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dc.contributor.authorWasko, Brian
dc.date.accessioned2021-07-15T15:47:56Z
dc.date.available2021-07-15T15:47:56Z
dc.date.issued2009
dc.identifier.citationWasko BM, Holland CL, Resnick MA, and Lewis LK. Inhibition of DNA double-strand break repair by the Ku heterodimer in mrx mutants of Saccharomyces cerevisiae. DNA Repair (Amst). 2009 Feb 1;8(2):162-9.en_US
dc.identifier.urihttps://hdl.handle.net/10657.1/2568
dc.description.abstractYeast rad50 and mre11 nuclease mutants are hypersensitive to physical and chemical agents that induce DNA double-strand breaks (DSBs). This sensitivity was suppressed by elevating intracellular levels of TLC1, the RNA subunit of telomerase. Suppression required proteins linked to homologous recombination, including Rad51, Rad52, Rad59 and Exo1, but not genes of the nonhomologous end-joining (NHEJ) repair pathway. Deletion mutagenesis experiments demonstrated that the 5’ end of TLC1 RNA was essential and a segment containing a binding site for the Yku70/Yku80 complex was sufficient for suppression. A mutant TLC1 RNA unable to associate with Yku80 protein did not increase resistance. These and other genetic studies indicated that association of the Ku heterodimer with broken DNA ends inhibits recombination in mrx mutants, but not in repair-proficient cells or in other DNA repair single mutants. In support of this model, DNA damage resistance of mrx cells was enhanced when YKU70 was coinactivated. Defective recombination repair of DSBs in mrx cells thus arises from at least two separate processes: loss of mrx nuclease-associated DNA end-processing and inhibition of the Exo1-mediated secondary recombination pathway by Ku.en_US
dc.publisherDNA Repairen_US
dc.subjecttelomerase, exonuclease, DNA repair, end-joining, homologous recombinationen_US
dc.titleInhibition of DNA double-strand break repair by the Ku heterodimer in mrx mutants of Saccharomyces cerevisiaeen_US
dc.typeArticleen_US


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