Werner's syndrome protein (WRN) migrates Holliday junctions and co-localizes with RPA upon replication arrest.

Abstract:

:Individuals affected by the autosomal recessive disorder Werner's syndrome (WS) develop many of the symptoms characteristic of premature ageing. Primary fibroblasts cultured from WS patients exhibit karyotypic abnormalities and a reduced replicative life span. The WRN gene encodes a 3'-5' DNA helicase, and is a member of the RecQ family, which also includes the product of the Bloom's syndrome gene (BLM). In this work, we show that WRN promotes the ATP-dependent translocation of Holliday junctions, an activity that is also exhibited by BLM. In cells arrested in S-phase with hydroxyurea, WRN localizes to discrete nuclear foci that coincide with those formed by the single-stranded DNA binding protein replication protein A. These results are consistent with a model in which WRN prevents aberrant recombination events at sites of stalled replication forks by dissociating recombination intermediates.

journal_name

EMBO Rep

journal_title

EMBO reports

authors

Constantinou A,Tarsounas M,Karow JK,Brosh RM,Bohr VA,Hickson ID,West SC

doi

10.1093/embo-reports/kvd004

keywords:

subject

Has Abstract

pub_date

2000-07-01 00:00:00

pages

80-4

issue

1

eissn

1469-221X

issn

1469-3178

pii

embor632

journal_volume

1

pub_type

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