Evidence map›Paper›PMID 34389686›Full record

ArticleLife science alliance2021

Dystrophin involvement in peripheral circadian SRF signalling.

Corinne A Betts, Aarti Jagannath, Tirsa LE van Westering, Melissa Bowerman, Subhashis Banerjee, Jinhong Meng, Maria Sofia Falzarano, Lara Cravo, Graham McClorey, Katharina E Meijboom and 12 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Life science alliance, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.3field-weighted citation impact, top 44% 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

7 citing papers in PubMed, 7 citations in OpenAlex.

  1. Article
  2. Article
  3. Improvement of Spontaneous Locomotor Activity in a Murine Model of Duchenne Muscular Dystrophy by N-Acetylglucosamine Alone and in Combination With Prednisolone.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
    Article
  4. Review
  5. Article
  6. Review
  7. Dystrophin missense mutations alter focal adhesion tension and mechanotransduction.Proceedings of the National Academy of Sciences of the United States of America · 2022
    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

22 authors at 6 institutions in 2 countries.

Corinne A BettsDepartment of Paediatrics, University of Oxford, South Parks Road, Oxford, UK corinne.betts@paediatrics.ox.ac.uk.ORCID 0000-0003-0579-8843
Aarti JagannathSleep and Circadian Neuroscience Institute (SCNi), Nuffield Department of Clinical Neurosciences, Oxford Molecular Pathology Institute, Dunn School of Pathology, University of Oxford, Oxford, UK.
Tirsa LE van WesteringDepartment of Paediatrics, University of Oxford, South Parks Road, Oxford, UK.
Melissa BowermanDepartment of Paediatrics, University of Oxford, South Parks Road, Oxford, UK.
Subhashis BanerjeeDepartment of Paediatrics, University of Oxford, South Parks Road, Oxford, UK.ORCID 0000-0001-8971-0006
Jinhong MengDubowitz Neuromuscular Centre, Molecular Neurosciences Section, Developmental Neuroscience Programme, University College London Great Ormond Street Institute of Child Health, London, UK.
Maria Sofia FalzaranoDepartment of Medical Sciences, Unit of Medical Genetics, University of Ferrara, Ferrara, Italy.
Lara CravoDepartment of Paediatrics, University of Oxford, South Parks Road, Oxford, UK.ORCID 0000-0002-0815-0869
Graham McCloreyDepartment of Paediatrics, University of Oxford, South Parks Road, Oxford, UK.
Katharina E MeijboomDepartment of Paediatrics, University of Oxford, South Parks Road, Oxford, UK.
Amarjit BhomraDepartment of Paediatrics, University of Oxford, South Parks Road, Oxford, UK.
Wooi Fang LimDepartment of Paediatrics, University of Oxford, South Parks Road, Oxford, UK.ORCID 0000-0002-1238-3040
Carlo RinaldiDepartment of Paediatrics, University of Oxford, South Parks Road, Oxford, UK.
John R CounsellDubowitz Neuromuscular Centre, Molecular Neurosciences Section, Developmental Neuroscience Programme, University College London Great Ormond Street Institute of Child Health, London, UK.ORCID 0000-0001-9208-101X
Katarzyna ChwaleniaDepartment of Paediatrics, University of Oxford, South Parks Road, Oxford, UK.
Elizabeth O'DonovanMedical Research Council, Laboratory of Molecular Biology, Francis Crick Avenue, Cambridge, UK.
Amer F SalehMedical Research Council, Laboratory of Molecular Biology, Francis Crick Avenue, Cambridge, UK.
Michael J GaitMedical Research Council, Laboratory of Molecular Biology, Francis Crick Avenue, Cambridge, UK.
Jennifer E MorganDubowitz Neuromuscular Centre, Molecular Neurosciences Section, Developmental Neuroscience Programme, University College London Great Ormond Street Institute of Child Health, London, UK.
Alessandra FerliniDepartment of Medical Sciences, Unit of Medical Genetics, University of Ferrara, Ferrara, Italy.
Russell G FosterSleep and Circadian Neuroscience Institute (SCNi), Nuffield Department of Clinical Neurosciences, Oxford Molecular Pathology Institute, Dunn School of Pathology, University of Oxford, Oxford, UK.ORCID 0000-0001-6055-2067
Matthew Ja WoodDepartment of Paediatrics, University of Oxford, South Parks Road, Oxford, UK.
University of Oxford · GBGreat Ormond Street Hospital · GBMRC Laboratory of Molecular Biology · GBUniversity of Ferrara · ITAstraZeneca (United Kingdom) · GBRobert Jones and Agnes Hunt Orthopaedic Hospital · GB

Funding

British Heart FoundationMedical Research Council MC_PC_16063Medical Research Council MC_U105178803Medical Research Council MR/N024850/1Medical Research Council MRN0248501Medical Research Council U105178803Wellcome Trust 205162/Z/16/ZWellcome Trust 210774/Z/18/Z
6 · The paper itself

Abstract

Absence of dystrophin, an essential sarcolemmal protein required for muscle contraction, leads to the devastating muscle-wasting disease Duchenne muscular dystrophy. Dystrophin has an actin-binding domain, which binds and stabilises filamentous-(F)-actin, an integral component of the RhoA-actin-serum-response-factor-(SRF) pathway. This pathway plays a crucial role in circadian signalling, whereby the suprachiasmatic nucleus (SCN) transmits cues to peripheral tissues, activating SRF and transcription of clock-target genes. Given dystrophin binds F-actin and disturbed SRF-signalling disrupts clock entrainment, we hypothesised dystrophin loss causes circadian deficits. We show for the first time alterations in the RhoA-actin-SRF-signalling pathway, in dystrophin-deficient myotubes and dystrophic mouse models. Specifically, we demonstrate reduced F/G-actin ratios, altered MRTF levels, dysregulated core-clock and downstream target-genes, and down-regulation of key circadian genes in muscle biopsies from Duchenne patients harbouring an array of mutations. Furthermore, we show dystrophin is absent in the SCN of dystrophic mice which display disrupted circadian locomotor behaviour, indicative of disrupted SCN signalling. Therefore, dystrophin is an important component of the RhoA-actin-SRF pathway and novel mediator of circadian signalling in peripheral tissues, loss of which leads to circadian dysregulation.

Indexed as

Signal TransductionActinsAnimalsCell LineDystrophinMiceMyoblasts, SkeletalrhoA GTP-Binding ProteinSerum Response FactorUtrophinActinsDystrophinrhoA GTP-Binding ProteinSerum Response FactorUtrophin

Identifiers

PMID34389686
PMCPMC8363758
OpenAlexW3190591004

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.