Smc5/6 maintains stalled replication forks in a recombination-competent conformation

The Smc5/6 structural maintenance of chromosomes complex is required for efficient homologous recombination (HR). Defects in Smc5/6 result in chromosome mis‐segregation and fragmentation. By characterising two Schizosaccharomyces pombe smc6 mutants, we define two separate functions for Smc5/6 in HR....

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Bibliographic Details
Published in:The EMBO journal Vol. 28; no. 2; pp. 144 - 155
Main Authors: Irmisch, Anja, Ampatzidou, Eleni, Mizuno, Ken'ichi, O'Connell, Matthew J, Murray, Johanne M
Format: Journal Article
Language:English
Published: Chichester, UK John Wiley & Sons, Ltd 21.01.2009
Nature Publishing Group UK
Springer Nature B.V
Nature Publishing Group
Subjects:
Cell Cycle Proteins - genetics
Cell Cycle Proteins - physiology
Chromatin - genetics
Chromatin - physiology
Chromosomal Proteins, Non-Histone - genetics
Chromosomal Proteins, Non-Histone - physiology
Chromosomes
Deoxyribonucleic acid
DNA
DNA Damage
DNA Replication - genetics
DNA Replication - physiology
EMBO13
Genetic recombination
Genomics
Molecular biology
Mutation
Nucleic Acid Conformation
Rad52
Rad52 DNA Repair and Recombination Protein - genetics
Rad52 DNA Repair and Recombination Protein - metabolism
recombination
Recombination, Genetic
replication fork stalling
Schizosaccharomyces - genetics
Schizosaccharomyces - physiology
Schizosaccharomyces pombe Proteins - genetics
Schizosaccharomyces pombe Proteins - physiology
Smc5/6
replication fork stalling
Rad52
recombination
Smc5/6
ISSN:0261-4189, 1460-2075, 1460-2075
Online Access:Get full text
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Summary:The Smc5/6 structural maintenance of chromosomes complex is required for efficient homologous recombination (HR). Defects in Smc5/6 result in chromosome mis‐segregation and fragmentation. By characterising two Schizosaccharomyces pombe smc6 mutants, we define two separate functions for Smc5/6 in HR. The first represents the previously described defect in processing recombination‐dependent DNA intermediates when replication forks collapse, which leads to increased rDNA recombination. The second novel function defines Smc5/6 as a positive regulator of recombination in the rDNA and correlates mechanistically with a requirement to load RPA and Rad52 onto chromatin genome‐wide when replication forks are stably stalled by nucleotide depletion. Rad52 is required for all HR repair, but Rad52 loading in response to replication fork stalling is unexpected and does not correlate with damage‐induced foci. We propose that Smc5/6 is required to maintain stalled forks in a stable recombination‐competent conformation primed for replication restart.
Bibliography:ArticleID:EMBJ2008273
Supplementary Information
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ark:/67375/WNG-TS7WF72V-5
ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
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ISSN:0261-4189
1460-2075
1460-2075
DOI:10.1038/emboj.2008.273