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Coordination of stress-mediated gene expression and DNA replication by signaling kinases

AutorDuch, Alba; Barroso, Sonia ; García-Rubio, María L. ; Aguilera, Andrés ; Posas, Francesc
Fecha de publicación2017
CitaciónFEBS3+ (2017)
XL SEBBM Congress (2017)
ResumenExposure of cells to increases in extracellular osmolarity results in the activation of the Hog1 stress-activated protein kinase (SAPK). Activation of Hog1 is required to generate a set of osmoadaptive responses essential for survival under high osmolarity. Adaptation to osmostress requires the induction of a large number of genes, which indicates the necessity to regulate several aspects of the cell physiology. In addition to gene expression, the SAPK also controls cell cycle. Here, we showed that the SAPK is able to modulate cell cycle delay in different phases of the cell cycle including S phase. During S phase, Hog1 targets Mrc1, a protein of the replication complex, to control DNA replication (Duch et al., 2013). The control of replication through Mrc1 is required to coordinate stress-responsive gene induction with duplication of DNA upon osmostress. Remarkably, we have recently found that Mrc1 is also important to delay replication in response to other environmental stresses suggesting a conserved mechanism of S phase regulation upon transcriptional outbursts. By a systematic biochemical assay, we have identified several kinases that are able to phosphorylate Mrc1 in the same phosphorylation sites than Hog1. This indicates that Mrc1 can integrate signals from multiple kinases to delay replication when an outburst of transcription occurs during S phase. All together highlights the relevance of the signaling kinases in the coordination of transcription and replication.
DescripciónResumen del póster presentado al 1st Joint Meeting of the French-Portuguese-Spanish Biochemical and Molecular Biology Societies y al XL Spanish Society of Biochemistry and Molecular Biology (SEBBM) Congress, celebrado en Barcelona (España) del 23 al 26 de octubre de 2017.-- et al.
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