Resection activity of the Sgs1 helicase alters the affinity of DNA ends for homologous recombination proteins in Saccharomyces cerevisiae.

ABSTRACT: The RecQ helicase family is critical during DNA damage repair, and mutations in these proteins are associated with Bloom, Werner, or Rothmund-Thompson syndromes in humans, leading to cancer predisposition and/or premature aging. In the budding yeast Saccharomyces cerevisiae, mutations in the RecQ homolog, SGS1, phenocopy many of the defects observed in the human syndromes. One challenge to studying RecQ helicases is that their disruption leads to a pleiotropic phenotype. Using yeast, we show that the separation-of-function allele of SGS1, sgs1-D664Δ, has impaired activity at DNA ends, resulting in a resection processivity defect. Compromising Sgs1 resection function in the absence of the Sae2 nuclease causes slow growth, which is alleviated by making the DNA ends accessible to Exo1 nucleas

SUBMITTER: Bernstein KA 

PROVIDER: S-EPMC3832270 | biostudies-literature | 2013 Dec

REPOSITORIES: biostudies-literature