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

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&#...

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Main Authors: Constantinou, A, Tarsounas, M, Karow, J, Brosh, R, Bohr, V, Hickson, I, West, S
Format: Journal article
Language:English
Published: 2000
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author Constantinou, A
Tarsounas, M
Karow, J
Brosh, R
Bohr, V
Hickson, I
West, S
author_facet Constantinou, A
Tarsounas, M
Karow, J
Brosh, R
Bohr, V
Hickson, I
West, S
author_sort Constantinou, A
collection OXFORD
description 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.
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spelling oxford-uuid:4bb41b1f-91d3-489d-8e70-380b7b0b7cee2022-03-26T15:45:03ZWerner's syndrome protein (WRN) migrates Holliday junctions and co-localizes with RPA upon replication arrest.Journal articlehttp://purl.org/coar/resource_type/c_dcae04bcuuid:4bb41b1f-91d3-489d-8e70-380b7b0b7ceeEnglishSymplectic Elements at Oxford2000Constantinou, ATarsounas, MKarow, JBrosh, RBohr, VHickson, IWest, SIndividuals 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.
spellingShingle Constantinou, A
Tarsounas, M
Karow, J
Brosh, R
Bohr, V
Hickson, I
West, S
Werner's syndrome protein (WRN) migrates Holliday junctions and co-localizes with RPA upon replication arrest.
title Werner's syndrome protein (WRN) migrates Holliday junctions and co-localizes with RPA upon replication arrest.
title_full Werner's syndrome protein (WRN) migrates Holliday junctions and co-localizes with RPA upon replication arrest.
title_fullStr Werner's syndrome protein (WRN) migrates Holliday junctions and co-localizes with RPA upon replication arrest.
title_full_unstemmed Werner's syndrome protein (WRN) migrates Holliday junctions and co-localizes with RPA upon replication arrest.
title_short Werner's syndrome protein (WRN) migrates Holliday junctions and co-localizes with RPA upon replication arrest.
title_sort werner s syndrome protein wrn migrates holliday junctions and co localizes with rpa upon replication arrest
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