Evidence map›Paper›PMID 17553984›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2007

Nuclear factor I coordinates multiple phases of cerebellar granule cell development via regulation of cell adhesion molecules.

Wei Wang, Debra Mullikin-Kilpatrick, James E Crandall, Richard M Gronostajski, E David Litwack, Daniel L Kilpatrick

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
2.4field-weighted citation impact, top 14% 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

49 citing papers in PubMed, 83 citations in OpenAlex.

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  6. The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023
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  19. Consensus Paper: Cerebellar Development.Cerebellum (London, England) · 2016
    Review
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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 4 institutions in 1 country.

Wei WangDepartment of Cellular and Molecular Physiology and Program in Neuroscience, University of Massachusetts Medical School, Worcester, Massachusetts 01655, USA.
Debra Mullikin-Kilpatrick
James E Crandall
Richard M Gronostajski
E David Litwack
Daniel L Kilpatrick
University of Massachusetts Chan Medical School · USEunice Kennedy Shriver Center · USUniversity at Buffalo, State University of New York · USUniversity of Maryland, Baltimore · US

Funding

PILOT AND FEASIBILITY PROGRAMP30DK032520 · NIDDK · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI CZECH, MICHAEL P · 1986 to 2010
$14.6M
Transcriptional regulation of pontine developmentR01NS050515 · NINDS · UNIVERSITY OF MARYLAND BALTIMORE · PI LITWACK, E DAVID · 2006 to 2009
$1.3M
Transcriptional Control of Terminal DifferentiationR01CA079999 · NCI · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI KILPATRICK, DANIEL L · 2001 to 2004
$1.1M
NCI NIH HHS CA79999NCI NIH HHS R01 CA079999NIDDK NIH HHS DK32520NIDDK NIH HHS P30 DK032520NINDS NIH HHS R01 NS050515
6 · The paper itself

Abstract

A central question is how various stages of neuronal development are integrated as a differentiation program. Here we show that the nuclear factor I (NFI) family of transcriptional regulators is expressed and functions throughout the postmitotic development of cerebellar granule neurons (CGNs). Expression of an NFI dominant repressor in CGN cultures blocked axon outgrowth and dendrite formation and decreased CGN migration. Inhibition of NFI transactivation also disrupted extension and fasciculation of parallel fibers as well as CGN migration to the internal granule cell layer in cerebellar slices. In postnatal day 17 Nfia-deficient mice, parallel fibers were greatly diminished and disoriented, CGN dendrite formation was dramatically impaired, and migration from the external germinal layer (EGL) was retarded. Axonal marker expression also was disrupted within the EGL of embryonic day 18 Nfib-null mice. NFI regulation of axon extension was observed under conditions of homotypic cell contact, implicating cell surface proteins as downstream mediators of its actions in CGNs. Consistent with this, the cell adhesion molecules ephrin B1 and N-cadherin were identified as NFI gene targets in CGNs using inhibitor and Nfi mutant analysis as well as chromatin immunoprecipitation. Functional inhibition of ephrin B1 or N-cadherin interfered with CGN axon extension and guidance, migration, and dendritogenesis in cell culture as well as in situ. These studies define NFI as a key regulator of postmitotic CGN development, in particular of axon formation, dendritogenesis, and migratory behavior. Furthermore, they reveal how a single transcription factor family can control and integrate multiple aspects of neuronal differentiation through the regulation of cell adhesion molecules.

Indexed as

AnimalsCell Adhesion MoleculesCell MovementCells, CulturedCerebellumDrosophilaMiceMice, Inbred C57BLMice, KnockoutMice, TransgenicNFI Transcription FactorsRatsCell Adhesion MoleculesNFI Transcription Factors

Identifiers

PMID17553984
PMCPMC6672151
OpenAlexW1965294797

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.