Osmostress
induced transcription by Hog1-mediated recruitment of the RNA Pol II.
Francesc Posas (1),
Paula M. Alepuz (1), Eulàlia de Nadal (1), Meritxell Zapater (1), Gustav
Ammerer (2)
(1) CEXS, Universitat Pompeu Fabra, Dr. Aiguader 80, Barcelona, 08003, Spain
(francesc.posas@cexs.upf.es); (2) Department of Biochemistry and Molecular Cell
Biology, Ludwig Boltzmann-Forschungsstelle. University of Vienna, A1030 Vienna,
Austria.
In budding yeast, the MAP kinase Hog1 coordinates the transcriptional program required for cell survival upon osmostress. Several transcription factors act downstream of the MAPK. The Hot1 transcription factor acts under the control of the MAP kinase and regulates a subset of Hog1-responsive genes. In response to high osmolarity Hot1 targets Hog1 to specific osmostress responsive promoters. We have found that assembly of the general transcription machinery at Hot1-dependent promoters depends on the presence of Hot1 and active Hog1 MAPK. Unexpectedly, recruitment of RNA polymerase II complex to target promoters does not depend on the phosphorylation of the Hot1 activator by the MAP Kinase. Hog1 interacts with the RNA Pol II and with general components of the transcription machinery, both in vitro and in vivo. Moreover, when tethered to a promoter as a LexA fusion protein, Hog1 activates transcription in a stress regulated manner. Thus, anchoring of active Hog1 to promoters by the Hot1 activator is essential for recruitment and activation of RNA Pol II. We also have found that the mammalian p38 interacts with the RNA polymerase II, which might suggest a conserved mechanism for regulation of gene expression by SAPKs among eukaryotic cells.