Repositorio de producción científica de la Universidad de Sevilla

CDK targets Sae2 to control DNA-end resection and homologous recombination

Opened Access CDK targets Sae2 to control DNA-end resection and homologous recombination


buscar en

Exportar a
Autor: Huertas Sánchez, Pablo
Cortés Ledesma, Felipe
Sartori, Alessandro A.
Aguilera López, Andrés
Jackson, Stephen P.
Departamento: Universidad de Sevilla. Departamento de Genética
Fecha: 2008
Publicado en: Nature, 455 (7213), 689-692.
Tipo de documento: Artículo
Resumen: DNA double-strand breaks (DSBs) are repaired by two principal mechanisms: non-homologous end-joining (NHEJ) and homologous recombination (HR)1. HR is the most accurate DSB repair mechanism but is generally restricted to the S and G2 phases of the cell cycle, when DNA has been replicated and a sister chromatid is available as a repair template2-5. By contrast, NHEJ operates throughout the cell cycle but assumes most importance in G1 (refs 4​, ​6). The choice between repair pathways is governed by cyclin-dependent protein kinases (CDKs)2,3,5,7, with a major site of control being at the level of DSB resection, an event that is necessary for HR but not NHEJ, and which takes place most effectively in S and G2 (refs 2​, ​5). Here we establish that cell-cycle control of DSB resection in Saccharomyces cerevisiae results from the phosphorylation by CDK of an evolutionarily conserved motif in the Sae2 protein. We show that mutating Ser 267 of Sae2 to a non-phosphorylatable residue causes phenot...
[Ver más]
Cita: Huertas Sánchez, P., Cortés Ledesma, F., Sartori, A.A., Aguilera López, A. y Jackson, S.P. (2008). CDK targets Sae2 to control DNA-end resection and homologous recombination. Nature, 455 (7213), 689-692.
Tamaño: 1.334Mb
Formato: PDF


DOI: 10.1038/nature07215

Ver versión del editor

Mostrar el registro completo del ítem

Esta obra está bajo una Licencia Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 Internacional

Este registro aparece en las siguientes colecciones