Mouse WRN helicase domain is not required for spontaneous homologous recombination-mediated DNA deletion

Adam D. Brown, Alison B. Claybon, Alexander J.R. Bishop

Research output: Contribution to journalArticle

4 Scopus citations

Abstract

Werner syndrome is a rare disorder that manifests as premature aging and age-related diseases. WRN is the gene mutated in WS, and is one of five human RecQ helicase family members. WS cells exhibit genomic instability and altered proliferation, and in vitro studies suggest that WRN has a role in suppressing homologous recombination. However, more recent studies propose that other RecQ helicases (including WRN) promote early events of homologous recombination. To study the role of WRN helicase on spontaneous homologous recombination, we obtained a mouse with a deleted WRN helicase domain and combined it with the in vivo pink-eyed unstable homologous recombination system. In this paper, we demonstrate that WRN helicase is not necessary for suppressing homologous recombination in vivo contrary to previous reports using a similar mouse model.

Original languageEnglish (US)
Article number356917
JournalJournal of Nucleic Acids
Volume2010
DOIs
StatePublished - 2010

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology

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