Stress causes a general down-regulation of gene expression in cells, together with the induction of a set of stress-responsive genes. How do cells know which specific genes to activate when they are silencing most of the others? The (yeast) answer is called Hog1, as shown in a recent paper published in Genome Biology by the Cell Signalling research group at the UPF.
The authors, led by Francesc Posas, used yeast as a model organism to study the response to osmostress, and they focused on Hog1, a stress-activated protein kinase which is related to p38. Using chromatin immunoprecipitation (ChIP) followed by sequencing (ChIP-Seq) they did genome-wide localization studies of RNA polymerase II (RNA Pol II) and Hog1. The results show that upon stress, RNA Pol II localization shifts toward stress-responsive genes relative to housekeeping genes, and that this relocalization required Hog1, which also localized to stress-responsive loci.
Posas and colleagues also looked at the re-organization of nucleosomes by micrococcal nuclease followed by sequencing (MNase-Seq). The analysis showed that, even though chromatin structure was not significantly altered at a genome-wide level in response to stress, there was pronounced chromatin remodeling at stress-responsive loci, which displayed Hog1 association.
The authors conclude that Hog1 serves to bypass the general down-regulation of gene expression that occurs in response to osmostress, and does so both by targeting RNA Pol II machinery and by inducing chromatin remodeling at stress-responsive loci.
Nadal-Ribelles M, Conde N, Flores O, Gonzalez-Vallinas J, Eyras E, Orozco M, de Nadal E, Posas F. Hog1 bypasses stress-mediated down-regulation of transcription by RNA polymerase II redistribution and chromatin remodeling. Genome Biol. 2012 Nov 18;13(11):R106