregation, and its deregulation may contribute to cancer.

67 citations


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