Evidence map›Paper›PMID 24961800›Full record

ArticleDevelopment (Cambridge, England)2014

Coordinated repression and activation of two transcriptional programs stabilizes cell fate during myogenesis.

Lucia Ciglar, Charles Girardot, Bartek Wilczyński, Martina Braun, Eileen E M Furlong

Open access · hybridAbstract read
In one paragraph

Article in Development (Cambridge, England), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.6field-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

18 citing papers in PubMed, 30 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Review
  9. Annual review of genetics · 2019
    Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Dual functionality ofGenes & development · 2017
    Article
  16. FlyBase at 25: looking to the future.Nucleic acids research · 2017
    Article
  17. Article
  18. Specification of the somatic musculature in Drosophila.Wiley interdisciplinary reviews. Developmental biology
    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

5 authors at 1 institution in 1 country.

Lucia CiglarEuropean Molecular Biology Laboratory, Genome Biology Unit, Heidelberg 69117, Germany.
Charles GirardotEuropean Molecular Biology Laboratory, Genome Biology Unit, Heidelberg 69117, Germany.
Bartek WilczyńskiEuropean Molecular Biology Laboratory, Genome Biology Unit, Heidelberg 69117, Germany.
Martina BraunEuropean Molecular Biology Laboratory, Genome Biology Unit, Heidelberg 69117, Germany.
Eileen E M FurlongEuropean Molecular Biology Laboratory, Genome Biology Unit, Heidelberg 69117, Germany furlong@embl.de.
European Molecular Biology Laboratory · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Molecular models of cell fate specification typically focus on the activation of specific lineage programs. However, the concurrent repression of unwanted transcriptional networks is also essential to stabilize certain cellular identities, as shown in a number of diverse systems and phyla. Here, we demonstrate that this dual requirement also holds true in the context of Drosophila myogenesis. By integrating genetics and genomics, we identified a new role for the pleiotropic transcriptional repressor Tramtrack69 in myoblast specification. Drosophila muscles are formed through the fusion of two discrete cell types: founder cells (FCs) and fusion-competent myoblasts (FCMs). When tramtrack69 is removed, FCMs appear to adopt an alternative muscle FC-like fate. Conversely, ectopic expression of this repressor phenocopies muscle defects seen in loss-of-function lame duck mutants, a transcription factor specific to FCMs. This occurs through Tramtrack69-mediated repression in FCMs, whereas Lame duck activates a largely distinct transcriptional program in the same cells. Lineage-specific factors are therefore not sufficient to maintain FCM identity. Instead, their identity appears more plastic, requiring the combination of instructive repressive and activating programs to stabilize cell fate.

Indexed as

AnimalsCell DifferentiationChromatin ImmunoprecipitationDrosophilaDrosophila ProteinsEmbryo, NonmammalianGene Expression Regulation, DevelopmentalIn Situ Hybridization, FluorescenceMesodermMuscle DevelopmentMyoblastsMyogenic Regulatory FactorsRepressor ProteinsDrosophila Proteinslmd protein, DrosophilaMyogenic Regulatory FactorsRepressor Proteinsttk protein, DrosophilaDrosophilaEnhancerMyoblast cell fate specificationTramtrack69Transcriptional networksTranscriptional repression

Identifiers

PMID24961800
PMCPMC4146391
OpenAlexW2047625632

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.