Hog1 controls global reallocation of RNA Pol II upon osmotic shock in Saccharomyces cerevisiae.

When challenged with osmotic shock, Saccharomyces cerevisiae induces hundreds of genes, despite a concurrent reduction in overall transcriptional capacity. The stress-responsive MAP kinase Hog1 activates expression of specific genes through interactions with chromatin remodeling enzymes, transcription factors, and RNA polymerase II. However, it is not clear whether Hog1 is involved more globally in modulating the cell's transcriptional program during stress, in addition to activating specific genes. Here we show that large-scale redistribution of RNA Pol II from housekeeping to stress genes requires Hog1. We demonstrate that decreased RNA Pol II occupancy is the default outcome for highly expressed genes upon stress and that Hog1 is partially required for this effect. We find that Hog1 and RNA Pol II colocalize to open reading frames that bypass global transcriptional repression. These activation targets are specified by promoter binding of two osmotic stress-responsive transcription factors. The combination of reduced global transcription with a gene-specific override mechanism allows cells to rapidly switch their transcriptional program in response to stress.