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 nuclease. Furthermore, fluorescent microscopy studies reveal that, when Sgs1 resection activity is compromised in sae2Δ cells, Mre11 repair foci persist. We suggest a model where the role of Sgs1 in end resection along with Sae2 is important for removing Mre11 from DNA ends during repair.
journal_name
Geneticsjournal_title
Geneticsauthors
Bernstein KA,Mimitou EP,Mihalevic MJ,Chen H,Sunjaveric I,Symington LS,Rothstein Rdoi
10.1534/genetics.113.157370subject
Has Abstractpub_date
2013-12-01 00:00:00pages
1241-51issue
4eissn
0016-6731issn
1943-2631pii
genetics.113.157370journal_volume
195pub_type
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