Evidence map›Paper›PMID 32160911›Full record

ArticleGenome biology2020

Smarcad1 mediates microbiota-induced inflammation in mouse and coordinates gene expression in the intestinal epithelium.

Juri Kazakevych, Jérémy Denizot, Anke Liebert, Mariana Portovedo, Mia Mosavie, Payal Jain, Claudia Stellato, Claire Fraser, Renan Oliveira Corrêa, Marina Célestine and 6 more

Open access · goldAbstract read
In one paragraph

Article in Genome biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

17 citing papers in PubMed, 20 citations in OpenAlex.

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  16. Long non-coding RNAs: the tentacles of chromatin remodeler complexes.Cellular and molecular life sciences : CMLS · 2021
    Review
  17. Epigenome-metabolome-microbiome axis in health and IBD.Current opinion in microbiology · 2020
    Review
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

16 authors at 4 institutions in 4 countries.

Juri KazakevychNuclear Dynamics, Babraham Institute, Cambridge, CB22 3AT, UK.
Jérémy DenizotNuclear Dynamics, Babraham Institute, Cambridge, CB22 3AT, UK.
Anke LiebertNuclear Dynamics, Babraham Institute, Cambridge, CB22 3AT, UK.
Mariana PortovedoLaboratory of Immunoinflammation, Institute of Biology, UNICAMP, Campinas, 13083-862, Brazil.
Mia MosavieSchool of Biological Sciences, University of Essex, Colchester, CO4 3SQ, UK.
Payal JainNuclear Dynamics, Babraham Institute, Cambridge, CB22 3AT, UK.
Claudia StellatoNuclear Dynamics, Babraham Institute, Cambridge, CB22 3AT, UK.
Claire FraserNuclear Dynamics, Babraham Institute, Cambridge, CB22 3AT, UK.
Renan Oliveira CorrêaLaboratory of Immunoinflammation, Institute of Biology, UNICAMP, Campinas, 13083-862, Brazil.
Marina CélestineNuclear Dynamics, Babraham Institute, Cambridge, CB22 3AT, UK.
Raphaël MattiuzNuclear Dynamics, Babraham Institute, Cambridge, CB22 3AT, UK.
Hanneke OkkenhaugImaging Facility, Babraham Institute, Cambridge, CB22 3AT, UK.
J Ross MillerNuclear Dynamics, Babraham Institute, Cambridge, CB22 3AT, UK.
Marco Aurélio Ramirez VinoloLaboratory of Immunoinflammation, Institute of Biology, UNICAMP, Campinas, 13083-862, Brazil.
Marc VeldhoenLymphocyte Signalling and Development, Babraham Institute, Cambridge, CB22 3AT, UK.
Patrick Varga-WeiszNuclear Dynamics, Babraham Institute, Cambridge, CB22 3AT, UK. patrick.varga-weisz@essex.ac.uk.
Babraham Institute · GBUniversidade Estadual de Campinas (UNICAMP) · BRInstituto de Medicina Molecular João Lobo AntunesUniversity of Essex · GB

Funding

Biotechnology and Biological Sciences Research Council BB/F020236/1Biotechnology and Biological Sciences Research Council BB/N013565/1Biotechnology and Biological Sciences Research Council BBS/E/B/000C0404Biotechnology and Biological Sciences Research Council BBS/E/B/000C0405Medical Research Council G0701175Medical Research Council MR/N009398/1
6 · The paper itself

Abstract

backgroundHow intestinal epithelial cells interact with the microbiota and how this is regulated at the gene expression level are critical questions. Smarcad1 is a conserved chromatin remodeling factor with a poorly understood tissue function. As this factor is highly expressed in the stem and proliferative zones of the intestinal epithelium, we explore its role in this tissue.

resultsSpecific deletion of Smarcad1 in the mouse intestinal epithelium leads to colitis resistance and substantial changes in gene expression, including a striking increase of expression of several genes linked to innate immunity. Absence of Smarcad1 leads to changes in chromatin accessibility and significant changes in histone H3K9me3 over many sites, including genes that are differentially regulated upon Smarcad1 deletion. We identify candidate members of the gut microbiome that elicit a Smarcad1-dependent colitis response, including members of the poorly understood TM7 phylum.

conclusionsOur study sheds light onto the role of the chromatin remodeling machinery in intestinal epithelial cells in the colitis response and shows how a highly conserved chromatin remodeling factor has a distinct role in anti-microbial defense. This work highlights the importance of the intestinal epithelium in the colitis response and the potential of microbial species as pharmacological and probiotic targets in the context of inflammatory diseases.

Indexed as

Gene Expression RegulationAnimalsColitisDNA HelicasesGene DeletionHistonesIntestinal MucosaMiceMicrobiotaRegulatory Elements, TranscriptionalDNA HelicasesHistonesSmarcad1 protein, mouse

Identifiers

PMID32160911
PMCPMC7065452
OpenAlexW3011964638

What OpenQuestion holds

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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.