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pubmed-article:21317047pubmed:dateCreated2011-3-22lld:pubmed
pubmed-article:21317047pubmed:abstractTextRecombination between inverted repeats is RAD52 dependent, but reduced only modestly in the rad51? mutant. RAD59 is required for RAD51-independent inverted-repeat recombination, but no clear mechanism for how recombination occurs in the absence of RAD51 has emerged. Because Rad59 is thought to function as an accessory factor for the single-strand annealing activity of Rad52 one possible mechanism for spontaneous recombination could be by strand annealing between repeats at a stalled replication fork. Here we demonstrate the importance of the Rad52 single-strand annealing activity for generating recombinants by showing suppression of the rad52?, rad51? rad52? and rad52? rad59? inverted-repeat recombination defects by the rfa1-D228Y mutation. In addition, formation of recombinants in the rad51? mutant was sensitive to the distance between the inverted repeats, consistent with a replication-based mechanism. Deletion of RAD5 or RAD18, which are required for error-free post-replication repair, reduced the recombination rate in the rad59? mutant, but not in wild type. These data are consistent with RAD51-independent recombinants arising by a faulty template switch mechanism that is distinct from nascent strand template switching.lld:pubmed
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pubmed-article:21317047pubmed:authorpubmed-author:SymingtonLorr...lld:pubmed
pubmed-article:21317047pubmed:authorpubmed-author:MottChristina...lld:pubmed
pubmed-article:21317047pubmed:copyrightInfoCopyright © 2011 Elsevier B.V. All rights reserved.lld:pubmed
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pubmed-article:21317047pubmed:year2011lld:pubmed
pubmed-article:21317047pubmed:articleTitleRAD51-independent inverted-repeat recombination by a strand-annealing mechanism.lld:pubmed
pubmed-article:21317047pubmed:affiliationDepartment of Microbiology & Immunology, Columbia University Medical Center, 701 W. 168th St, New York, NY 10032, USA.lld:pubmed
pubmed-article:21317047pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:21317047pubmed:publicationTypeResearch Support, N.I.H., Extramurallld:pubmed
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