Sas3 and Ada2(Gcn5)-dependent histone H3 acetylation is required for transcription elongation at the de-repressed FLO1 gene

Michael Church, Kim C Smith, Mohamed M Mubarack, Sari Pennings, Alastair B Fleming

Research output: Contribution to journalArticlepeer-review

Abstract

The S. cerevisiae FLO1 gene encodes a cell wall protein that imparts cell-cell adhesion. FLO1
transcription is regulated via the antagonistic activities of the Tup1-Cyc8 co-repressor and Swi-Snf
co-activator complexes. Tup1-Cyc8 represses transcription through the organisation of strongly
positioned, hypoacetylated nucleosomes across gene promoters. Swi-Snf catalyses remodelling of
these nucleosomes in a mechanism involving histone acetylation that is poorly understood. Here,
we show that FLO1 de-repression is accompanied by Swi-Snf recruitment, promoter histone eviction,
and Sas3 and Ada2(Gcn5)-dependent histone H3K14 acetylation. In the absence of H3K14
acetylation, Swi-Snf recruitment and histone eviction proceed, but transcription is reduced,
suggesting these processes, while essential, are not sufficient for de-repression. Further analysis in
the absence of H3K14 acetylation reveals RNAP II recruitment at the FLO1 promoter still occurs, but
RNAP II is absent from the gene-coding region, demonstrating Sas3 and Ada2-dependent histone H3
acetylation is required for transcription elongation. Analysis of the transcription kinetics at other
genes reveals shared mechanisms coupled to a distinct role for histone H3 acetylation, essential at
FLO1, downstream of initiation. We propose histone H3 acetylation in the coding region provides
rate-limiting control during the transition from initiation to elongation which dictates whether the
gene is permissive for transcription.
Original languageEnglish
JournalNucleic Acids Research
Volume45
Issue number8
DOIs
Publication statusPublished - 23 Jan 2017

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