Evidence map›Paper›PMID 25607881›Full record

ArticlePLoS genetics2015

Fascin1-dependent Filopodia are required for directional migration of a subset of neural crest cells.

Elena F Boer, Elizabeth D Howell, Thomas F Schilling, Cicely A Jette, Rodney A Stewart

Abstract read
In one paragraph

Article in PLoS genetics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
–field-weighted citation impact
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

25 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Review
  13. Article
  14. Neural crest development: insights from the zebrafish.Developmental dynamics : an official publication of the American Association of Anatomists · 2020
    Review
  15. PeerJ · 2019
    Article
  16. Endodermal pouch-expressedBiology open · 2018
    Article
  17. Article
  18. Article
  19. Article
  20. Signaling filopodia in vertebrate embryonic development.Cellular and molecular life sciences : CMLS · 2016
    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

5 authors.

Elena F BoerDepartment of Oncological Sciences, Huntsman Cancer Institute, University of Utah, Salt Lake City, Utah, United States of America.
Elizabeth D HowellDepartment of Oncological Sciences, Huntsman Cancer Institute, University of Utah, Salt Lake City, Utah, United States of America.
Thomas F SchillingDepartment of Developmental and Cell Biology, University of California, Irvine, Irvine, California, United States of America.
Cicely A JetteDepartment of Oncological Sciences, Huntsman Cancer Institute, University of Utah, Salt Lake City, Utah, United States of America.
Rodney A StewartDepartment of Oncological Sciences, Huntsman Cancer Institute, University of Utah, Salt Lake City, Utah, United States of America.

Funding

THE ROLE OF ATROPHIN-2 IN CARTILAGE PATTERNING AND POLARITY IN ZEBRAFISHR01DE013828 · NIDCR · UNIVERSITY OF CALIFORNIA-IRVINE · PI SCHILLING, THOMAS F · 2001 to 2025
$9.1M
DEVELOPMENTAL BIOLOGY TRAINING PROGRAMT32HD007491 · NICHD · UTAH STATE HIGHER EDUCATION SYSTEM--UNIVERSITY OF UTAH · PI James Alan Gagnon, Kristen M Kwan · 1995 to 2026
$8.0M
HSRD VA CDA 13-025NICHD NIH HHS 5T32 HD07491NICHD NIH HHS T32 HD007491NIDCR NIH HHS R01 DE013828NIDCR NIH HHS R01 DE13828
6 · The paper itself

Abstract

Directional migration of neural crest (NC) cells is essential for patterning the vertebrate embryo, including the craniofacial skeleton. Extensive filopodial protrusions in NC cells are thought to sense chemo-attractive/repulsive signals that provide directionality. To test this hypothesis, we generated null mutations in zebrafish fascin1a (fscn1a), which encodes an actin-bundling protein required for filopodia formation. Homozygous fscn1a zygotic null mutants have normal NC filopodia due to unexpected stability of maternal Fscn1a protein throughout NC development and into juvenile stages. In contrast, maternal/zygotic fscn1a null mutant embryos (fscn1a MZ) have severe loss of NC filopodia. However, only a subset of NC streams display migration defects, associated with selective loss of craniofacial elements and peripheral neurons. We also show that fscn1a-dependent NC migration functions through cxcr4a/cxcl12b chemokine signaling to ensure the fidelity of directional cell migration. These data show that fscn1a-dependent filopodia are required in a subset of NC cells to promote cell migration and NC derivative formation, and that perdurance of long-lived maternal proteins can mask essential zygotic gene functions during NC development.

Indexed as

AnimalsBody PatterningCell MovementEpithelial-Mesenchymal TransitionGene Expression Regulation, DevelopmentalMicrofilament ProteinsMutationNeural CrestPseudopodiaSignal TransductionZebrafishZebrafish Proteinsfscn1a protein, zebrafishMicrofilament ProteinsZebrafish Proteins

Identifiers

PMID25607881
PMCPMC4301650

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.