Eukaryotic Cell
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EC Accepts, published online ahead of print on 28 March 2008
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Eukaryotic Cell doi:10.1128/EC.00465-07
Copyright (c) 2008, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.

The transcription factors Pcr1 and Atf1 have distinct roles in stress- and Sty1-dependent gene regulation

Miriam Sansó, Madelaine Gogol, José Ayté, Chris Seidel, and Elena Hidalgo*

Oxidative Stress and Cell Cycle Group, Departament de Ciències Experimentals i de la Salut, Universitat Pompeu Fabra, C/Dr. Aiguader 88, E-08003 Barcelona, Spain; Stowers Institute for Medical Research, Kansas City, USA

* To whom correspondence should be addressed. Email: elena.hidalgo{at}upf.edu.


   Abstract

The MAP kinase Sty1 is essential for the regulation of transcriptional responses that promote cell survival in response to different types of environmental stimuli in Schizosaccharomyces pombe. Upon stress activation, Sty1 reversibly accumulates in the nucleus, where it stimulates gene expression via the Atf1 transcription factor. Atf1 protein forms a heterodimer with Pcr1, but the specific role of this association is controversial. We have carried out a comparative analysis of strains lacking these proteins individually. We demonstrate that Atf1 and Pcr1 have similar but not identical roles in S. pombe, since cells lacking Pcr1 do not share all the phenotypes reported for {Delta}atf1 cells. Northern blot and microarray analysis demonstrate that the response to specific stresses of cells lacking either Pcr1 or Atf1 do not fully overlap; and even though most Atf1-dependent genes induced by osmotic stress are also Pcr1-dependent, a subset of genes require only the presence of Atf1 for their induction. Whereas binding of Atf1 to most stress-dependent genes requires the presence of Pcr1, we demonstrate here that Atf1 can bind to the Pcr1-independent promoters in a {Delta}pcr1 strain in vivo. Furthermore, these analyses show that both proteins have a global repressive effect on stress-dependent and stress-independent genes.







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