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© Research
Publication : The EMBO journal

Srs2 mediates PCNA-SUMO-dependent inhibition of DNA repair synthesis

Scientific Fields
Diseases
Organisms
Applications
Technique

Published in The EMBO journal - 08 Feb 2013

Burkovics P, Sebesta M, Sisakova A, Plault N, Szukacsov V, Robert T, Pinter L, Marini V, Kolesar P, Haracska L, Gangloff S, Krejci L

Link to Pubmed [PMID] – 23395907

EMBO J. 2013 Mar;32(5):742-55

Completion of DNA replication needs to be ensured even when challenged with fork progression problems or DNA damage. PCNA and its modifications constitute a molecular switch to control distinct repair pathways. In yeast, SUMOylated PCNA (S-PCNA) recruits Srs2 to sites of replication where Srs2 can disrupt Rad51 filaments and prevent homologous recombination (HR). We report here an unexpected additional mechanism by which S-PCNA and Srs2 block the synthesis-dependent extension of a recombination intermediate, thus limiting its potentially hazardous resolution in association with a cross-over. This new Srs2 activity requires the SUMO interaction motif at its C-terminus, but neither its translocase activity nor its interaction with Rad51. Srs2 binding to S-PCNA dissociates Polδ and Polη from the repair synthesis machinery, thus revealing a novel regulatory mechanism controlling spontaneous genome rearrangements. Our results suggest that cycling cells use the Siz1-dependent SUMOylation of PCNA to limit the extension of repair synthesis during template switch or HR and attenuate reciprocal DNA strand exchanges to maintain genome stability.

http://www.ncbi.nlm.nih.gov/pubmed/23395907