Evidence map›Paper›PMID 33431884›Full record

ArticleNature communications2021

Transcription shapes genome-wide histone acetylation patterns.

Benjamin J E Martin, Julie Brind'Amour, Anastasia Kuzmin, Kristoffer N Jensen, Zhen Cheng Liu, Matthew Lorincz, LeAnn J Howe

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 104 papers.

0numbers the graph read from it
0cells of the map it votes in
104citing papers in PubMed
9.5field-weighted citation impact, top 1% 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

104 citing papers in PubMed, 152 citations in OpenAlex.

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44 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 1 institution in 1 country.

Benjamin J E MartinDepartment of Biochemistry and Molecular Biology, Life Sciences Institute, Molecular Epigenetics Group, University of British Columbia, 2350 Health Sciences Mall, Vancouver, BC, V6T 1Z3, Canada.ORCID http://orcid.org/0000-0002-2296-6346
Julie Brind'AmourDepartment of Medical Genetics, Life Sciences Institute, Molecular Epigenetics Group, University of British Columbia, 2350 Health Sciences Mall, Vancouver, BC, V6T 1Z3, Canada.ORCID http://orcid.org/0000-0002-9522-8571
Anastasia KuzminDepartment of Biochemistry and Molecular Biology, Life Sciences Institute, Molecular Epigenetics Group, University of British Columbia, 2350 Health Sciences Mall, Vancouver, BC, V6T 1Z3, Canada.
Kristoffer N JensenDepartment of Medical Genetics, Life Sciences Institute, Molecular Epigenetics Group, University of British Columbia, 2350 Health Sciences Mall, Vancouver, BC, V6T 1Z3, Canada.
Zhen Cheng LiuDepartment of Biochemistry and Molecular Biology, Life Sciences Institute, Molecular Epigenetics Group, University of British Columbia, 2350 Health Sciences Mall, Vancouver, BC, V6T 1Z3, Canada.
Matthew LorinczDepartment of Medical Genetics, Life Sciences Institute, Molecular Epigenetics Group, University of British Columbia, 2350 Health Sciences Mall, Vancouver, BC, V6T 1Z3, Canada.ORCID http://orcid.org/0000-0003-0885-0467
LeAnn J HoweDepartment of Biochemistry and Molecular Biology, Life Sciences Institute, Molecular Epigenetics Group, University of British Columbia, 2350 Health Sciences Mall, Vancouver, BC, V6T 1Z3, Canada. ljhowe@mail.ubc.ca.ORCID http://orcid.org/0000-0001-5866-6030
University of British Columbia · CA

Funding

CIHR PJT-162253
6 · The paper itself

Abstract

Histone acetylation is a ubiquitous hallmark of transcription, but whether the link between histone acetylation and transcription is causal or consequential has not been addressed. Using immunoblot and chromatin immunoprecipitation-sequencing in S. cerevisiae, here we show that the majority of histone acetylation is dependent on transcription. This dependency is partially explained by the requirement of RNA polymerase II (RNAPII) for the interaction of H4 histone acetyltransferases (HATs) with gene bodies. Our data also confirms the targeting of HATs by transcription activators, but interestingly, promoter-bound HATs are unable to acetylate histones in the absence of transcription. Indeed, HAT occupancy alone poorly predicts histone acetylation genome-wide, suggesting that HAT activity is regulated post-recruitment. Consistent with this, we show that histone acetylation increases at nucleosomes predicted to stall RNAPII, supporting the hypothesis that this modification is dependent on nucleosome disruption during transcription. Collectively, these data show that histone acetylation is a consequence of RNAPII promoting both the recruitment and activity of histone acetyltransferases.

Indexed as

Genome, FungalTranscription, GeneticAcetylationAnimalsChromatinHistone AcetyltransferasesHistonesMiceSaccharomyces cerevisiaeTrans-ActivatorsChromatinHistone AcetyltransferasesHistonesTrans-Activators

Identifiers

PMID33431884
PMCPMC7801501
OpenAlexW3119357692

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.