BURKOVICS, Peter, Marek ŠEBESTA, Alexandra SISÁKOVÁ, Nicolas PLAULT, Valeria SZUKACSOV, Thomas ROBERT, Lajos PINTER, María Victoria MARINI PALOMEQUE, Peter KOLESÁR, Lajos HARACSKA, Serge GANGLOFF and Lumír KREJČÍ. Srs2 mediates PCNA-SUMO-dependent inhibition of DNA repair synthesis. EMBO JOURNAL. NEW YORK: NATURE PUBLISHING GROUP, 2013, vol. 32, No 5, p. 742-755. ISSN 0261-4189. doi:10.1038/emboj.2013.9.
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Basic information
Original name Srs2 mediates PCNA-SUMO-dependent inhibition of DNA repair synthesis
Authors BURKOVICS, Peter (348 Hungary, belonging to the institution), Marek ŠEBESTA (703 Slovakia, belonging to the institution), Alexandra SISÁKOVÁ (703 Slovakia, belonging to the institution), Nicolas PLAULT (250 France), Valeria SZUKACSOV (348 Hungary), Thomas ROBERT (250 France), Lajos PINTER (348 Hungary), María Victoria MARINI PALOMEQUE (858 Uruguay, belonging to the institution), Peter KOLESÁR (703 Slovakia, belonging to the institution), Lajos HARACSKA (348 Hungary), Serge GANGLOFF (250 France) and Lumír KREJČÍ (203 Czech Republic, guarantor, belonging to the institution).
Other information
Original language English
Type of outcome Article in a journal
Field of Study Genetics and molecular biology
Country of publisher United States of America
Confidentiality degree is not subject to a state or trade secret
Impact factor Impact factor: 10.748
RIV identification code RIV/00216224:14110/13:00066406
Organization unit Faculty of Medicine
Doi http://dx.doi.org/10.1038/emboj.2013.9
UT WoS 000316468000014
Keywords in English DNA repair synthesis; genome stability; PCNA SUMOylation; Srs2; SUMO interacting motif
Tags podil
Tags International impact, Reviewed
Changed by Changed by: prof. Ing. Petr Dvořák, CSc., učo 47260. Changed: 14/2/2014 08:57.
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 Pol delta and Pol eta 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.
GAP207/12/2323, research and development projectName: Endonuleazová a translokázová aktivita v restričních-modifikáčních komplexéch typu I
Investor: Czech Science Foundation
GA13-26629S, research and development projectName: SUMO a stability genomu
Investor: Czech Science Foundation
GA301/09/1917, research and development projectName: Štěpení replikačních-rekombinačních DNA meziproduktů a jejich úloha při nestabilitě genomu
Investor: Czech Science Foundation
GD203/09/H046, research and development projectName: Biochemie na rozcestí mezi in silico a in vitro
Investor: Czech Science Foundation
ME10048, research and development projectName: Vliv post-translačních modifikací na DNA opravu a rekombinaci.
Investor: Ministry of Education, Youth and Sports of the CR, Research and Development Programme KONTAKT (ME)
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