Titre
Identification and purification of two distinct complexes containing the five RAD51 paralogs.
Type
article
Institution
UNIL/CHUV/Unisanté + institutions partenaires
Périodique
Auteur(s)
Masson, J.Y.
Auteure/Auteur
Tarsounas, M.C.
Auteure/Auteur
Stasiak, A.Z.
Auteure/Auteur
Stasiak, A.
Auteure/Auteur
Shah, R.
Auteure/Auteur
McIlwraith, M.J.
Auteure/Auteur
Benson, F.E.
Auteure/Auteur
West, S.C.
Auteure/Auteur
Liens vers les personnes
Liens vers les unités
ISSN
0890-9369
Statut éditorial
Publié
Date de publication
2001-12
Volume
15
Numéro
24
Première page
3296
Dernière page/numéro d’article
3307
Langue
anglais
Notes
Publication types: Journal Article ; Research Support, Non-U.S. Gov't
Publication Status: ppublish
Publication Status: ppublish
Résumé
Cells defective in any of the RAD51 paralogs (RAD51B, RAD51C, RAD51D, XRCC2, and XRCC3) are sensitive to DNA cross-linking agents and to ionizing radiation. Because the paralogs are required for the assembly of DNA damage-induced RAD51 foci, and mutant cell lines are defective in homologous recombination and show genomic instability, their defect is thought to be caused by an inability to promote efficient recombinational repair. Here, we show that the five paralogs exist in two distinct complexes in human cells: one contains RAD51B, RAD51C, RAD51D, and XRCC2 (defined as BCDX2), whereas the other consists of RAD51C with XRCC3. Both protein complexes have been purified to homogeneity and their biochemical properties investigated. BCDX2 binds single-stranded DNA and single-stranded gaps in duplex DNA, in accord with the proposal that the paralogs play an early (pre-RAD51) role in recombinational repair. Moreover, BCDX2 complex binds specifically to nicks in duplex DNA. We suggest that the extreme sensitivity of paralog-defective cell lines to cross-linking agents is owing to defects in the processing of incised cross links and the consequential failure to initiate recombinational repair at these sites.
Sujets
PID Serval
serval:BIB_12EC1D985834
PMID
Open Access
Oui
Date de création
2008-01-24T09:36:22.741Z
Date de création dans IRIS
2025-05-20T13:41:58Z