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

Détails

ID Serval
serval:BIB_C4FC6771E90F
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Titre
Werner's syndrome protein (WRN) migrates Holliday junctions and co-localizes with RPA upon replication arrest
Périodique
EMBO Reports
Auteur(s)
Constantinou  A., Tarsounas  M., Karow  J. K., Brosh  R. M., Bohr  V. A., Hickson  I. D., West  S. C.
ISSN
1469-221X (Print)
Statut éditorial
Publié
Date de publication
07/2000
Volume
1
Numéro
1
Pages
80-4
Notes
Journal Article
Research Support, Non-U.S. Gov't --- Old month value: Jul
Résumé
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.
Mots-clé
Adenosine Triphosphatases/genetics/metabolism Adenosine Triphosphate/metabolism Bacterial Proteins/genetics/metabolism Cell Nucleus/metabolism DNA/genetics/*metabolism DNA Helicases/genetics/*metabolism *DNA Replication Hela Cells Humans Microscopy, Fluorescence RecQ Helicases Recombinant Proteins/genetics/metabolism *Recombination, Genetic Werner Syndrome/genetics/*metabolism
Pubmed
Web of science
Création de la notice
24/01/2008 15:50
Dernière modification de la notice
03/03/2018 21:14
Données d'usage