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Unloading of homologous recombination factors is required for restoring double-stranded DNA at damage repair loci

Y. Vasianovich, V. Altmannova, O. Kotenko, MD. Newton, L. Krejci, S. Makovets,

. 2017 ; 36 (2) : 213-231. [pub] 20161208

Language English Country England, Great Britain

Document type Journal Article

Persistent link   https://www.medvik.cz/link/bmc17031236

Cells use homology-dependent DNA repair to mend chromosome breaks and restore broken replication forks, thereby ensuring genome stability and cell survival. DNA break repair via homology-based mechanisms involves nuclease-dependent DNA end resection, which generates long tracts of single-stranded DNA required for checkpoint activation and loading of homologous recombination proteins Rad52/51/55/57. While recruitment of the homologous recombination machinery is well characterized, it is not known how its presence at repair loci is coordinated with downstream re-synthesis of resected DNA We show that Rad51 inhibits recruitment of proliferating cell nuclear antigen (PCNA), the platform for assembly of the DNA replication machinery, and that unloading of Rad51 by Srs2 helicase is required for efficient PCNA loading and restoration of resected DNA As a result, srs2Δ mutants are deficient in DNA repair correlating with extensive DNA processing, but this defect in srs2Δ mutants can be suppressed by inactivation of the resection nuclease Exo1. We propose a model in which during re-synthesis of resected DNA, the replication machinery must catch up with the preceding processing nucleases, in order to close the single-stranded gap and terminate further resection.

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$a Cells use homology-dependent DNA repair to mend chromosome breaks and restore broken replication forks, thereby ensuring genome stability and cell survival. DNA break repair via homology-based mechanisms involves nuclease-dependent DNA end resection, which generates long tracts of single-stranded DNA required for checkpoint activation and loading of homologous recombination proteins Rad52/51/55/57. While recruitment of the homologous recombination machinery is well characterized, it is not known how its presence at repair loci is coordinated with downstream re-synthesis of resected DNA We show that Rad51 inhibits recruitment of proliferating cell nuclear antigen (PCNA), the platform for assembly of the DNA replication machinery, and that unloading of Rad51 by Srs2 helicase is required for efficient PCNA loading and restoration of resected DNA As a result, srs2Δ mutants are deficient in DNA repair correlating with extensive DNA processing, but this defect in srs2Δ mutants can be suppressed by inactivation of the resection nuclease Exo1. We propose a model in which during re-synthesis of resected DNA, the replication machinery must catch up with the preceding processing nucleases, in order to close the single-stranded gap and terminate further resection.
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$a Altmannová, Veronika $u Department of Biology, Masaryk University, Brno, Czech Republic. International Clinical Research Center, St. Anne's University Hospital in Brno, Brno, Czech Republic. $7 mub2011626283
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$a Kotenko, Oleksii $u Institute of Cell Biology, School of Biological Sciences, University of Edinburgh, Edinburgh, UK.
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$a Krejci, Lumir $u Department of Biology, Masaryk University, Brno, Czech Republic. International Clinical Research Center, St. Anne's University Hospital in Brno, Brno, Czech Republic. National Centre for Biomolecular Research, Masaryk University, Brno, Czech Republic.
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$a Makovets, Svetlana $u Institute of Cell Biology, School of Biological Sciences, University of Edinburgh, Edinburgh, UK smakovet@staffmail.ed.ac.uk.
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