期刊
PLOS GENETICS
卷 9, 期 12, 页码 -出版社
PUBLIC LIBRARY SCIENCE
DOI: 10.1371/journal.pgen.1004071
关键词
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资金
- National Institute of Environmental Health Sciences [T32 ES007058-33]
- BBSRC [BB/G00353X/1]
- Charles A. King Trust
- MRC
- NIH NIGMS [GM084955]
- NIH [R01 GM088248]
- BBSRC [BB/G00353X/1] Funding Source: UKRI
- MRC [G0902043] Funding Source: UKRI
- Biotechnology and Biological Sciences Research Council [BB/G00353X/1] Funding Source: researchfish
- Medical Research Council [G0902043] Funding Source: researchfish
During meiosis, Structural Maintenance of Chromosome (SMC) complexes underpin two fundamental features of meiosis: homologous recombination and chromosome segregation. While meiotic functions of the cohesin and condensin complexes have been delineated, the role of the third SMC complex, Smc5/6, remains enigmatic. Here we identify specific, essential meiotic functions for the Smc5/6 complex in homologous recombination and the regulation of cohesin. We show that Smc5/6 is enriched at centromeres and cohesin-association sites where it regulates sister-chromatid cohesion and the timely removal of cohesin from chromosomal arms, respectively. Smc5/6 also localizes to recombination hotspots, where it promotes normal formation and resolution of a subset of joint-molecule intermediates. In this regard, Smc5/6 functions independently of the major crossover pathway defined by the MutL gamma complex. Furthermore, we show that Smc5/6 is required for stable chromosomal localization of the XPF-family endonuclease, Mus81-Mms4(Eme1). Our data suggest that the Smc5/6 complex is required for specific recombination and chromosomal processes throughout meiosis and that in its absence, attempts at cell division with unresolved joint molecules and residual cohesin lead to severe recombination-induced meiotic catastrophe.
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