CDK targets Sae2 to control DNA-end resection and homologous recombination
Pablo Huertas,
Felipe Cortés-Ledesma,
Alessandro A. Sartori,
Andrés Aguilera and
Stephen P. Jackson ()
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Pablo Huertas: The Wellcome Trust and Cancer Research UK Gurdon Institute, University of Cambridge, Tennis Court Road, Cambridge CB2 1QN, UK
Felipe Cortés-Ledesma: Centro Andaluz de Biología Molecular y Medicina Regenerativa CABIMER, Universidad de Sevilla-CSIC, Avenida Américo Vespucio s/n, 41092 Sevilla, Spain
Alessandro A. Sartori: The Wellcome Trust and Cancer Research UK Gurdon Institute, University of Cambridge, Tennis Court Road, Cambridge CB2 1QN, UK
Andrés Aguilera: Centro Andaluz de Biología Molecular y Medicina Regenerativa CABIMER, Universidad de Sevilla-CSIC, Avenida Américo Vespucio s/n, 41092 Sevilla, Spain
Stephen P. Jackson: The Wellcome Trust and Cancer Research UK Gurdon Institute, University of Cambridge, Tennis Court Road, Cambridge CB2 1QN, UK
Nature, 2008, vol. 455, issue 7213, 689-692
Abstract:
DNA repair: pathways in balance DNA can be repaired by two fundamentally different mechanisms, depending on whether a homologous template is available or not. Given that DNA is duplicated in S phase, homologous recombination is restricted to S and G2 phases of the cell cycle. The activity of cyclin-dependent kinases (CDKs) is also cell-cycle regulated, and the yeast CDK Cdc28 controls DNA resection, an early step of homologous recombination. In this work, Huertas et al. show that the target of Cdc28 in regulating DNA resection is Sae2, a protein with endonuclease activity that was first identified as being required for meiotic recombination. These results support models in which the commitment to DSB resection is highly regulated to ensure that the cell engages the most appropriate DNA repair pathway at the right time, thereby optimizing genome stability.
Date: 2008
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DOI: 10.1038/nature07215
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