Evidence map›Paper›PMID 25336744›Full record

ArticleDevelopment (Cambridge, England)2014

The tumor suppressor Nf2 regulates corpus callosum development by inhibiting the transcriptional coactivator Yap.

Alfonso Lavado, Michelle Ware, Joshua Paré, Xinwei Cao

Open access · bronzeAbstract 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 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
2.2field-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

14 citing papers in PubMed, 38 citations in OpenAlex.

  1. A PAK family kinase and the Hippo/Yorkie pathway modulate WNT signaling to functionally integrate body axes during regeneration.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  2. CaCell death & disease · 2022
    Article
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  14. Role of Yes-associated protein 1 in gliomas: pathologic and therapeutic aspects.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015
    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

4 authors at 1 institution in 1 country.

Alfonso LavadoDepartment of Developmental Neurobiology, St. Jude Children's Research Hospital, Memphis, TN 38105, USA.
Michelle WareDepartment of Developmental Neurobiology, St. Jude Children's Research Hospital, Memphis, TN 38105, USA.
Joshua ParéDepartment of Developmental Neurobiology, St. Jude Children's Research Hospital, Memphis, TN 38105, USA.
Xinwei CaoDepartment of Developmental Neurobiology, St. Jude Children's Research Hospital, Memphis, TN 38105, USA Xinwei.cao@stjude.org.
St. Jude Children's Research Hospital · US

Funding

Viral Vector Technology (VVTSR)P30CA021765 · NCI · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI CHARLES ROBERTS · 1985 to 2026
$166.9M
Function & regulation of Hippo pathway effectors YAP/TAZ during brain developmentR01NS086938 · NINDS · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI CAO, XINWEI · 2014 to 2018
$1.9M
NCI NIH HHS P30 CA021765NCI NIH HHS P30 CA021765-34NINDS NIH HHS R01 NS086938NINDS NIH HHS R01NS086938
6 · The paper itself

Abstract

The corpus callosum connects cerebral hemispheres and is the largest axon tract in the mammalian brain. Callosal malformations are among the most common congenital brain anomalies and are associated with a wide range of neuropsychological deficits. Crossing of the midline by callosal axons relies on a proper midline environment that harbors guidepost cells emitting guidance cues to instruct callosal axon navigation. Little is known about what controls the formation of the midline environment. We find that two components of the Hippo pathway, the tumor suppressor Nf2 (Merlin) and the transcriptional coactivator Yap (Yap1), regulate guidepost development and expression of the guidance cue Slit2 in mouse. During normal brain development, Nf2 suppresses Yap activity in neural progenitor cells to promote guidepost cell differentiation and prevent ectopic Slit2 expression. Loss of Nf2 causes malformation of midline guideposts and Slit2 upregulation, resulting in callosal agenesis. Slit2 heterozygosity and Yap deletion both restore callosal formation in Nf2 mutants. Furthermore, selectively elevating Yap activity in midline neural progenitors is sufficient to disrupt guidepost formation, upregulate Slit2 and prevent midline crossing. The Hippo pathway is known for its role in controlling organ growth and tumorigenesis. Our study identifies a novel role of this pathway in axon guidance. Moreover, by linking axon pathfinding and neural progenitor behaviors, our results provide an example of the intricate coordination between growth and wiring during brain development.

Indexed as

Adaptor Proteins, Signal TransducingAnimalsCell Cycle ProteinsCorpus CallosumEpendymoglial CellsFemaleLimbic LobeMiceNervous SystemNeurofibromatosis 2PhosphoproteinsPregnancyTranscription FactorsYAP-Signaling ProteinsAdaptor Proteins, Signal TransducingCell Cycle ProteinsPhosphoproteinsTranscription FactorsYap1 protein, mouseYAP-Signaling ProteinsCommissureGlial wedgeGuidepost neuronsIndusium griseumNervous systemRadial glia

Identifiers

PMID25336744
PMCPMC4302891
OpenAlexW2147027546

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.