The Bloom's syndrome gene product promotes branch migration of holliday junctions

Détails

ID Serval
serval:BIB_7B2737F40C27
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Titre
The Bloom's syndrome gene product promotes branch migration of holliday junctions
Périodique
Proceedings of the National Academy of Sciences of the United States of America
Auteur(s)
Karow  J. K., Constantinou  A., Li  J. L., West  S. C., Hickson  I. D.
ISSN
0027-8424 (Print)
Statut éditorial
Publié
Date de publication
06/2000
Volume
97
Numéro
12
Pages
6504-8
Notes
Journal Article
Research Support, Non-U.S. Gov't --- Old month value: Jun 6
Résumé
Bloom's syndrome (BS) is an autosomal recessive disorder associated with dwarfism, immunodeficiency, reduced fertility, and elevated levels of many types of cancer. BS cells show marked genomic instability; in particular, hyperrecombination between sister chromatids and homologous chromosomes. This instability is thought to result from defective processing of DNA replication intermediates. The gene mutated in BS, BLM, encodes a member of the RecQ family of DExH box DNA helicases, which also includes the Werner's syndrome gene product. We have investigated the mechanism by which BLM suppresses hyperrecombination. Here, we show that BLM selectively binds Holliday junctions in vitro and acts on recombination intermediates containing a Holliday junction to promote ATP-dependent branch migration. We present a model in which BLM disrupts potentially recombinogenic molecules that arise at sites of stalled replication forks. Our results have implications for the role of BLM as an anti-recombinase in the suppression of tumorigenesis.
Mots-clé
Adenosine Triphosphatases/*physiology Bloom Syndrome/*genetics DNA Helicases/*physiology Humans *Recombination, Genetic
Pubmed
Web of science
Open Access
Oui
Création de la notice
24/01/2008 15:50
Dernière modification de la notice
08/05/2019 20:48
Données d'usage