Evidence map›Paper›PMID 27302134›Full record

ArticleNucleic acids research2016

MyoD reprogramming requires Six1 and Six4 homeoproteins: genome-wide cis-regulatory module analysis.

Marc Santolini, Iori Sakakibara, Morgane Gauthier, Francesc Ribas-Aulinas, Hirotaka Takahashi, Tatsuya Sawasaki, Vincent Mouly, Jean-Paul Concordet, Pierre-Antoine Defossez, Vincent Hakim and 1 more

Open access · goldAbstract read
In one paragraph

Article in Nucleic acids research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.4field-weighted citation impact, top 18% 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

20 citing papers in PubMed, 33 citations in OpenAlex.

  1. When everything is a master regulator, nothing is.Molecular biology of the cell · 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.

Marc SantoliniInstitut Cochin, Université Paris-Descartes, Centre National de la Recherche Scientifique (CNRS), UMR 8104, Paris, France Institut National de la Santé et de la Recherche Médicale (INSERM) U1016, Paris, France Ecole Normale Supérieure, CNRS, Laboratoire de Physique Statistique, PSL Research University, Université Pierre-et-Marie Curie, Paris, France.
Iori SakakibaraInstitut Cochin, Université Paris-Descartes, Centre National de la Recherche Scientifique (CNRS), UMR 8104, Paris, France Institut National de la Santé et de la Recherche Médicale (INSERM) U1016, Paris, France Division of Integrative Pathophysiology, Proteo-Science Center, Graduate School of Medicine, Ehime University, Ehime, Japan.
Morgane GauthierInstitut Cochin, Université Paris-Descartes, Centre National de la Recherche Scientifique (CNRS), UMR 8104, Paris, France Institut National de la Santé et de la Recherche Médicale (INSERM) U1016, Paris, France.
Francesc Ribas-AulinasInstitut Cochin, Université Paris-Descartes, Centre National de la Recherche Scientifique (CNRS), UMR 8104, Paris, France Institut National de la Santé et de la Recherche Médicale (INSERM) U1016, Paris, France.
Hirotaka TakahashiProteo-Science Center, Ehime University, Ehime 791-8577, Japan.
Tatsuya SawasakiProteo-Science Center, Ehime University, Ehime 791-8577, Japan.
Vincent MoulySorbonne Universités, UPMC Univ Paris 06, INSERM UMRS974, CNRS FRE3617, Center for Research in Myology, 75013 Paris, France.
Jean-Paul ConcordetInstitut Cochin, Université Paris-Descartes, Centre National de la Recherche Scientifique (CNRS), UMR 8104, Paris, France Institut National de la Santé et de la Recherche Médicale (INSERM) U1016, Paris, France.
Pierre-Antoine DefossezUniversity Paris Diderot, Sorbonne Paris Cité, UMR 7216 CNRS, 75013 Paris, France.
Vincent HakimEcole Normale Supérieure, CNRS, Laboratoire de Physique Statistique, PSL Research University, Université Pierre-et-Marie Curie, Paris, France hakim@lps.ens.fr.
Pascal MaireInstitut Cochin, Université Paris-Descartes, Centre National de la Recherche Scientifique (CNRS), UMR 8104, Paris, France Institut National de la Santé et de la Recherche Médicale (INSERM) U1016, Paris, France pascal.maire@inserm.fr.
Université Paris Cité · FRCentre National de la Recherche Scientifique · FREhime University · JPSorbonne Université · FRUniversité Paris Sciences et Lettres · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Myogenic regulatory factors of the MyoD family have the ability to reprogram differentiated cells toward a myogenic fate. In this study, we demonstrate that Six1 or Six4 are required for the reprogramming by MyoD of mouse embryonic fibroblasts (MEFs). Using microarray experiments, we found 761 genes under the control of both Six and MyoD. Using MyoD ChIPseq data and a genome-wide search for Six1/4 MEF3 binding sites, we found significant co-localization of binding sites for MyoD and Six proteins on over a thousand mouse genomic DNA regions. The combination of both datasets yielded 82 genes which are synergistically activated by Six and MyoD, with 96 associated MyoD+MEF3 putative cis-regulatory modules (CRMs). Fourteen out of 19 of the CRMs that we tested demonstrated in Luciferase assays a synergistic action also observed for their cognate gene. We searched putative binding sites on these CRMs using available databases and de novo search of conserved motifs and demonstrated that the Six/MyoD synergistic activation takes place in a feedforward way. It involves the recruitment of these two families of transcription factors to their targets, together with partner transcription factors, encoded by genes that are themselves activated by Six and MyoD, including Mef2, Pbx-Meis and EBF.

Indexed as

GenomeAnimalsBase SequenceBinding SitesCells, CulturedCellular ReprogrammingChromatin ImmunoprecipitationEmbryo, MammalianFibroblastsHomeodomain ProteinsHumansLuciferasesMice, KnockoutMuscle DevelopmentMutationMyoD ProteinHomeodomain ProteinsLuciferasesMyoD ProteinNuclear ProteinsSix1 protein, mouseSix4 protein, mouseTrans-ActivatorsTranscription Factors

Identifiers

PMID27302134
PMCPMC5062961
OpenAlexW2427716423

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.