Failures in the replication of genetic material during cell division leads to the activation of the checkpoint (checkpoint) of replication, conserved in eukaryotes. When it detects replicative stress cellular responses are activated to preserve the integrity of the genome, including the stabilization of replication forks, the activation of a specific transcriptional program and the slowing of the cycle to prevent entry into mitosis in the absence of adequate replication genetics. The principal effector in Schizosaccharomyces pombe Cds1 kinase is homologous to mammalian Chk2, which plays an essential role in stabilizing replication forks under stress. This kinase regulates events in brackets recombinogénicos stops and coordinates the resumption of replication when stress ceases and cells undergo an adaptation process.

Flp1 is a dual specificity phosphatase Cdc14. Previous work group Avelino Bueno, Cancer Research Center in Salamanca (USAL-CSIC) have shown that the action of Cdc25 in S. Flp1 pombe can coordinate mitotic exit with cytokinesis. In this paper, we demonstrate the close relationship of Cds1 in Flp1/Cdc14 with replicative stress, and describes for the first time, the involvement of Flp1 / Cdc14 in the replication checkpoint. The study shows how the cellular response to replicative stress induces Flp1 exit from the nucleolus to the nucleus through a mechanism directly controlled by Cds1. Well, this change of location is necessary for full activation of the checkpoint. In addition, altered protein levels or location Flp1 under these conditions results in defects such as outbreaks of recombination, indicating a dysregulation of stress response.