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Mol. Cell. Biol. doi:10.1128/MCB.00089-07
Copyright (c) 2007, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.

Selective requirement for SAGA in Hog1-mediated gene expression depending on the severity of the external osmostress conditions

Cell signaling unit, Departament de Ciències Experimentals i de la Salut, Universitat Pompeu Fabra (UPF), Parc de Recerca Biomèdica de Barcelona (PRBB) E-08003 Barcelona, Spain; Swiss Federal Institute of Technology Zurich (ETH), Institute of Biochemistry, Zurich, Switzerland

^* To whom correspondence should be addressed. Email: francesc.posas{at}upf.edu.

	Abstract

Regulation of gene expression by the Hog1 stress-activated protein kinase is essential for proper cell adaptation to osmostress. Hog1 coordinates an extensive transcriptional program through the modulation of transcription. To identify systematically novel components of the transcriptional machinery required for osmostress-mediated gene expression, we performed an exhaustive genome-wide genetic screening searching for mutations that render cells osmosensitive at high osmolarity and displayed reduced expression of osmoresponsive genes. The SAGA and Mediator complexes were identified as putative novel regulators of osmostress-mediated transcription. Interestingly, whereas Mediator is essential for osmostress gene expression, the requirement for SAGA is different depending on the strength of the extracellular osmotic conditions. At mild osmolarity, SAGA mutants only show very slight defects on RNA PolII recruitment and gene expression, whereas at severe osmotic conditions, SAGA mutants show completely impaired RNA PolII recruitment and transcription of osmoresponsive genes. Thus, our results define an essential role for Mediator in osmostress gene expression and a selective role for SAGA under severe osmostress. Our results indicate that the requirement for a transcriptional complex to regulate a promoter might be determined in function of the strength of the stimuli perceived by the cell through the regulation of interactions between transcriptional complexes.

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