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Genetic instability is prevented by Mrc1-dependent spatio-temporal separation of replicative and repair activities of homologous recombination: Homologous recombination tolerates replicative stress by Mrc1-regulated replication and repair activities operating at S and G2 in distinct subnuclear compartments

AutorPrado, Félix
Palabras claveDNA checkpoints
Homologous recombination
Rad51
Repair centers
Replication
Fecha de publicación26-feb-2014
EditorJohn Wiley & Sons
CitaciónBioEssays 36: 451- 462 (2014)
ResumenHomologous recombination (HR) is required to protect and restart stressed replication forks. Paradoxically, the Mrc1 branch of the S phase checkpoints, which is activated by replicative stress, prevents HR repair at breaks and arrested forks. Indeed, the mechanisms underlying HR can threaten genome integrity if not properly regulated. Thus, understanding how cells avoid genetic instability associated with replicative stress, a hallmark of cancer, is still a challenge. Here I discuss recent results that support a model by which HR responds to replication stress through replicative and repair activities that operate at different stages of the cell cycle (S and G2, respectively) and in distinct subnuclear structures. Remarkably, the replication checkpoint appears to control this scenario by inhibiting the assembly of HR repair centers at stressed forks during S phase, thereby avoiding genetic instability
Versión del editorhttp://dx.doi.org/10.1002/bies.201300161
URIhttp://hdl.handle.net/10261/123623
DOI10.1002/bies.201300161
Identificadoresdoi: 10.1002/bies.201300161
issn: 1521-1878
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