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Rad52 sumoylation and its involvement in the efficient induction of homologous recombination.
DNA Repair (Amst). 2008 Jun 01; 7(6):879-89.DR

Abstract

The protein Rad52 is a key player in various types of homologous recombination and is essential to maintenance of genomic integrity. Although evidence indicates that Rad52 is modified by SUMO, the physiological relevance of this sumoylation remains unclear. Here, we identify the conditions under which Rad52 sumoylation is induced, and clarify the role of this modification in homologous recombination. Oligomerization of Rad52 was a prerequisite for sumoylation, and the modification occurred in the cell proceeding S phase being exposed to the DNA-damaging agent methyl methanesulfonate (MMS). Following exposure to MMS, sumoylated Rad52 accumulated in rad51 cells, but not in the recombination-related gene mutants, rad54, rad55, rad59, sgs1, or srs2. The accumulation of sumoylated Rad52 was suppressed in rad51 cells expressing Rad51-K191R, an ATPase-defective protein presumed to be recruited to ssDNA. Although the sumoylation defective mutant rad52-3KR (K10R/K11R/K220R) showed no defect in mating-type switching, which did not lead to Rad52 sumoylation in wild-type cells, the mutant did demonstrate a partial defect in MMS-induced interchromosomal homologous recombination.

Authors+Show Affiliations

Molecular Cell Biology Laboratory, Graduate School of Pharmaceutical Sciences, Tohoku University, Aoba 6-3, Aramaki, Aoba-ku, Sendai 980-8578, Japan.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

18396468

Citation

Ohuchi, Takashi, et al. "Rad52 Sumoylation and Its Involvement in the Efficient Induction of Homologous Recombination." DNA Repair, vol. 7, no. 6, 2008, pp. 879-89.
Ohuchi T, Seki M, Branzei D, et al. Rad52 sumoylation and its involvement in the efficient induction of homologous recombination. DNA Repair (Amst). 2008;7(6):879-89.
Ohuchi, T., Seki, M., Branzei, D., Maeda, D., Ui, A., Ogiwara, H., Tada, S., & Enomoto, T. (2008). Rad52 sumoylation and its involvement in the efficient induction of homologous recombination. DNA Repair, 7(6), 879-89. https://doi.org/10.1016/j.dnarep.2008.02.005
Ohuchi T, et al. Rad52 Sumoylation and Its Involvement in the Efficient Induction of Homologous Recombination. DNA Repair (Amst). 2008 Jun 1;7(6):879-89. PubMed PMID: 18396468.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Rad52 sumoylation and its involvement in the efficient induction of homologous recombination. AU - Ohuchi,Takashi, AU - Seki,Masayuki, AU - Branzei,Dana, AU - Maeda,Daisuke, AU - Ui,Ayako, AU - Ogiwara,Hideaki, AU - Tada,Shusuke, AU - Enomoto,Takemi, Y1 - 2008/04/08/ PY - 2007/12/26/received PY - 2008/02/04/revised PY - 2008/02/13/accepted PY - 2008/4/9/pubmed PY - 2008/8/6/medline PY - 2008/4/9/entrez SP - 879 EP - 89 JF - DNA repair JO - DNA Repair (Amst) VL - 7 IS - 6 N2 - The protein Rad52 is a key player in various types of homologous recombination and is essential to maintenance of genomic integrity. Although evidence indicates that Rad52 is modified by SUMO, the physiological relevance of this sumoylation remains unclear. Here, we identify the conditions under which Rad52 sumoylation is induced, and clarify the role of this modification in homologous recombination. Oligomerization of Rad52 was a prerequisite for sumoylation, and the modification occurred in the cell proceeding S phase being exposed to the DNA-damaging agent methyl methanesulfonate (MMS). Following exposure to MMS, sumoylated Rad52 accumulated in rad51 cells, but not in the recombination-related gene mutants, rad54, rad55, rad59, sgs1, or srs2. The accumulation of sumoylated Rad52 was suppressed in rad51 cells expressing Rad51-K191R, an ATPase-defective protein presumed to be recruited to ssDNA. Although the sumoylation defective mutant rad52-3KR (K10R/K11R/K220R) showed no defect in mating-type switching, which did not lead to Rad52 sumoylation in wild-type cells, the mutant did demonstrate a partial defect in MMS-induced interchromosomal homologous recombination. SN - 1568-7864 UR - https://www.unboundmedicine.com/medline/citation/18396468/Rad52_sumoylation_and_its_involvement_in_the_efficient_induction_of_homologous_recombination_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S1568-7864(08)00060-8 DB - PRIME DP - Unbound Medicine ER -