Evidence map›Paper›PMID 27434165›Full record

ArticleFly2016

Revisiting the role of the Gcm transcription factor, from master regulator to Swiss army knife.

Pierre B Cattenoz, Angela Giangrande

Abstract read
In one paragraph

Article in Fly, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
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

3 citing papers in PubMed.

  1. Article
  2. Article
  3. 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

2 authors.

Pierre B Cattenoza Department of Functional Genomics and Cancer , Institut de Génétique et de Biologie Moléculaire et Cellulaire , Illkirch , France.
Angela Giangrandea Department of Functional Genomics and Cancer , Institut de Génétique et de Biologie Moléculaire et Cellulaire , Illkirch , France.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Master genes are known to induce the differentiation of a multipotent cell into a specific cell type. These molecules are often transcription factors that switch on the regulatory cascade that triggers cell specification. Gcm was first described as the master gene of the glial fate in Drosophila as it induces the differentiation of neuroblasts into glia in the developing nervous system. Later on, Gcm was also shown to regulate the differentiation of blood, tendon and peritracheal cells as well as that of neuronal subsets. Thus, the glial master gene is used in at least 4 additional systems to promote differentiation. To understand the numerous roles of Gcm, we recently reported a genome-wide screen of Gcm direct targets in the Drosophila embryo. This screen provided new insight into the role and mode of action of this powerful transcription factor, notably on the interactions between Gcm and major differentiation pathways such as the Hedgehog, Notch and JAK/STAT. Here, we discuss the mode of action of Gcm in the different systems, we present new tissues that require Gcm and we revise the concept of 'master gene'.

Indexed as

AnimalsCell DifferentiationDNA-Binding ProteinsDrosophilaDrosophila ProteinsEmbryo, NonmammalianGenes, RegulatorSignal TransductionTranscription FactorsDNA-Binding ProteinsDrosophila ProteinsGCM protein, DrosophilaTranscription FactorsDamIDGcmhedgehoghigh-throughput screenimmune systemJAK/STATnervous systemNotch

Identifiers

PMID27434165
PMCPMC5036930

What OpenQuestion holds

Textmetadata
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.