Evidence map›Paper›PMID 22069186›Full record

ArticleDevelopment (Cambridge, England)2011

Roles of Hedgehog pathway components and retinoic acid signalling in specifying zebrafish ventral spinal cord neurons.

Samantha England, Manuel F Batista, John K Mich, James K Chen, Katharine E Lewis

Open access · bronzeAbstract read
In one paragraph

Article in Development (Cambridge, England), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

26 citing papers in PubMed, 44 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Retinoic acid, RARs and early development.Journal of molecular endocrinology · 2022
    Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Retinoic acid signaling pathways.Development (Cambridge, England) · 2019
    Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. 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

5 authors at 3 institutions in 2 countries.

Samantha EnglandBiology Department, Syracuse University, 107 College Place, Syracuse, NY 13244, USA.
Manuel F Batista
John K Mich
James K Chen
Katharine E Lewis
Stanford University · USUniversity of Cambridge · GBSyracuse University · US

Funding

Medical Research Council G0801283Wellcome Trust 079971
6 · The paper itself

Abstract

In mouse, Hedgehog (Hh) signalling is required for most ventral spinal neurons to form. Here, we analyse the spinal cord phenotype of zebrafish maternal-zygotic smoothened (MZsmo) mutants that completely lack Hh signalling. We find that most V3 domain cells and motoneurons are lost, whereas medial floorplate still develops normally and V2, V1 and V0v cells form in normal numbers. This phenotype resembles that of mice that lack both Hh signalling and Gli repressor activity. Ventral spinal cord progenitor domain transcription factors are not expressed at 24 hpf in zebrafish MZsmo mutants. However, pMN, p2 and p1 domain markers are expressed at early somitogenesis stages in these mutants. This suggests that Gli repressor activity does not extend into zebrafish ventral spinal cord at these stages, even in the absence of Hh signalling. Consistent with this, ectopic expression of Gli3R represses ventral progenitor domain expression at these early stages and knocking down Gli repressor activity rescues later expression. We investigated whether retinoic acid (RA) signalling specifies ventral spinal neurons in the absence of Hh signalling. The results suggest that RA is required for the correct number of many different spinal neurons to form. This is probably mediated, in part, by an effect on cell proliferation. However, V0v, V1 and V2 cells are still present, even in the absence of both Hh and RA signalling. We demonstrate that Gli1 has a Hh-independent role in specifying most of the remaining motoneurons and V3 domain cells in embryos that lack Hh signalling, but removal of Gli1 activity does not affect more dorsal neurons.

Indexed as

AnimalsCell DifferentiationHedgehog ProteinsImmunohistochemistryIn Situ HybridizationMorpholinosNeuronsOncogene Proteinsp-AminoazobenzeneReceptors, G-Protein-CoupledSignal TransductionSmoothened ReceptorSpinal CordTrans-ActivatorsTretinoinVeratrum AlkaloidsC.I. Solvent Yellow 56cyclopamineHedgehog ProteinsMorpholinosOncogene Proteinsp-AminoazobenzeneReceptors, G-Protein-CoupledSmoothened Receptorsmo protein, zebrafishTrans-ActivatorsTretinoinVeratrum AlkaloidsZebrafish ProteinsZinc Finger Protein GLI1

Identifiers

PMID22069186
PMCPMC3210494
OpenAlexW2072915616

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.