Evidence map›Paper›PMID 22685423›Full record

ArticlePLoS genetics2012

Attenuation of Notch and Hedgehog signaling is required for fate specification in the spinal cord.

Peng Huang, Fengzhu Xiong, Sean G Megason, Alexander F Schier

Open access · goldAbstract read
In one paragraph

Article in PLoS genetics, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

50 citing papers in PubMed, 91 citations in OpenAlex.

  1. Article
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  3. Sonic hedgehog signaling promotes basal epidermalbioRxiv : the preprint server for biology · 2025
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  11. Review
  12. iScience · 2023
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  13. Thyroid hormone regulates proximodistal patterning in fin rays.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Frontiers in cell and developmental biology · 2021
    Review
  19. Review
  20. Review
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

4 authors at 3 institutions in 1 country.

Peng HuangDepartment of Molecular and Cellular Biology, Center for Brain Science, Harvard Stem Cell Institute, Broad Institute, Center for Systems Biology, Harvard University, Cambridge, Massachusetts, USA. huang@mcb.harvard.edu
Fengzhu Xiong
Sean G Megason
Alexander F Schier
Harvard Stem Cell Institute · USCenter for Systems Biology · USHarvard University · US

Funding

GENETIC MECHANISMS OF AXIS FORMATION IN VERTEBRATESR01GM056211 · NIGMS · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI SCHIER, ALEXANDER F · 1997 to 2015
$5.1M
COMPARATIVE GENETICS OF GLI FUNCTIONR01DE016779 · NIDCR · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI SCHIER, ALEXANDER F · 2004 to 2008
$2.0M
NIDCR NIH HHS 5R01DE016779NIDCR NIH HHS R01 DE016779NIGMS NIH HHS R01 GM056211
6 · The paper itself

Abstract

During the development of the spinal cord, proliferative neural progenitors differentiate into postmitotic neurons with distinct fates. How cells switch from progenitor states to differentiated fates is poorly understood. To address this question, we studied the differentiation of progenitors in the zebrafish spinal cord, focusing on the differentiation of Kolmer-Agduhr″ (KA″) interneurons from lateral floor plate (LFP) progenitors. In vivo cell tracking demonstrates that KA″ cells are generated from LFP progenitors by both symmetric and asymmetric cell divisions. A photoconvertible reporter of signaling history (PHRESH) reveals distinct temporal profiles of Hh response: LFP progenitors continuously respond to Hh, while KA″ cells lose Hh response upon differentiation. Hh signaling is required in LFP progenitors for KA″ fate specification, but prolonged Hh signaling interferes with KA″ differentiation. Notch signaling acts permissively to maintain LFP progenitor cells: activation of Notch signaling prevents differentiation, whereas inhibition of Notch signaling results in differentiation of ectopic KA″ cells. These results indicate that neural progenitors depend on Notch signaling to maintain Hh responsiveness and rely on Hh signaling to induce fate identity, whereas proper differentiation depends on the attenuation of both Notch and Hh signaling.

Indexed as

ZebrafishAnimalsAnimals, Genetically ModifiedCell DifferentiationCell DivisionCell LineageEmbryonic DevelopmentGene Expression Regulation, DevelopmentalHedgehog ProteinsInterneuronsPatched ReceptorsReceptors, Cell SurfaceReceptors, NotchSignal TransductionSpinal CordStem CellsHedgehog ProteinsPatched ReceptorsReceptors, Cell SurfaceReceptors, Notch

Identifiers

PMID22685423
PMCPMC3369957
OpenAlexW1976206791

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.