Evidence map›Paper›PMID 26416879›Full record

ArticleMolecular and cellular biology2015

PAK1 and CtBP1 Regulate the Coupling of Neuronal Activity to Muscle Chromatin and Gene Expression.

Jean-Luc Thomas, Vincent Moncollin, Aymeric Ravel-Chapuis, Carmen Valente, Daniela Corda, Alexandre Méjat, Laurent Schaeffer

Open access · bronzeAbstract read
In one paragraph

Article in Molecular and cellular biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

16 citing papers in PubMed, 26 citations in OpenAlex.

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  15. Traumatic muscle fibrosis: From pathway to prevention.The journal of trauma and acute care surgery · 2017
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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

7 authors at 5 institutions in 2 countries.

Jean-Luc ThomasUniversité de Lyon 1 and Laboratoire de Biologie Moléculaire de la Cellule, ENS Lyon, Lyon, France.
Vincent MoncollinUniversité de Lyon 1 and Laboratoire de Biologie Moléculaire de la Cellule, ENS Lyon, Lyon, France vincent.moncollin@ens-lyon.fr laurent.schaeffer@univ-lyon1.fr.
Aymeric Ravel-ChapuisUniversité de Lyon 1 and Laboratoire de Biologie Moléculaire de la Cellule, ENS Lyon, Lyon, France.
Carmen ValenteInstitute of Protein Biochemistry, National Research Council, Naples, Italy.
Daniela CordaInstitute of Protein Biochemistry, National Research Council, Naples, Italy.
Alexandre MéjatUniversité de Lyon 1 and Laboratoire de Biologie Moléculaire de la Cellule, ENS Lyon, Lyon, France.
Laurent SchaefferUniversité de Lyon 1 and Laboratoire de Biologie Moléculaire de la Cellule, ENS Lyon, Lyon, France Hospices Civils de Lyon, Service d'Anatomie et Cytologie Pathologiques, Hôpital Édouard Herriot, Lyon, France vincent.moncollin@ens-lyon.fr laurent.schaeffer@univ-lyon1.fr.
Laboratoire de Biologie et Modélisation de la Cellule · FRUniversité Claude Bernard Lyon 1 · FRÉcole Normale Supérieure de Lyon · FRInstitute of Protein Biochemistry · ITNational Research Council · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Acetylcholine receptor (AChR) expression in innervated muscle is limited to the synaptic region. Neuron-induced electrical activity participates in this compartmentalization by promoting the repression of AChR expression in the extrasynaptic regions. Here, we show that the corepressor CtBP1 (C-terminal binding protein 1) is present on the myogenin promoter together with repressive histone marks. shRNA-mediated downregulation of CtBP1 expression is sufficient to derepress myogenin and AChR expression in innervated muscle. Upon denervation, CtBP1 is displaced from the myogenin promoter and relocates to the cytoplasm, while repressive histone marks are replaced by activating ones concomitantly to the activation of myogenin expression. We also observed that upon denervation the p21-activated kinase 1 (PAK1) expression is upregulated, suggesting that phosphorylation by PAK1 may be involved in the relocation of CtBP1. Indeed, preventing CtBP1 Ser158 phosphorylation induces CtBP1 accumulation in the nuclei and abrogates the activation of myogenin and AChR expression. Altogether, these findings reveal a molecular mechanism to account for the coordinated control of chromatin modifications and muscle gene expression by presynaptic neurons via a PAK1/CtBP1 pathway.

Indexed as

Muscle DenervationActive Transport, Cell NucleusAlcohol OxidoreductasesAnimalsCell NucleusChromatinCytoplasmDNA-Binding ProteinsHistonesMiceMuscle, SkeletalMyogeninp21-Activated KinasesPhosphorylationPromoter Regions, GeneticReceptors, CholinergicAlcohol OxidoreductasesChromatinC-terminal binding proteinDNA-Binding ProteinsHistonesMyogeninp21-Activated KinasesPak1 protein, mouseReceptors, CholinergicRNA, Small Interfering

Identifiers

PMID26416879
PMCPMC4648822
OpenAlexW2178902488

What OpenQuestion holds

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Registered trials

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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.