Accumulation of unacetylatable Snf2p at the INO1 promoter is detrimental to remodeler recycling supply for CUP1 induction

• Published in: PloS one Vol. 15; no. 3; p. e0230572
• Main Authors: Esposito, Michelle, Sherr, Goldie Libby, Esposito, Anthony, Kaluski, George, Ellington, Farris, Shen, Chang-Hui
• Format: Journal Article
• Language: English
• Published: United States Public Library of Science 25.03.2020; Public Library of Science (PLoS)
• Subjects: Acetylation; Analysis; Biochemical analysis; Biochemistry; Biology; Biology and Life Sciences; Chromatin; Community colleges; Copper; Crosstalk; Epigenetic inheritance; Gene expression; Gene regulation; Genes; Genetic aspects; Genetic regulation; Phosphorylation; Physical Sciences; Research and Analysis Methods; Toxicity; Transcription (Genetics); Transcription activation; Transcription factors; Yeasts; New York; United States > US; New Jersey
• ISSN: 1932-6203; 1932-6203
• DOI: 10.1371/journal.pone.0230572

Chromatin structure plays a decisive role in gene regulation through the actions of transcriptional activators, coactivators, and epigenetic machinery. These trans-acting factors contribute to gene expression through their interactions with chromatin structure. In yeast INO1 activation, transcriptional activators and coactivators have been defined through intense study but the mechanistic links within these trans-acting factors and their functional implications are not yet fully understood. In this study, we examined the crosstalk within transcriptional coactivators with regard to the implications of Snf2p acetylation during INO1 activation. Through various biochemical analysis, we demonstrated that both Snf2p and Ino80p chromatin remodelers accumulate at the INO1 promoter in the absence of Snf2p acetylation during induction. Furthermore, nucleosome density and histone acetylation patterns remained unaffected by Snf2p acetylation status. We also showed that cells experience increased sensitivity to copper toxicity when remodelers accumulate at the INO1 promoter due to the decreased CUP1 expression. Therefore, our data provide evidence for crosstalk within transcriptional co-activators during INO1 activation. In light of these findings, we propose a model in which acetylation-driven chromatin remodeler recycling allows for efficient regulation of genes that are dependent upon limited co-activators.