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Histone H3 K56 acetylation in wild-type histone shuffle strain (YBL574)

ABSTRACT: ChIP-on chip assays to measure the change in histone H3 K56 acetylation over the yeast genome in wild-type YBL574 yeast strains compared to H3K36A mutant strains.

ORGANISM(S): Saccharomyces cerevisiae

PROVIDER: GSE37039 | GEO | 2012/07/25

SECONDARY ACCESSION(S): PRJNA158291

REPOSITORIES: GEO

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Histone H3 K56 acetylation in wild-type histone shuffle strain (YBL574)

Project description:ChIP-on chip assays to measure the change in histone H3 K56 acetylation over the yeast genome in wild-type YBL574 yeast strains compared to H3K36A mutant strains. Two color experiment. Mutant vs WT cells. Biological replicates=3 per IP per cell type.

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Distinct transcriptional roles for Histone H3-K56 acetylation during the cell cycle

Project description:Dynamic disruption and reassembly of promoter-proximal nucleosomes is a conserved hallmark of transcriptionally active chromatin. Histone H3-K56 acetylation (H3K56Ac) enhances these turnover events and promotes nucleosome assembly during S phase. Here we sequence nascent transcripts to investigate the impact of H3K56Ac on transcription throughout the yeast cell cycle. Strikingly, we find that H3K56Ac is a genome-wide activator of transcription. H3K56Ac has a major impact on transcription initiation, but it also appears to promote elongation and/or termination. In contrast, H3K56Ac represses promiscuous transcription that occurs immediately following replication fork passage, in this case by promoting efficient nucleosome assembly. We also detect a stepwise increase in transcription as cells transit S phase and enter G2, but this response to increased gene dosage does not require H3K56Ac. Thus, a single histone mark can exert both positive and negative impacts on transcription that are coupled to different cell cycle events.

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FACT activity and histone H3-K56 acetylation promote optimal establishment of chromatin architecture independent of ongoing transcription in Saccharomyces cerevisiae [RNA-Seq]

Project description:FACT is a histone chaperone that can destabilize or assemble nucleosomes. Acetylation of histone H3-K56 weakens a histone:DNA contact that is central to FACT activity, suggesting that this modification could affect FACT functions. We tested this by asking how mutations of H3-K56 and FACT affect nucleosome structure, chromatin integrity, and transcription output. Mimics of unacetylated or permanently acetylated H3-K56 had different effects on FACT in vitro and in vivo as expected, but H3-K56 and FACT mutations caused surprisingly similar changes in transcription of individual genes. Notably, neither the changes in transcript levels nor the effects on nucleosome occupancy resulting from mutations conformed to the model that FACT is needed to overcome nucleosomal barriers during transcription initiation or elongation. Instead, the results suggest that both FACT and H3-K56ac are involved in establishing chromatin architecture prior to transcription and restoring it afterwards. They contribute to a process that optimizes transcription frequency, especially at conditionally expressed genes, and restores chromatin integrity after transcription, especially at the +1 nucleosome to block antisense transcription, but FACT appears to be less involved than expected in directly promoting transcription.

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