Mouse WRN Helicase Domain Is Not Required for Spontaneous Homologous Recombination-Mediated DNA Deletion. (26th July 2010)

• Record Type: Journal Article
• Authors: Brown, Adam D.; Claybon, Alison B.; Bishop, Alexander J. R.
• Other Names: Basu Ashis Academic Editor.
• Is Part Of: Journal of nucleic acids. Volume 2010(2010)
• Publication Date: 2010-07-26
• Subjects: Nucleic acids -- Periodicals; 572.805
• DOI: 10.4061/2010/356917
• Languages: English
• ISSNs: 2090-0201

Abstract

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.