Evidence map›Paper›PMID 36103831›Full record

ArticleCell reports2022

Histone H1 regulates non-coding RNA turnover on chromatin in a m6A-dependent manner.

José Miguel Fernández-Justel, Cristina Santa-María, Sara Martín-Vírgala, Shreya Ramesh, Alberto Ferrera-Lagoa, Mónica Salinas-Pena, Javier Isoler-Alcaraz, Magdalena M Maslon, Albert Jordan, Javier F Cáceres and 1 more

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.8field-weighted citation impact, top 14% 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

14 citing papers in PubMed, 24 citations in OpenAlex.

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  6. lncRNA TUG1 and kidney diseases.BMC nephrology · 2025
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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

11 authors at 5 institutions in 2 countries.

José Miguel Fernández-JustelCentro de Biología Molecular Severo Ochoa (CBMSO), Consejo Superior de Investigaciones Científicas/Universidad Autónoma de Madrid (CSIC/UAM), Nicolás Cabrera 1, 28049 Madrid, Spain.
Cristina Santa-MaríaCentro de Biología Molecular Severo Ochoa (CBMSO), Consejo Superior de Investigaciones Científicas/Universidad Autónoma de Madrid (CSIC/UAM), Nicolás Cabrera 1, 28049 Madrid, Spain.
Sara Martín-VírgalaCentro de Biología Molecular Severo Ochoa (CBMSO), Consejo Superior de Investigaciones Científicas/Universidad Autónoma de Madrid (CSIC/UAM), Nicolás Cabrera 1, 28049 Madrid, Spain.
Shreya RameshCentro de Biología Molecular Severo Ochoa (CBMSO), Consejo Superior de Investigaciones Científicas/Universidad Autónoma de Madrid (CSIC/UAM), Nicolás Cabrera 1, 28049 Madrid, Spain.
Alberto Ferrera-LagoaCentro de Biología Molecular Severo Ochoa (CBMSO), Consejo Superior de Investigaciones Científicas/Universidad Autónoma de Madrid (CSIC/UAM), Nicolás Cabrera 1, 28049 Madrid, Spain.
Mónica Salinas-PenaInstituto de Biología Molecular de Barcelona (IBMB-CSIC), Carrer de Baldiri Reixac, 15, 08028 Barcelona, Spain.
Javier Isoler-AlcarazCentro de Biología Molecular Severo Ochoa (CBMSO), Consejo Superior de Investigaciones Científicas/Universidad Autónoma de Madrid (CSIC/UAM), Nicolás Cabrera 1, 28049 Madrid, Spain.
Magdalena M MaslonMRC Human Genetics Unit, Institute of Genetics and Cancer, University of Edinburgh, Crewe South Road, Edinburgh EH4 2XU, UK.
Albert JordanInstituto de Biología Molecular de Barcelona (IBMB-CSIC), Carrer de Baldiri Reixac, 15, 08028 Barcelona, Spain.
Javier F CáceresMRC Human Genetics Unit, Institute of Genetics and Cancer, University of Edinburgh, Crewe South Road, Edinburgh EH4 2XU, UK.
María GómezCentro de Biología Molecular Severo Ochoa (CBMSO), Consejo Superior de Investigaciones Científicas/Universidad Autónoma de Madrid (CSIC/UAM), Nicolás Cabrera 1, 28049 Madrid, Spain. Electronic address: mgomez@cbm.csic.es.
Centro de Biología Molecular Severo Ochoa · ESConsejo Superior de Investigaciones Científicas · ESInstitut de Biologia Molecular de Barcelona · ESUniversidad Autónoma de Madrid · ESUniversity of Edinburgh · GB

Funding

Medical Research Council MC_UU_00007/7
6 · The paper itself

Abstract

Linker histones are highly abundant chromatin-associated proteins with well-established structural roles in chromatin and as general transcriptional repressors. In addition, it has been long proposed that histone H1 exerts context-specific effects on gene expression. Here, we identify a function of histone H1 in chromatin structure and transcription using a range of genomic approaches. In the absence of histone H1, there is an increase in the transcription of non-coding RNAs, together with reduced levels of m6A modification leading to their accumulation on chromatin and causing replication-transcription conflicts. This strongly suggests that histone H1 prevents non-coding RNA transcription and regulates non-coding transcript turnover on chromatin. Accordingly, altering the m6A RNA methylation pathway rescues the replicative phenotype of H1 loss. This work unveils unexpected regulatory roles of histone H1 on non-coding RNA turnover and m6A deposition, highlighting the intimate relationship between chromatin conformation, RNA metabolism, and DNA replication to maintain genome performance.

Indexed as

ChromatinHistonesMethylationRNA, UntranslatedTranscription FactorsChromatinHistonesRNA, UntranslatedTranscription Factorschromatin conformationchromatin RNAsCP: Molecular biologyhistone H1lncRNAsm6AmESCsreplication-transcription conflictsreplicative stressR-loops

Identifiers

PMID36103831
PMCPMC7613722
OpenAlexW4295905064

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.