Evidence map›Paper›PMID 11160433›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2001

Defects in sensory axon growth precede neuronal death in Brn3a-deficient mice.

S R Eng, K Gratwick, J M Rhee, N Fedtsova, L Gan, E E Turner

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
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

48 citing papers in PubMed, 103 citations in OpenAlex.

  1. Article
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  4. A wound-induced differentiation trajectory for neurons.Proceedings of the National Academy of Sciences of the United States of America · 2024
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  14. Frizzled3 is required for the development of multiple axon tracts in the mouse central nervous system.Proceedings of the National Academy of Sciences of the United States of America · 2014
    Article
  15. Article
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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 2 institutions in 1 country.

S R EngDepartment of Psychiatry and Program in Neuroscience, University of California, San Diego, USA.
K Gratwick
J M Rhee
N Fedtsova
L Gan
E E Turner
University of California, San Diego · USUniversity of Rochester · US

Funding

FELLOWSHIP IN GERIATRIC MENTAL HEALTHT32MH019934 · NIMH · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI Elizabeth W Twamley · 1994 to 2026
$9.5M
TRANSCRIPTION FACTORS IN CONTROL OF BRAIN DEVELOPMENTR01HD033442 · NICHD · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI TURNER, ERIC E. · 1997 to 2010
$2.5M
TRANSCRIPTIONAL CONTROL OF NEURONAL SURVIVAL IN THE CNSR03MH058447 · NIMH · UNIVERSITY OF CALIFORNIA SAN DIEGO · PI TURNER, ERIC E. · 1997 to 1998
–
NICHD NIH HHS HD33442NICHD NIH HHS R01 HD033442NIMH NIH HHS 5-T32-MH19934NIMH NIH HHS MH01581NIMH NIH HHS MH58447NIMH NIH HHS T32 MH019934
6 · The paper itself

Abstract

Brn3a/Brn-3.0 is a POU-domain transcription factor expressed in primary sensory neurons of the cranial and dorsal root ganglia and in specific neurons in the caudal CNS. Mice lacking Brn3a undergo extensive sensory neural death late in gestation and die at birth. To further examine Brn3a expression and the abnormalities that accompany its absence, we constructed a transgene containing 11 kb of Brn3a upstream regulatory sequence linked to a LacZ reporter. Here we show that these regulatory sequences direct transgene expression specifically to Brn3a peripheral sensory neurons of the cranial and dorsal root ganglia. Furthermore, expression of the 11 kb/LacZ reporter in the sensory neurons of the mesencephalic trigeminal, but not other Brn3a midbrain neurons, demonstrates that cell-specific transgene expression is targeted to a functional class of neurons rather than to an anatomical region. We then interbred the 11 kb/LacZ reporter strain with mice carrying a null mutant allele of Brn3a to generate 11 kb/LacZ, Brn3a knock-out mice. beta-Galactosidase expression in these mice reveals significant axonal growth defects, including excessive and premature branching of the major divisions of the trigeminal nerve and a failure to correctly innervate whisker follicles, all of which precede sensory neural death in these mice. These defects in Brn3a(-/-) mice resemble strongly those seen in mice lacking the mediators of sensory pathfinding semaphorin 3A and neuropilin-1. Here we show, however, that sensory neurons are able to express neuropilin-1 in the absence of Brn3a.

Indexed as

AnimalsAxonsbeta-GalactosidaseBrainCell DeathCrosses, GeneticDNA-Binding ProteinsFemaleGanglia, SpinalGenes, ReporterImmunohistochemistryMaleMiceMice, Inbred C57BLMice, KnockoutNerve Tissue Proteinsbeta-GalactosidaseDNA-Binding ProteinsNerve Tissue ProteinsNeuropilin-1Pou4f1 protein, mouseReceptor, trkCRNA, MessengerTranscription Factor Brn-3Transcription Factor Brn-3ATranscription Factors

Identifiers

PMID11160433
PMCPMC6763803
OpenAlexW2132264513

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.