Evidence map›Paper›PMID 28115623›Full record

ArticleNucleic acids research2017

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 Alhussain, Sari Pennings, Alastair B Fleming

Open access · goldAbstract read
In one paragraph

Article in Nucleic acids research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
2.4field-weighted citation impact, top 11% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

27 citing papers in PubMed, 37 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Review
  16. Article
  17. Review
  18. Article
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 1 institution in 1 country.

Michael ChurchSchool of Genetics and Microbiology, University of Dublin, Trinity College Dublin, College Green, Dublin 2, Ireland.
Kim C SmithSchool of Genetics and Microbiology, University of Dublin, Trinity College Dublin, College Green, Dublin 2, Ireland.
Mohamed M AlhussainSchool of Genetics and Microbiology, University of Dublin, Trinity College Dublin, College Green, Dublin 2, Ireland.
Sari PenningsQueen's Medical Research Institute, University of Edinburgh, Edinburgh, EH16 4TJ, UK.
Alastair B FlemingSchool of Genetics and Microbiology, University of Dublin, Trinity College Dublin, College Green, Dublin 2, Ireland.
University of Edinburgh · GB

Funding

Biotechnology and Biological Sciences Research CouncilWellcome Trust
6 · The paper itself

Abstract

The Saccharomyces 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 organization of strongly positioned, hypoacetylated nucleosomes across gene promoters. Swi-Snf catalyzes remodeling 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.

Indexed as

Gene Expression Regulation, FungalAcetylationCell WallChromosomal Proteins, Non-HistoneHistone AcetyltransferasesHistonesMannose-Binding LectinsNuclear ProteinsNucleosomesPromoter Regions, GeneticProtein BindingRepressor ProteinsRNA Polymerase IISaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsTranscription Elongation, GeneticADA2 protein, S cerevisiaeChromosomal Proteins, Non-HistoneCYC8 protein, S cerevisiaeFLO1 protein, S cerevisiaeHistone AcetyltransferasesHistonesMannose-Binding LectinsNuclear ProteinsNucleosomesRepressor ProteinsRNA Polymerase IISaccharomyces cerevisiae ProteinsSAS3 protein, S cerevisiaeSWI-SNF-B chromatin-remodeling complexTranscription FactorsTUP1 protein, S cerevisiae

Identifiers

PMID28115623
PMCPMC5416777
OpenAlexW2580335446

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.