Smc5-Smc6-Dependent Removal of Cohesin from Mitotic Chromosomes
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| Published in: | Molecular and Cellular Biology Vol. 29; no. 16; pp. 4363 - 4375 |
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| AbstractList | The function of the essential cohesin-related Smc5-Smc6 complex has remained elusive, though hypomorphic mutants have defects late in recombination, in checkpoint maintenance, and in chromosome segregation. Recombination and checkpoints are not essential for viability, and Smc5-Smc6-null mutants die in lethal mitoses. This suggests that the chromosome segregation defects may be the source of lethality in irradiated Smc5-Smc6 hypomorphs. We show that in smc6 mutants, following DNA damage in interphase, chromosome arm segregation fails due to an aberrant persistence of cohesin, which is normally removed by the Separase-independent pathway. This postanaphase persistence of cohesin is not dependent on DNA damage, since the synthetic lethality of smc6 hypomorphs with a topoisomerase II mutant, defective in mitotic chromosome structure, is also due to the retention of cohesin on undamaged chromosome arms. In both cases, Separase overexpression bypasses the defect and restores cell viability, showing that defective cohesin removal is a major determinant of the mitotic lethality of Smc5-Smc6 mutants. Article Usage Stats Services MCB Citing Articles Google Scholar PubMed Related Content Social Bookmarking CiteULike Delicious Digg Facebook Google+ Mendeley Reddit StumbleUpon Twitter current issue Spotlights in the Current Issue MCB About MCB Subscribers Authors Reviewers Advertisers Inquiries from the Press Permissions & Commercial Reprints ASM Journals Public Access Policy MCB RSS Feeds 1752 N Street N.W. • Washington DC 20036 202.737.3600 • 202.942.9355 fax • journals@asmusa.org Print ISSN: 0270-7306 Online ISSN: 1098-5549 Copyright © 2014 by the American Society for Microbiology. For an alternate route to MCB .asm.org, visit: MCB The function of the essential cohesin-related Smc5-Smc6 complex has remained elusive, though hypomorphic mutants have defects late in recombination, in checkpoint maintenance, and in chromosome segregation. Recombination and checkpoints are not essential for viability, and Smc5-Smc6-null mutants die in lethal mitoses. This suggests that the chromosome segregation defects may be the source of lethality in irradiated Smc5-Smc6 hypomorphs. We show that in smc6 mutants, following DNA damage in interphase, chromosome arm segregation fails due to an aberrant persistence of cohesin, which is normally removed by the Separase-independent pathway. This postanaphase persistence of cohesin is not dependent on DNA damage, since the synthetic lethality of smc6 hypomorphs with a topoisomerase II mutant, defective in mitotic chromosome structure, is also due to the retention of cohesin on undamaged chromosome arms. In both cases, Separase overexpression bypasses the defect and restores cell viability, showing that defective cohesin removal is a major determinant of the mitotic lethality of Smc5-Smc6 mutants. |
| Author | Johanne M. Murray Matthew J. O'Connell Anja Irmisch Emily A. Outwin |
| AuthorAffiliation | Department of Oncological Sciences, Mount Sinai School of Medicine, New York, New York, 1 Genome Damage and Stability Centre, University of Sussex, Falmer, Brighton, United Kingdom 2 |
| AuthorAffiliation_xml | – name: Department of Oncological Sciences, Mount Sinai School of Medicine, New York, New York, 1 Genome Damage and Stability Centre, University of Sussex, Falmer, Brighton, United Kingdom 2 |
| Author_xml | – sequence: 1 givenname: Emily A. surname: Outwin fullname: Outwin, Emily A. organization: Department of Oncological Sciences, Mount Sinai School of Medicine, New York, New York – sequence: 2 givenname: Anja surname: Irmisch fullname: Irmisch, Anja organization: Genome Damage and Stability Centre, University of Sussex, Falmer, Brighton, United Kingdom – sequence: 3 givenname: Johanne M. surname: Murray fullname: Murray, Johanne M. organization: Genome Damage and Stability Centre, University of Sussex, Falmer, Brighton, United Kingdom – sequence: 4 givenname: Matthew J. surname: O'Connell fullname: O'Connell, Matthew J. organization: Department of Oncological Sciences, Mount Sinai School of Medicine, New York, New York |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/19528228$$D View this record in MEDLINE/PubMed |
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| Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 Corresponding author. Mailing address: Department of Oncological Sciences, Mount Sinai School of Medicine, One Gustave L. Levy Place, Box 1130, New York, NY 10029. Phone: (212) 659-5468. Fax: (212) 987-2240. E-mail: matthew.oconnell@mssm.edu |
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Mendeley... The function of the essential cohesin-related Smc5-Smc6 complex has remained elusive, though hypomorphic mutants have defects late in recombination, in... |
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| SubjectTerms | Animals Cell Cycle - physiology Cell Cycle Proteins - genetics Cell Cycle Proteins - metabolism Chromosomal Proteins, Non-Histone - genetics Chromosomal Proteins, Non-Histone - metabolism Chromosome Segregation Chromosomes - metabolism Cohesins DNA Damage DNA Repair Endopeptidases - genetics Endopeptidases - metabolism Humans Mitosis - physiology Nuclear Proteins - genetics Nuclear Proteins - metabolism Phosphoproteins - genetics Phosphoproteins - metabolism Recombinant Fusion Proteins - genetics Recombinant Fusion Proteins - metabolism Schizosaccharomyces - genetics Schizosaccharomyces - metabolism Schizosaccharomyces pombe Proteins - genetics Schizosaccharomyces pombe Proteins - metabolism Separase |
| Title | Smc5-Smc6-Dependent Removal of Cohesin from Mitotic Chromosomes |
| URI | http://mcb.asm.org/content/29/16/4363.abstract https://www.tandfonline.com/doi/abs/10.1128/MCB.00377-09 https://www.ncbi.nlm.nih.gov/pubmed/19528228 https://search.proquest.com/docview/67522685 https://search.proquest.com/docview/746204335 https://pubmed.ncbi.nlm.nih.gov/PMC2725735 |
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