Evidence map›Paper›PMID 21205796›Full record

ArticleDevelopment (Cambridge, England)2011

F3/contactin and TAG1 play antagonistic roles in the regulation of sonic hedgehog-induced cerebellar granule neuron progenitor proliferation.

Dia Xenaki, Indira B Martin, Lynn Yoshida, Kyoji Ohyama, Gianfranco Gennarini, Martin Grumet, Takeshi Sakurai, Andrew J W Furley

Open access · bronzeAbstract read
In one paragraph

Article in Development (Cambridge, England), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed, 1 pooled it
2.4field-weighted citation impact, top 11% 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

28 citing papers in PubMed, 1 synthesis or guideline pooled it, 70 citations in OpenAlex.

  1. Pooled it
  2. MTCL2 Is Essential for the Bipolar-to-Multipolar Transition in the Dendrite Extension of Cerebellar Granule Neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2026
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  3. Review
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  18. Manduca Contactin Regulates Amyloid Precursor Protein-Dependent Neuronal Migration.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016
    Article
  19. Article
  20. 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

8 authors at 3 institutions in 3 countries.

Dia XenakiDepartment of Biomedical Science, University of Sheffield, Sheffield, UK.
Indira B Martin
Lynn Yoshida
Kyoji Ohyama
Gianfranco Gennarini
Martin Grumet
Takeshi Sakurai
Andrew J W Furley
University of Sheffield · GBRutgers, The State University of New Jersey · USUniversity of Bari Aldo Moro · IT

Funding

Biotechnology and Biological Sciences Research Council 50/G19549Biotechnology and Biological Sciences Research Council BB/D014867Cancer Research UK C7795/A7237Wellcome Trust GR077544AIA
6 · The paper itself

Abstract

Modulation of the sonic hedgehog (SHH) pathway is a crucial factor in cerebellar morphogenesis. Stimulation of granule neuron progenitor (GNP) proliferation is a central function of SHH signalling, but how this is controlled locally is not understood. We show that two sequentially expressed members of the contactin (CNTN) family of adhesion molecules, TAG1 and F3, act antagonistically to control SHH-induced proliferation: F3 suppresses SHH-induced GNP proliferation and induces differentiation, whereas TAG1 antagonises F3. Production of GNPs in TAG1-null mice is delayed and reduced. F3 and TAG1 colocalise on GNPs with the related L1-like adhesion molecule NrCAM, and F3 fails to suppress the SHH-induced proliferation of NrCAM-deficient GNPs. We show that F3 and SHH both primarily affect a group of intermediate GNPs (IPs), which, though actively dividing, also express molecules associated with differentiation, including β-tubulin III (TuJ1) and TAG1. In vivo, intermediate progenitors form a discrete layer in the middle of the external germinal layer (mEGL), while F3 becomes expressed on the axons of postmitotic granule neurons as they leave the inner EGL (iEGL). We propose, therefore, that F3 acts as a localised signal in the iEGL that induces SHH-stimulated cells in the overlying mEGL to exit cell cycle and differentiate. By contrast, expression of TAG1 on GNPs antagonises this signal in the mEGL, preventing premature differentiation and sustaining GNP expansion in a paracrine fashion. Together, these findings indicate that CNTN and L1-like proteins play a significant role in modulating SHH-induced neuronal precursor proliferation.

Indexed as

AnimalsCell DifferentiationCell ProliferationCells, CulturedCerebellumContactin 1Contactin 2Hedgehog ProteinsMiceMice, Mutant StrainsNeuronsSignal TransductionCntn2 protein, mouseContactin 1Contactin 2Hedgehog Proteins

Identifiers

PMID21205796
PMCPMC3014637
OpenAlexW2003369797

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.