Increased mobility of double-strand breaks requires Mec1, Rad9 and the homologous recombination machinery.

Détails

ID Serval
serval:BIB_30F64806AF33
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Titre
Increased mobility of double-strand breaks requires Mec1, Rad9 and the homologous recombination machinery.
Périodique
Nature Cell Biology
Auteur(s)
Dion V., Kalck V., Horigome C., Towbin B.D., Gasser S.M.
ISSN
1476-4679 (Electronic)
ISSN-L
1465-7392
Statut éditorial
Publié
Date de publication
2012
Volume
14
Numéro
5
Pages
502-509
Langue
anglais
Résumé
Chromatin mobility is thought to facilitate homology search during homologous recombination and to shift damage either towards or away from specialized repair compartments. However, unconstrained mobility of double-strand breaks could also promote deleterious chromosomal translocations. Here we use live time-lapse fluorescence microscopy to track the mobility of damaged DNA in budding yeast. We found that a Rad52-YFP focus formed at an irreparable double-strand break moves in a larger subnuclear volume than the undamaged locus. In contrast, Rad52-YFP bound at damage arising from a protein-DNA adduct shows no increase in movement. Mutant analysis shows that enhanced double-strand-break mobility requires Rad51, the ATPase activity of Rad54, the ATR homologue Mec1 and the DNA-damage-response mediator Rad9. Consistent with a role for movement in the homology-search step of homologous recombination, we show that recombination intermediates take longer to form in cells lacking Rad9.
Mots-clé
Cell Cycle Proteins/physiology, Chromatin/metabolism, DNA Damage, Intracellular Signaling Peptides and Proteins/physiology, Microscopy, Fluorescence, Protein-Serine-Threonine Kinases/physiology, Recombination, Genetic, Saccharomyces cerevisiae/metabolism, Saccharomyces cerevisiae Proteins/physiology
Pubmed
Web of science
Création de la notice
12/02/2014 16:11
Dernière modification de la notice
20/08/2019 13:15
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