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  • The EMBO Journal (2006) 25, 2338 - 2346
  • doi:10.1038/sj.emboj.7601095

Published online: 11 May 2006

Phosphorylation of Hsl1 by Hog1 leads to a G2 arrest essential for cell survival at high osmolarity

Josep Clotet1,2,a, Xavier Escoté2,a, Miquel Àngel Adrover2,a, Gilad Yaakov2, Eloi Garí3, Martí Aldea3, Eulàlia de Nadal2 and Francesc Posas2

  1. Department of Molecular and Cellular Biology, Universitat Internacional de Catalunya, Sant Cugat del Vallès, Spain
  2. Cell Signaling Unit, Departament de Ciències Experimentals i de la Salut, Universitat Pompeu Fabra (UPF), Barcelona, Spain
  3. Departament de Ciències Mèdiques Bàsiques, Universitat de Lleida, Lleida, Spain

Correspondence to:

Francesc Posas, Cell Signaling Unit, Departament de Ciències Experimentals i de la Salut, Universitat Pompeu Fabra (UPF), Dr. Aiguader, 80, 08003 Barcelona, Spain. Tel.: +34 93 542 2848; Fax: +34 93 542 2802; E-mail: francesc.posas@upf.edu

aThese authors have contributed equally to this work

Received 7 October 2005; Accepted 22 March 2006

Control of cell cycle progression by stress-activated protein kinases (SAPKs) is essential for cell adaptation to extracellular stimuli. Exposure of yeast to osmostress leads to activation of the Hog1 SAPK, which controls cell cycle at G1 by the targeting of Sic1. Here, we show that survival to osmostress also requires regulation of G2 progression. Activated Hog1 interacts and directly phosphorylates a residue within the Hsl7-docking site of the Hsl1 checkpoint kinase, which results in delocalization of Hsl7 from the septin ring and leads to Swe1 accumulation. Upon Hog1 activation, cells containing a nonphosphorylatable Hsl1 by Hog1 are unable to promote Hsl7 delocalization, fail to arrest at G2 and become sensitive to osmostress. Together, we present a novel mechanism that regulates the Hsl1–Hsl7 complex to integrate stress signals to mediate cell cycle arrest and, demonstrate that a single MAPK coordinately modulates different cell cycle checkpoints to improve cell survival upon stress.

  • Keywords:

    • cell cycle,
    • Hog1,
    • Hsl1,
    • osmostress,
    • SAPK