Reference: Ma W, et al. (2009) The transition of closely opposed lesions to double-strand breaks during long-patch base excision repair is prevented by the coordinated action of DNA polymerase delta and Rad27/Fen1. Mol Cell Biol 29(5):1212-21

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Abstract

DNA double-strand breaks can result from closely-opposed breaks induced directly in complementary strands. Alternatively, double-strand breaks could be generated during repair of clustered damage, where the repair of closely-opposed lesions has to be well-coordinated. Using single and multiple mutants of budding yeast that impede interaction of DNA polymerase delta and 5'-flap endonuclease Rad27/Fen1 with the PCNA sliding clamp, we show that the lack of coordination between these components during long-patch base excision repair of alkylation damage can result in many double-strand breaks within the chromosomes of non-dividing haploid cells. This contrasts with the efficient repair of non-clustered MMS-induced lesions, as measured by quantitative PCR and S1 nuclease cleavage of single-strand break sites. We conclude that closely-opposed single-strand lesions are a unique threat to the genome and that repair of closely-opposed strand damage requires greater spatial and temporal coordination between the participating proteins than widely-spaced damage in order to prevent the development of double-strand breaks.

Reference Type
Journal Article
Authors
Ma W, Panduri V, Sterling JF, Van Houten B, Gordenin DA, Resnick MA
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