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Ionizing radiation-induced foci formation of mammalian Rad51 and Rad54 depends on the Rad51 paralogs, but not on Rad52.
Mutat Res. 2005 Jul 01; 574(1-2):34-49.MR

Abstract

Homologous recombination is of major importance for the prevention of genomic instability during chromosome duplication and repair of DNA damage, especially double-strand breaks. Biochemical experiments have revealed that during the process of homologous recombination the RAD52 group proteins, including Rad51, Rad52 and Rad54, are involved in an essential step: formation of a joint molecule between the broken DNA and the intact repair template. Accessory proteins for this reaction include the Rad51 paralogs and BRCA2. The significance of homologous recombination for the cell is underscored by the evolutionary conservation of the Rad51, Rad52 and Rad54 proteins from yeast to humans. Upon treatment of cells with ionizing radiation, the RAD52 group proteins accumulate at the sites of DNA damage into so-called foci. For the yeast Saccharomyces cerevisiae, foci formation of Rad51 and Rad54 is abrogated in the absence of Rad52, while Rad51 foci formation does occur in the absence of the Rad51 paralog Rad55. By contrast, we show here that in mammalian cells, Rad52 is not required for foci formation of Rad51 and Rad54. Furthermore, radiation-induced foci formation of Rad51 and Rad54 is impaired in all Rad51 paralog and BRCA2 mutant cell lines tested, while Rad52 foci formation is not influenced by a mutation in any of these recombination proteins. Despite their evolutionary conservation and biochemical similarities, S. cerevisiae and mammalian Rad52 appear to differentially contribute to the DNA-damage response.

Authors+Show Affiliations

Department of Cell Biology and Genetics, Erasmus MC, University Medical Center, P.O. Box 1738, 3000 DR Rotterdam, The Netherlands.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

15914205

Citation

van Veelen, Lieneke R., et al. "Ionizing Radiation-induced Foci Formation of Mammalian Rad51 and Rad54 Depends On the Rad51 Paralogs, but Not On Rad52." Mutation Research, vol. 574, no. 1-2, 2005, pp. 34-49.
van Veelen LR, Essers J, van de Rakt MW, et al. Ionizing radiation-induced foci formation of mammalian Rad51 and Rad54 depends on the Rad51 paralogs, but not on Rad52. Mutat Res. 2005;574(1-2):34-49.
van Veelen, L. R., Essers, J., van de Rakt, M. W., Odijk, H., Pastink, A., Zdzienicka, M. Z., Paulusma, C. C., & Kanaar, R. (2005). Ionizing radiation-induced foci formation of mammalian Rad51 and Rad54 depends on the Rad51 paralogs, but not on Rad52. Mutation Research, 574(1-2), 34-49.
van Veelen LR, et al. Ionizing Radiation-induced Foci Formation of Mammalian Rad51 and Rad54 Depends On the Rad51 Paralogs, but Not On Rad52. Mutat Res. 2005 Jul 1;574(1-2):34-49. PubMed PMID: 15914205.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Ionizing radiation-induced foci formation of mammalian Rad51 and Rad54 depends on the Rad51 paralogs, but not on Rad52. AU - van Veelen,Lieneke R, AU - Essers,Jeroen, AU - van de Rakt,Mandy W M M, AU - Odijk,Hanny, AU - Pastink,Albert, AU - Zdzienicka,Małgorzata Z, AU - Paulusma,Coen C, AU - Kanaar,Roland, Y1 - 2005/04/09/ PY - 2004/08/30/received PY - 2004/12/08/revised PY - 2005/01/10/accepted PY - 2005/5/26/pubmed PY - 2005/7/19/medline PY - 2005/5/26/entrez SP - 34 EP - 49 JF - Mutation research JO - Mutat Res VL - 574 IS - 1-2 N2 - Homologous recombination is of major importance for the prevention of genomic instability during chromosome duplication and repair of DNA damage, especially double-strand breaks. Biochemical experiments have revealed that during the process of homologous recombination the RAD52 group proteins, including Rad51, Rad52 and Rad54, are involved in an essential step: formation of a joint molecule between the broken DNA and the intact repair template. Accessory proteins for this reaction include the Rad51 paralogs and BRCA2. The significance of homologous recombination for the cell is underscored by the evolutionary conservation of the Rad51, Rad52 and Rad54 proteins from yeast to humans. Upon treatment of cells with ionizing radiation, the RAD52 group proteins accumulate at the sites of DNA damage into so-called foci. For the yeast Saccharomyces cerevisiae, foci formation of Rad51 and Rad54 is abrogated in the absence of Rad52, while Rad51 foci formation does occur in the absence of the Rad51 paralog Rad55. By contrast, we show here that in mammalian cells, Rad52 is not required for foci formation of Rad51 and Rad54. Furthermore, radiation-induced foci formation of Rad51 and Rad54 is impaired in all Rad51 paralog and BRCA2 mutant cell lines tested, while Rad52 foci formation is not influenced by a mutation in any of these recombination proteins. Despite their evolutionary conservation and biochemical similarities, S. cerevisiae and mammalian Rad52 appear to differentially contribute to the DNA-damage response. SN - 0027-5107 UR - https://www.unboundmedicine.com/medline/citation/15914205/Ionizing_radiation_induced_foci_formation_of_mammalian_Rad51_and_Rad54_depends_on_the_Rad51_paralogs_but_not_on_Rad52_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0027-5107(05)00087-4 DB - PRIME DP - Unbound Medicine ER -