Pro-recombination Role of Srs2 Protein Requires SUMO (Small ubiquitin-like Modifier) but Is Independent of PCNA (Proliferating Cell Nuclear Antigen) Interaction
| Autoři | |
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| Rok publikování | 2016 |
| Druh | Článek v odborném periodiku |
| Časopis / Zdroj | Journal of Biological Chemistry |
| Fakulta / Pracoviště MU | |
| Citace | |
| Doi | http://dx.doi.org/10.1074/jbc.M115.685891 |
| Obor | Genetika a molekulární biologie |
| Klíčová slova | DNA repair; Homologous recombination; Possible mechanisms; Post-translational modifications; Proliferating cell nuclear antigens; Recombination factors; Small ubiquitin-like modifiers; Sumoylation |
| Popis | 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. |
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