The yeast MAP kinase Hog1 coordinates the transcriptional program required for cell survival upon osmotic stress, although the mechanisms by which these kinesis regulate gene expression are not clearly defined. The group at the Universitat Pompeu Fabra led by Francesc Posas had already described two different control mechanisms of gene expression by MAP kinesis: direct modification of transcription factors and direct recruitment to specific promoters by the MAP kinase RNA complex Polii. In this new work shows that the MAP kinase Hog1 induces gene expression in response to stress, through a mechanism involving recruitment of the complex of the his tone deacetylase Rpd3-Sin3 to promoters of genes regulated by osmotic stress.

Cells deficient in this complex are sensitive to high osmolarity and, as seen through the use of DNA chips, show a deficient expression of stress response genes. In addition, Hog1 interacts physically with Rpd3 in vivo and in vitro and in conditions of stress, recruit the deacetylase to the promoters of stress genes. Binding of the Rpd3-Sin3 complex to these promoters allows the “deacetylation of histones”, which allows the entry of the RNA Polii and induction of gene expression. These data indicate that recruitment of his tone deacetylase Rpd3 to the promoters by the MAPK Hog1 is necessary to induce gene expression after stress, and that the activity of his tone deacetylase is essential for gene induction in response to stress.