Evidence map›Paper›PMID 22554084›Full record

ArticleNeural development2012

Fbxw7 regulates Notch to control specification of neural precursors for oligodendrocyte fate.

Julia L Snyder, Christina A Kearns, Bruce Appel

Abstract read
In one paragraph

Article in Neural development, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

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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

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3 · Its place in the literature

Who cites it

41 citing papers in PubMed.

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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

3 authors.

Julia L SnyderDepartment of Biological Sciences, Vanderbilt University, Nashville, TN, USA.
Christina A Kearns
Bruce Appel

Funding

ZEBRAFISH TRANSGENIC CORE - ROCKY MOUNTAIN NEUROLOGICAL DISORDERS CORE CENTERP30NS048154 · NINDS · UNIVERSITY OF COLORADO DENVER · PI RIBERA, ANGELES BADELL · 2004 to 2020
$10.1M
Training Program in Stem Cell and Regenerative Developmental BiologyT32HD007502 · NICHD · VANDERBILT UNIVERSITY · PI WRIGHT, CHRISTOPHER V · 1997 to 2022
$5.4M
Genetic Analysis of Oligodendrocyte SpecificationR01NS046668 · NINDS · VANDERBILT UNIVERSITY · PI APPEL, BRUCE H · 2004 to 2019
$4.8M
NICHD NIH HHS T32 HD007502NINDS NIH HHS NS046668NINDS NIH HHS P30 NS048154
6 · The paper itself

Abstract

backgroundIn the developing vertebrate nervous system elevated levels of Notch signaling activity can block neurogenesis and promote formation of glial cells. The mechanisms that limit Notch activity to balance formation of neurons and glia from neural precursors are poorly understood.

resultsBy screening for mutations that disrupt oligodendrocyte development in zebrafish we found one allele, called vu56, that produced excess oligodendrocyte progenitor cells (OPCs). Positional cloning revealed that the vu56 allele is a mutation of fbxw7, which encodes the substrate recognition component of a ubiquitin ligase that targets Notch and other proteins for degradation. To investigate the basis of the mutant phenotype we performed in vivo, time-lapse imaging, which revealed that the increase in OPC number resulted from production of extra OPCs by ventral spinal cord precursors and not from changes in OPC proliferation or death. Notch signaling activity was elevated in spinal cord precursors of fbxw7 mutant zebrafish and inhibition of Notch signaling suppressed formation of excess OPCs.

conclusionNotch signaling promotes glia cell formation from neural precursors in vertebrate embryos. Our data indicate that Fbxw7 helps attenuate Notch signaling during zebrafish neural development thereby limiting the number of OPCs.

Indexed as

AnimalsBase SequenceCell Cycle ProteinsCell DifferentiationCell LineageF-Box ProteinsF-Box-WD Repeat-Containing Protein 7Gene Expression Regulation, DevelopmentalMolecular Sequence DataOligodendrogliaReceptor, Notch1Sequence AlignmentSignal TransductionStem CellsTranscription FactorsUbiquitin-Protein Ligase ComplexesCell Cycle ProteinsF-Box ProteinsF-Box-WD Repeat-Containing Protein 7Fbxw7 protein, zebrafishReceptor, Notch1Transcription FactorsUbiquitin-Protein Ligase ComplexesUbiquitin-Protein LigasesZebrafish Proteins

Identifiers

PMID22554084
PMCPMC3404928

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LicenceCC BY
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Registered trials

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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.