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Rad51 inhibits translocation formation by non-conservative homologous recombination in Saccharomyces cerevisiae.
PLoS One. 2010 Jul 29; 5(7):e11889.Plos

Abstract

Chromosomal translocations are a primary biological response to ionizing radiation (IR) exposure, and are likely to result from the inappropriate repair of the DNA double-strand breaks (DSBs) that are created. An abundance of repetitive sequences in eukaryotic genomes provides ample opportunity for such breaks to be repaired by homologous recombination (HR) between non-allelic repeats. Interestingly, in the budding yeast, Saccharomyces cerevisiae the central strand exchange protein, Rad51 that is required for DSB repair by gene conversion between unlinked repeats that conserves genomic structure also suppresses translocation formation by several HR mechanisms. In particular, Rad51 suppresses translocation formation by single-strand annealing (SSA), perhaps the most efficient mechanism for translocation formation by HR in both yeast and mammalian cells. Further, the enhanced translocation formation that emerges in the absence of Rad51 displays a distinct pattern of genetic control, suggesting that this occurs by a separate mechanism. Since hypomorphic mutations in RAD51 in mammalian cells also reduce DSB repair by conservative gene conversion and stimulate non-conservative repair by SSA, this mechanism may also operate in humans and, perhaps contribute to the genome instability that propels the development of cancer.

Authors+Show Affiliations

Department of Molecular and Cellular Biology, Beckman Research Institute, City of Hope National Medical Center, Duarte, California, United States of America.No affiliation info available

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, Non-P.H.S.

Language

eng

PubMed ID

20686691

Citation

Manthey, Glenn M., and Adam M. Bailis. "Rad51 Inhibits Translocation Formation By Non-conservative Homologous Recombination in Saccharomyces Cerevisiae." PloS One, vol. 5, no. 7, 2010, pp. e11889.
Manthey GM, Bailis AM. Rad51 inhibits translocation formation by non-conservative homologous recombination in Saccharomyces cerevisiae. PLoS One. 2010;5(7):e11889.
Manthey, G. M., & Bailis, A. M. (2010). Rad51 inhibits translocation formation by non-conservative homologous recombination in Saccharomyces cerevisiae. PloS One, 5(7), e11889. https://doi.org/10.1371/journal.pone.0011889
Manthey GM, Bailis AM. Rad51 Inhibits Translocation Formation By Non-conservative Homologous Recombination in Saccharomyces Cerevisiae. PLoS One. 2010 Jul 29;5(7):e11889. PubMed PMID: 20686691.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Rad51 inhibits translocation formation by non-conservative homologous recombination in Saccharomyces cerevisiae. AU - Manthey,Glenn M, AU - Bailis,Adam M, Y1 - 2010/07/29/ PY - 2010/05/13/received PY - 2010/07/07/accepted PY - 2010/8/6/entrez PY - 2010/8/6/pubmed PY - 2010/10/29/medline SP - e11889 EP - e11889 JF - PloS one JO - PLoS One VL - 5 IS - 7 N2 - Chromosomal translocations are a primary biological response to ionizing radiation (IR) exposure, and are likely to result from the inappropriate repair of the DNA double-strand breaks (DSBs) that are created. An abundance of repetitive sequences in eukaryotic genomes provides ample opportunity for such breaks to be repaired by homologous recombination (HR) between non-allelic repeats. Interestingly, in the budding yeast, Saccharomyces cerevisiae the central strand exchange protein, Rad51 that is required for DSB repair by gene conversion between unlinked repeats that conserves genomic structure also suppresses translocation formation by several HR mechanisms. In particular, Rad51 suppresses translocation formation by single-strand annealing (SSA), perhaps the most efficient mechanism for translocation formation by HR in both yeast and mammalian cells. Further, the enhanced translocation formation that emerges in the absence of Rad51 displays a distinct pattern of genetic control, suggesting that this occurs by a separate mechanism. Since hypomorphic mutations in RAD51 in mammalian cells also reduce DSB repair by conservative gene conversion and stimulate non-conservative repair by SSA, this mechanism may also operate in humans and, perhaps contribute to the genome instability that propels the development of cancer. SN - 1932-6203 UR - https://www.unboundmedicine.com/medline/citation/20686691/Rad51_inhibits_translocation_formation_by_non_conservative_homologous_recombination_in_Saccharomyces_cerevisiae_ L2 - https://dx.plos.org/10.1371/journal.pone.0011889 DB - PRIME DP - Unbound Medicine ER -