Open AccessAccumulation of unacetylatable Snf2p at the INO1 promoter is detrimental to remodeler recycling supply for CUP1 induction
Author(s) -
Michelle Esposito,
Goldie Libby Sherr,
Anthony M. Esposito,
George Kaluski,
Farris Ellington,
ChangHui Shen
Publication year - 2020
Publication title -
plos one
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.99
H-Index - 332
ISSN - 1932-6203
DOI - 10.1371/journal.pone.0230572
Subject(s) - acetylation , biology , chromatin , histone , nucleosome , epigenetics , transcriptional regulation , regulation of gene expression , gene , promoter , crosstalk , genetics , transcription (linguistics) , microbiology and biotechnology , gene expression , linguistics , physics , philosophy , optics
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.