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Nut/Hos1 and Sas2/Rpd3 control H3 acetylation of two different sets of osmotic stress-induced genes

ABSTRACT: Epigenetic information is able to interact with the cellular environment and therefore it could be especially useful for reprogramming gene expression in response to a physiological perturbation. In fact, genes induced or repressed by osmotic stress undergo significant changes in the levels of various histone modifications, especially the acetylation levels of histone H3. Exposure of yeast to high osmolarity results in the activation of p38-related SAPK, Hog1, which plays a central role in the control of gene expression. Therefore, two types of mechanisms converge in gene regulation by stress: that of the epigenetic signals and that of the trans-acting protein factor. We have evaluated the connection between the presence of Hog1 and the changes on acetylation of histone H3 in stress-regulated genes. Furthermore, we asked which enzymatic activities are involved in the changes produced in the acetylation of H3 linked to gene activation by osmotic stress. We have demonstrated that increase of acetylation of lysines 9 and 14 of H3 produced on induced genes during stress positively correlates between them and are largely dependent on Hog1 at genome-wide level. Conversely, decrease in acetylation on repressed genes was not dependent on Hog1. However, the absence of Hog1 produces different and even opposite effects on the induction and acetylation of H3 of each gene, which suggests that Hog1 influences both processes through different mechanisms. Additionally, we found that in genes up-regulated during osmotic stress in a Msn2/Msn4-independent manner, the state of acetylation of lysine 9 of H3 was altered in strains deficient in Nut1 HAT and Hos1 HDAC; meanwhile for Msn2/Msn4-dependent induced genes H3k9 acetylation varies in strains deficient in Sas2 HAT and Rpd3 HDAC. During induction by osmotic stress at least two different mechanism act on H3k9 acetylation of two differentiated set of induced genes, one of them would act through Nut1/Hos1, while the other through Sas2/Rpd3. The results presented here show new and unexpected participants in the process of the regulation of gene in response to environmental perturbations.

ORGANISM(S): Saccharomyces cerevisiae

PROVIDER: GSE127742 | GEO | 2019/07/01

REPOSITORIES: GEO

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Project description:Exposure of Saccharomyces cerevisiae to alkaline pH represents a stress condition that generates a compensatory reaction. Here we examine a possible role of the protein kinase-A (PKA) pathway in this response. The phenotypic analysis reveals that mutations that activate the PKA pathway (ira1 ira2, bcy1) tend to cause sensitivity to alkaline pH, whereas its deactivation develops tolerance to this stress. We observe that alkalinization causes a transient decrease in cAMP, the main regulator of the pathway. Alkaline pH causes rapid nuclear localization of the PKA-regulated Msn2 transcription factor which, together with Msn4, mediates a general stress response by binding to STRE sequences in many promoters. Consequently, a synthetic STRE-LacZ reporter shows a rapid induction in response to alkaline stress. An msn2 msn4 mutant is sensitive to alkaline pH, and transcriptomic analysis reveals that after 10 minutes of alkaline stress, the expression of many induced genes (47%) depends, at least in part, on the presence of Msn2 and Msn4. Taken together, these results demonstrate that inhibition of the PKA pathway by alkaline pH represents a substantial part of the adaptive response to this kind of stress and that this response involves Msn2/Msn4-mediated gene remodeling. However, the relevance of attenuation of PKA in high pH tolerance is not restricted to regulation of Msn2 function. Eight samples were analyzed: WT and the MCY5278 mutant strain, lacking both Msn2 and Msn4, in the presence of 20 mM KOH (pH 8) and in the presence of 20 mM KCl (non-induced conditions) for 10 and 30 min of stress. 2 biological replicates were analyzed for each condition, and dye-swapping was carried out for each comparison of samples. We compared the expression profiles of: 1) WT +KOH vs. WT +KCl after 10 min 2) msn2 msn4 mutant +KOH vs. msn2 msn4 +KCl after 10 min 3)WT +KOH vs. WT +KCl after 30 min 4) msn2 msn4 mutant +KOH vs. msn2 msn4 +KCl after 30 min Total number of chips analyzed: 16.

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Nut/Hos1 and Sas2/Rpd3 control H3 acetylation of two different sets of osmotic stress-induced genes

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