دورية أكاديمية
أعرض في EDS

Meiotic crossover control by concerted action of Rad51-Dmc1 in homolog template bias and robust homeostatic regulation.

التفاصيل البيبلوغرافية
العنوان: Meiotic crossover control by concerted action of Rad51-Dmc1 in homolog template bias and robust homeostatic regulation.
المؤلفون: Lao JP; Howard Hughes Medical Institute and Department of Microbiology & Molecular Genetics, University of California, Davis, Davis, California, United States of America ; Genetics Graduate Group, University of California, Davis, Davis, California, United States of America., Cloud V; Committee on Genetics, University of Chicago, Cummings Life Science Center, Chicago, Illinois, United States of America ; Department of Radiation and Cellular Oncology, University of Chicago, Cummings Life Science Center, Chicago, Illinois, United States of America., Huang CC; Howard Hughes Medical Institute and Department of Microbiology & Molecular Genetics, University of California, Davis, Davis, California, United States of America., Grubb J; Department of Radiation and Cellular Oncology, University of Chicago, Cummings Life Science Center, Chicago, Illinois, United States of America., Thacker D; Weil Graduate School of Medical Sciences of Cornell University, New York, New York, United States of America ; Memorial Sloan-Kettering Cancer Center, New York, New York, United States of America., Lee CY; Program in Cell Cycle and Cancer Biology, Oklahoma Medical Research Foundation, Oklahoma City, Oklahoma, United States of America., Dresser ME; Program in Cell Cycle and Cancer Biology, Oklahoma Medical Research Foundation, Oklahoma City, Oklahoma, United States of America ; Department of Cell Biology, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma, United States of America., Hunter N; Howard Hughes Medical Institute and Department of Microbiology & Molecular Genetics, University of California, Davis, Davis, California, United States of America ; Genetics Graduate Group, University of California, Davis, Davis, California, United States of America ; Department of Molecular & Cellular Biology, University of California, Davis, Davis, California, United States of America ; Department of Cell Biology & Human Anatomy, University of California, Davis, Davis, California, United States of America., Bishop DK; Committee on Genetics, University of Chicago, Cummings Life Science Center, Chicago, Illinois, United States of America ; Department of Radiation and Cellular Oncology, University of Chicago, Cummings Life Science Center, Chicago, Illinois, United States of America ; Department of Molecular Genetics and Cell Biology, University of Chicago, Cummings Life Science Center, Chicago, Illinois, United States of America.
المصدر: PLoS genetics [PLoS Genet] 2013; Vol. 9 (12), pp. e1003978. Date of Electronic Publication: 2013 Dec 19.
نوع المنشور: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
اللغة: English
بيانات الدورية: Publisher: Public Library of Science Country of Publication: United States NLM ID: 101239074 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1553-7404 (Electronic) Linking ISSN: 15537390 NLM ISO Abbreviation: PLoS Genet Subsets: MEDLINE
أسماء مطبوعة: Original Publication: San Francisco, CA : Public Library of Science, c2005-
مواضيع طبية MeSH: Crossing Over, Genetic*, Cell Cycle Proteins/*genetics , DNA-Binding Proteins/*genetics , Meiosis/*genetics , Rad51 Recombinase/*genetics , Saccharomyces cerevisiae Proteins/*genetics, Cell Cycle Proteins/metabolism ; Chromatids/genetics ; Chromosome Pairing/genetics ; Chromosome Segregation/genetics ; DNA Breaks, Double-Stranded ; DNA Repair/genetics ; DNA-Binding Proteins/metabolism ; Homeostasis ; Homologous Recombination/genetics ; Rad51 Recombinase/metabolism ; Saccharomyces cerevisiae ; Saccharomyces cerevisiae Proteins/metabolism ; Synaptonemal Complex/genetics
مستخلص: During meiosis, repair of programmed DNA double-strand breaks (DSBs) by recombination promotes pairing of homologous chromosomes and their connection by crossovers. Two DNA strand-exchange proteins, Rad51 and Dmc1, are required for meiotic recombination in many organisms. Studies in budding yeast imply that Rad51 acts to regulate Dmc1's strand exchange activity, while its own exchange activity is inhibited. However, in a dmc1 mutant, elimination of inhibitory factor, Hed1, activates Rad51's strand exchange activity and results in high levels of recombination without participation of Dmc1. Here we show that Rad51-mediated meiotic recombination is not subject to regulatory processes associated with high-fidelity chromosome segregation. These include homolog bias, a process that directs strand exchange between homologs rather than sister chromatids. Furthermore, activation of Rad51 does not effectively substitute for Dmc1's chromosome pairing activity, nor does it ensure formation of the obligate crossovers required for accurate homolog segregation. We further show that Dmc1's dominance in promoting strand exchange between homologs involves repression of Rad51's strand-exchange activity. This function of Dmc1 is independent of Hed1, but requires the meiotic kinase, Mek1. Hed1 makes a relatively minor contribution to homolog bias, but nonetheless this is important for normal morphogenesis of synaptonemal complexes and efficient crossing-over especially when DSB numbers are decreased. Super-resolution microscopy shows that Dmc1 also acts to organize discrete complexes of a Mek1 partner protein, Red1, into clusters along lateral elements of synaptonemal complexes; this activity may also contribute to homolog bias. Finally, we show that when interhomolog bias is defective, recombination is buffered by two feedback processes, one that increases the fraction of events that yields crossovers, and a second that we propose involves additional DSB formation in response to defective homolog interactions. Thus, robust crossover homeostasis is conferred by integrated regulation at initiation, strand-exchange and maturation steps of meiotic recombination.
Competing Interests: The authors have declared that no competing interests exist.
التعليقات: Comment in: PLoS Genet. 2014 Jan;10(1):e1004104. (PMID: 24465222)
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معلومات مُعتمدة: GM074223 United States GM NIGMS NIH HHS; United States HHMI Howard Hughes Medical Institute; GM050936 United States GM NIGMS NIH HHS; R01 GM050936 United States GM NIGMS NIH HHS; R01 GM074223 United States GM NIGMS NIH HHS
المشرفين على المادة: 0 (Cell Cycle Proteins)
0 (DMC1 protein, S cerevisiae)
0 (DNA-Binding Proteins)
0 (Saccharomyces cerevisiae Proteins)
EC 2.7.7.- (Rad51 Recombinase)
تواريخ الأحداث: Date Created: 20131225 Date Completed: 20140820 Latest Revision: 20211021
رمز التحديث: 20221213
مُعرف محوري في PubMed: PMC3868528
DOI: 10.1371/journal.pgen.1003978
PMID: 24367271
قاعدة البيانات: MEDLINE
الوصف
تدمد:1553-7404
DOI:10.1371/journal.pgen.1003978