J 2016

Pro-recombination Role of Srs2 Protein Requires SUMO (Small ubiquitin-like Modifier) but Is Independent of PCNA (Proliferating Cell Nuclear Antigen) Interaction

KOLESÁR, Peter, Veronika ALTMANNOVÁ, Sonia SILVA, Michael LISBY, Lumír KREJČÍ et. al.

Basic information

Original name

Pro-recombination Role of Srs2 Protein Requires SUMO (Small ubiquitin-like Modifier) but Is Independent of PCNA (Proliferating Cell Nuclear Antigen) Interaction

Authors

KOLESÁR, Peter (703 Slovakia, belonging to the institution), Veronika ALTMANNOVÁ (203 Czech Republic, belonging to the institution), Sonia SILVA (208 Denmark), Michael LISBY (208 Denmark) and Lumír KREJČÍ (203 Czech Republic, guarantor, belonging to the institution)

Edition

Journal of Biological Chemistry, Bethesda, American Society for Biochemistry and Molecular Biology Inc. 2016, 0021-9258

Other information

Language

English

Type of outcome

Článek v odborném periodiku

Field of Study

Genetics and molecular biology

Country of publisher

United States of America

Confidentiality degree

není předmětem státního či obchodního tajemství

Impact factor

Impact factor: 4.125

RIV identification code

RIV/00216224:14110/16:00088201

Organization unit

Faculty of Medicine

DOI

UT WoS

000383447600032

Keywords in English

DNA repair; Homologous recombination; Possible mechanisms; Post-translational modifications; Proliferating cell nuclear antigens; Recombination factors; Small ubiquitin-like modifiers; Sumoylation

Tags

Tags

International impact, Reviewed
Změněno: 28/11/2016 16:09, Ing. Mgr. Věra Pospíšilíková

Abstract

V originále

Srs2 plays many roles in DNA repair, the proper regulation and coordination of which is essential. Post-translational modification by small ubiquitin-like modifier (SUMO) is one such possible mechanism. Here, we investigate the role of SUMO in Srs2 regulation and show that the SUMO-interacting motif (SIM) of Srs2 is important for the interaction with several recombination factors. Lack of SIM, but not proliferating cell nuclear antigen (PCNA)-interacting motif (PIM), leads to increased cell death under circumstances requiring homologous recombination for DNA repair. Simultaneous mutation of SIM in a srs2 deltaPIM strain leads to a decrease in recombination, indicating a pro-recombination role of SUMO. Thus SIM has an ambivalent function in Srs2 regulation; it not only mediates interaction with SUMO-PCNA to promote the anti-recombination function but it also plays a PCNA-independent pro-recombination role, probably by stimulating the formation of recombination complexes. The fact that deletion of PIM suppresses the phenotypes of Srs2 lacking SIM suggests that proper balance between the anti-recombination PCNA-bound and pro-recombination pools of Srs2 is crucial. Notably, sumoylation of Srs2 itself specifically stimulates recombination at the rDNA locus.

Links

EE2.3.30.0009, research and development project
Name: Zaměstnáním čerstvých absolventů doktorského studia k vědecké excelenci
EE2.3.30.0037, research and development project
Name: Zaměstnáním nejlepších mladých vědců k rozvoji mezinárodní spolupráce
GAP207/12/2323, research and development project
Name: Endonuleazová a translokázová aktivita v restričních-modifikáčních komplexéch typu I
Investor: Czech Science Foundation
GA13-26629S, research and development project
Name: SUMO a stability genomu
Investor: Czech Science Foundation
MUNI/M/1894/2014, interní kód MU
Name: Development of new MUS81 nuclease inhibitors as chemical biology probe with clinical progression
Investor: Masaryk University, INTERDISCIPLINARY - Interdisciplinary research projects
ROZV/20/LF/2015, interní kód MU
Name: LF - Příspěvek IP 2015
Investor: Ministry of Education, Youth and Sports of the CR