Recruitment of a chromatin remodelling complex by the Hog1 MAP kinase to stress genes

Abstract

For efficient transcription, RNA PolII must overcome the presence of nucleosomes. The p38-related MAPK Hog1 is an important regulator of transcription upon osmostress in yeast and thereby it is involved in initiation and elongation. However, the role of this protein kinase in elongation has remained unclear. Here, we show that during stress there is a dramatic change in the nucleosome organization of stress-responsive loci that depends on Hog1 and the RSC chromatin remodelling complex. Upon stress, the MAPK Hog1 physically interacts with RSC to direct its association with the ORF of osmo-responsive genes. In RSC mutants, PolII accumulates on stress promoters but not in coding regions. RSC mutants also display reduced stress gene expression and enhanced sensitivity to osmostress. Cell survival under acute osmostress might thus depend on a burst of transcription that in turn could occur only with efficient nucleosome eviction. Our results suggest that the selective targeting of the RSC complex by Hog1 provides the necessary mechanistic basis for this event.

Casein Kinase II Regulation of the Hot1 Transcription Factor Promotes Stochastic Gene Expression

“…In a similar manner, the association of Hot1 with gene promoters occurs independently of its phosphorylation by Hog1 (17,18). Formation of a Hot1-Hog1 complex is predicted to allow Hog1 phosphorylation of other key factors involved in transitioning Hot1 gene targets to an active state (16,28). We speculate that the Hot1-CK2 complex positions CK2 to target additional factors that promote an inactive state for Hot1 gene targets.…”

cAMP-response Element-binding Protein (CREB) Controls MSK1-mediated Phosphorylation of Histone H3 at the c-fos Promoter in Vitro

“…Such kinases are now considered to be a transient but active component of the transcriptional machinery (49) and to regulate a broad range of transcriptional processes that occur on chromatin (50,51). For instance, the Hog1 kinase, once recruited to the promoter, facilitates subsequent recruitment of RNAPII (51), the Rpd3 histone deacetylase complex (52) and the RSC chromatin remodeling complex (53).…”

Severe osmotic compression triggers a slowdown of intracellular signaling, which can be explained by molecular crowding

“…The final cell volume is set by the mechanical equilibration of external, internal, and turgor pressures (10,11). Hyperosmotic stress alters a variety of cellular processes, such as disrupting the cytoskeleton structure (12,13), inducing chromatin remodeling (14,15), and triggering cell cycle arrest (16,17) and apoptosis (18,19). The high-osmolarity glycerol (HOG) pathway of the budding yeast Saccharomyces cerevisiae (Fig.…”