Evidence map›Paper›PMID 32690000›Full record

ArticleBMC molecular and cell biology2020

Differential contribution of p300 and CBP to regulatory element acetylation in mESCs.

Sara Martire, Jennifer Nguyen, Aishwarya Sundaresan, Laura A Banaszynski

Open access · goldAbstract read
In one paragraph

Article in BMC molecular and cell biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed
3.8field-weighted citation impact, top 5% 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

50 citing papers in PubMed, 76 citations in OpenAlex.

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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

4 authors at 1 institution in 1 country.

Sara MartireCecil H. and Ida Green Center for Reproductive Biology Sciences, Department of Obstetrics and Gynecology, Children's Medical Center Research Institute, Hamon Center for Regenerative Science and Medicine, University of Texas Southwestern Medical Center, Dallas, TX, 75390, USA.
Jennifer NguyenCecil H. and Ida Green Center for Reproductive Biology Sciences, Department of Obstetrics and Gynecology, Children's Medical Center Research Institute, Hamon Center for Regenerative Science and Medicine, University of Texas Southwestern Medical Center, Dallas, TX, 75390, USA.
Aishwarya SundaresanCecil H. and Ida Green Center for Reproductive Biology Sciences, Department of Obstetrics and Gynecology, Children's Medical Center Research Institute, Hamon Center for Regenerative Science and Medicine, University of Texas Southwestern Medical Center, Dallas, TX, 75390, USA.
Laura A BanaszynskiCecil H. and Ida Green Center for Reproductive Biology Sciences, Department of Obstetrics and Gynecology, Children's Medical Center Research Institute, Hamon Center for Regenerative Science and Medicine, University of Texas Southwestern Medical Center, Dallas, TX, 75390, USA. laura.banaszynski@utsouthwestern.edu.ORCID http://orcid.org/0000-0002-5189-8848
Children's Medical Center · US

Funding

Chromatin Dynamics and Genome RegulationR35GM124958 · NIGMS · UT SOUTHWESTERN MEDICAL CENTER · PI Laura Banaszynski · 2017 to 2026
$4.4M
Congressionally Directed Medical Research Programs KC170230NIGMS NIH HHS 1R35GM124958NIGMS NIH HHS R35 GM124958Welch Foundation I-2025
6 · The paper itself

Abstract

backgroundThe transcription coactivators CREB binding protein (CBP) and p300 are highly homologous acetyltransferases that mediate histone 3 lysine 27 acetylation (H3K27ac) at regulatory elements such as enhancers and promoters. Although in most cases, CBP and p300 are considered to be functionally identical, both proteins are indispensable for development and there is evidence of tissue-specific nonredundancy. However, characterization of chromatin and transcription states regulated by each protein is lacking.

resultsIn this study we analyze the individual contribution of p300 and CBP to the H3K27ac landscape, chromatin accessibility, and transcription in mouse embryonic stem cells (mESC). We demonstrate that p300 is the predominant H3K27 acetyltransferase in mESCs and that loss of acetylation in p300KD mESCs is more pronounced at enhancers compared to promoters. While loss of either CBP or p300 has little effect on the open state of chromatin, we observe that distinct gene sets are transcriptionally dysregulated upon depletion of p300 or CBP. Transcriptional dysregulation is generally correlated with dysregulation of promoter acetylation upon depletion of p300 (but not CBP) and appears to be relatively independent of dysregulated enhancer acetylation. Interestingly, both our transcriptional and genomic analyses demonstrate that targets of the p53 pathway are stabilized upon depletion of p300, suggesting an unappreciated view of the relationship between p300 and p53 in mESCs.

conclusionsThis genomic study sheds light on distinct functions of two important transcriptional regulators in the context of a developmentally relevant cell type. Given the links to both developmental disorders and cancer, we believe that our study may promote new ways of thinking about how these proteins function in settings that lead to disease.

Indexed as

AcetylationAnimalsBase SequenceCell LineChromatinCREB-Binding ProteinE1A-Associated p300 ProteinEnhancer Elements, GeneticGene Expression RegulationHistonesMiceMice, Inbred C57BLMouse Embryonic Stem CellsProtein BindingRegulatory Sequences, Nucleic AcidTranscription, GeneticChromatinCREB-Binding ProteinE1A-Associated p300 ProteinEp300 protein, mouseHistonesTumor Suppressor Protein p53AcetyltransferaseChromatinEmbryonic stem cellEnhancer

Identifiers

PMID32690000
PMCPMC7370441
OpenAlexW3043608523

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.