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Werner's syndrome protein (WRN) migrates Holliday junctions and co‐localizes with RPA upon replication arrest
Author(s) -
Constantinou Angelos,
Tarsounas Madalena,
Karow Julia K,
Brosh Robert M,
Bohr Vilhelm A,
Hickson Ian D,
West Stephen C
Publication year - 2000
Publication title -
embo reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.584
H-Index - 184
eISSN - 1469-3178
pISSN - 1469-221X
DOI - 10.1093/embo-reports/kvd004
Subject(s) - holliday junction , werner syndrome , helicase , bloom syndrome , recq helicase , biology , homologous recombination , dna replication , gene , dna , genetics , premature aging , microbiology and biotechnology , dna repair , rna
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.