Pro-recombination role of Srs2 requires SUMO but is independent of PCNA interaction

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00159816%3A_____%2F16%3A00064071" target="_blank" >RIV/00159816:_____/16:00064071 - isvavai.cz</a>

Výsledek na webu

<a href="http://dx.doi.org/10.1074/jbc.M115.685891" target="_blank" >http://dx.doi.org/10.1074/jbc.M115.685891</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1074/jbc.M115.685891" target="_blank" >10.1074/jbc.M115.685891</a>

Jazyk výsledku

angličtina

Název v původním jazyce

Pro-recombination role of Srs2 requires SUMO but is independent of PCNA interaction

Popis výsledku v původním jazyce

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 SUMO's role 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 PCNA-interacting motif (PIM), leads to increased cell death under circumstances requiring homologous recombination for DNA repair. Simultaneous mutation of SIM in a srs2dPIM 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.

Název v anglickém jazyce

Pro-recombination role of Srs2 requires SUMO but is independent of PCNA interaction

Popis výsledku anglicky

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 SUMO's role 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 PCNA-interacting motif (PIM), leads to increased cell death under circumstances requiring homologous recombination for DNA repair. Simultaneous mutation of SIM in a srs2dPIM 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.

Druh

J_x - Nezařazeno - Článek v odborném periodiku (Jimp, Jsc a Jost)

CEP obor

CE - Biochemie

OECD FORD obor

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Projekt

Výsledek vznikl pri realizaci vícero projektů. Více informací v záložce Projekty.

Návaznosti

P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)

Rok uplatnění

2016

Kód důvěrnosti údajů

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Název periodika

Journal of Biological Chemistry

ISSN

0021-9258

e-ISSN

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Svazek periodika

291

Číslo periodika v rámci svazku

14

Stát vydavatele periodika

US - Spojené státy americké

Počet stran výsledku

14

Strana od-do

7594-7607

Kód UT WoS článku

000383447600032

EID výsledku v databázi Scopus

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