Evidence map›Paper›PMID 24832538›Full record

ArticlePloS one2014

Tcf3 represses Wnt-β-catenin signaling and maintains neural stem cell population during neocortical development.

Atsushi Kuwahara, Hiroshi Sakai, Yuanjiang Xu, Yasuhiro Itoh, Yusuke Hirabayashi, Yukiko Gotoh

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed, 1 pooled it
2.1field-weighted citation impact, top 13% 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

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

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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

6 authors at 1 institution in 1 country.

Atsushi KuwaharaLaboratory of Cell Signaling, Institute of Molecular and Cellular Biosciences, The University of Tokyo, Tokyo, Japan.
Hiroshi SakaiLaboratory of Cell Signaling, Institute of Molecular and Cellular Biosciences, The University of Tokyo, Tokyo, Japan.
Yuanjiang XuLaboratory of Cell Signaling, Institute of Molecular and Cellular Biosciences, The University of Tokyo, Tokyo, Japan.
Yasuhiro ItohLaboratory of Cell Signaling, Institute of Molecular and Cellular Biosciences, The University of Tokyo, Tokyo, Japan.
Yusuke HirabayashiLaboratory of Cell Signaling, Institute of Molecular and Cellular Biosciences, The University of Tokyo, Tokyo, Japan.
Yukiko GotohLaboratory of Cell Signaling, Institute of Molecular and Cellular Biosciences, The University of Tokyo, Tokyo, Japan.
The University of Tokyo · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

During mouse neocortical development, the Wnt-β-catenin signaling pathway plays essential roles in various phenomena including neuronal differentiation and proliferation of neural precursor cells (NPCs). Production of the appropriate number of neurons without depletion of the NPC population requires precise regulation of the balance between differentiation and maintenance of NPCs. However, the mechanism that suppresses Wnt signaling to prevent premature neuronal differentiation of NPCs is poorly understood. We now show that the HMG box transcription factor Tcf3 (also known as Tcf7l1) contributes to this mechanism. Tcf3 is highly expressed in undifferentiated NPCs in the mouse neocortex, and its expression is reduced in intermediate neuronal progenitors (INPs) committed to the neuronal fate. We found Tcf3 to be a repressor of Wnt signaling in neocortical NPCs in a reporter gene assay. Tcf3 bound to the promoter of the proneural bHLH gene Neurogenin1 (Neurog1) and repressed its expression. Consistent with this, Tcf3 repressed neuronal differentiation and increased the self-renewal activity of NPCs. We also found that Wnt signal stimulation reduces the level of Tcf3, and increases those of Tcf1 (also known as Tcf7) and Lef1, positive mediators of Wnt signaling, in NPCs. Together, these results suggest that Tcf3 antagonizes Wnt signaling in NPCs, thereby maintaining their undifferentiated state in the neocortex and that Wnt signaling promotes the transition from Tcf3-mediated repression to Tcf1/Lef1-mediated enhancement of Wnt signaling, constituting a positive feedback loop that facilitates neuronal differentiation.

Indexed as

Wnt Signaling PathwayAnimalsBasic Helix-Loop-Helix Proteinsbeta CateninCell DifferentiationCell ProliferationCell SeparationFlow CytometryHepatocyte Nuclear Factor 1-alphaIn Situ HybridizationLymphoid Enhancer-Binding Factor 1MiceMice, Inbred ICRNerve Tissue ProteinsNeural Stem CellsNeuronsBasic Helix-Loop-Helix Proteinsbeta CateninCTNNB1 protein, mouseHepatocyte Nuclear Factor 1-alphaHnf1a protein, mouseLef1 protein, mouseLymphoid Enhancer-Binding Factor 1Nerve Tissue ProteinsNeurog1 protein, mouseProto-Oncogene Proteins c-mycTcf3 protein, mouseWnt3A ProteinWnt3a protein, mouse

Identifiers

PMID24832538
PMCPMC4022625
OpenAlexW1968541727

What OpenQuestion holds

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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.