Evidence map›Paper›PMID 19934013›Full record

ArticleDevelopment (Cambridge, England)2009

N-cadherin acts in concert with Slit1-Robo2 signaling in regulating aggregation of placode-derived cranial sensory neurons.

Celia E Shiau, Marianne Bronner-Fraser

Abstract read
In one paragraph

Article in Development (Cambridge, England), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.

0numbers the graph read from it
0cells of the map it votes in
59citing papers in PubMed
3.3field-weighted citation impact, top 7% 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

59 citing papers in PubMed, 90 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Elp1 function in placode-derived neurons is critical for proper trigeminal ganglion development.Developmental dynamics : an official publication of the American Association of Anatomists · 2025
    Article
  6. Article
  7. Article
  8. From neural crest migration to the onset of gangliogenesis.Current topics in developmental biology · 2025
    Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Review
  19. Trans-Axonal Signaling in Neural Circuit Wiring.International journal of molecular sciences · 2020
    Review
  20. Molecular cancer research : MCR · 2020
    Article
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

2 authors at 1 institution in 1 country.

Celia E ShiauDivision of Biology 139-74, California Institute of Technology, Pasadena, CA 91125, USA.
Marianne Bronner-Fraser
California Institute of Technology · US

Funding

PREDOCTORAL TRAINING IN BIOLOGY AND CHEMISTRYT32GM007616 · NIGMS · CALIFORNIA INSTITUTE OF TECHNOLOGY · PI STERNBERG, PAUL WARREN · 1985 to 2019
$22.9M
Ectodermal Placode Development into Sensory StructuresR01DE016459 · NIDCR · CALIFORNIA INSTITUTE OF TECHNOLOGY · PI BRONNER, MARIANNE · 2004 to 2014
$3.8M
NIDCR NIH HHS DE16459NIDCR NIH HHS R01 DE016459NIGMS NIH HHS 5T32 GM07616NIGMS NIH HHS T32 GM007616
6 · The paper itself

Abstract

Vertebrate cranial sensory ganglia have a dual origin from the neural crest and ectodermal placodes. In the largest of these, the trigeminal ganglion, Slit1-Robo2 signaling is essential for proper ganglion assembly. Here, we demonstrate a crucial role for the cell adhesion molecule N-cadherin and its interaction with Slit1-Robo2 during gangliogenesis in vivo. A common feature of chick trigeminal and epibranchial ganglia is the expression of N-cadherin and Robo2 on placodal neurons and Slit1 on neural crest cells. Interestingly, N-cadherin localizes to intercellular adherens junctions between placodal neurons during ganglion assembly. Depletion of N-cadherin causes loss of proper ganglion coalescence, similar to that observed after loss of Robo2, suggesting that the two pathways might intersect. Consistent with this possibility, blocking or augmenting Slit-Robo signaling modulates N-cadherin protein expression on the placodal cell surface concomitant with alteration in placodal adhesion. Lack of an apparent change in total N-cadherin mRNA or protein levels suggests post-translational regulation. Co-expression of N-cadherin with dominant-negative Robo abrogates the Robo2 loss-of-function phenotype of dispersed ganglia, whereas loss of N-cadherin reverses the aberrant aggregation induced by increased Slit-Robo expression. Our study suggests a novel mechanism whereby N-cadherin acts in concert with Slit-Robo signaling in mediating the placodal cell adhesion required for proper gangliogenesis.

Indexed as

AnimalsCadherinsCell AdhesionChick EmbryoGene Expression Regulation, DevelopmentalNerve Tissue ProteinsNeural CrestNeurogenesisReceptors, ImmunologicSensory Receptor CellsSignal TransductionTrigeminal GanglionCadherinsNerve Tissue ProteinsReceptors, Immunologic

Identifiers

PMID19934013
PMCPMC2781051
OpenAlexW1996698511

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.