Evidence map›Paper›PMID 24306105›Full record

ArticleDevelopment (Cambridge, England)2014

Ion channels contribute to the regulation of cell sheet forces during Drosophila dorsal closure.

Ginger L Hunter, Janice M Crawford, Julian Z Genkins, Daniel P Kiehart

Abstract read
In one paragraph

Article in Development (Cambridge, England), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
2.6field-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

33 citing papers in PubMed, 61 citations in OpenAlex.

  1. Review
  2. TRPA1 for Butterfly Eyespot Formation.International journal of molecular sciences · 2026
    Article
  3. A steady-state pool of calcium-dependent actin is maintained by Homer and controls epithelial mechanosensation.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Optochemical Control of Cell Contractility in Drosophila Embryos.Methods in molecular biology (Clifton, N.J.) · 2022
    Article
  9. Review
  10. Article
  11. Measuring mechanical stress in living tissues.Nature reviews. Physics · 2020
    Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Mathematical models of dorsal closure.Progress in biophysics and molecular biology · 2018
    Review
  18. Article
  19. Article
  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 1 institution in 1 country.

Ginger L HunterDepartment of Biology, Duke University, Durham, NC 27708, USA.
Janice M Crawford
Julian Z Genkins
Daniel P Kiehart
Duke University · US

Funding

Training Program in Developmental & Stem Cell BiologyT32HD040372 · NICHD · DUKE UNIVERSITY · PI Terry H Lechler · 2001 to 2026
$8.9M
Morphogenesis: Biophysics and Genetics of Dorsal ClosureR01GM033830 · NIGMS · HARVARD UNIVERSITY · PI KIEHART, DANIEL PETER · 1985 to 2017
$7.2M
NICHD NIH HHS T32 HD040372NICHD NIH HHS T32 HD 040372-09NIGMS NIH HHS R01 GM033830NIGMS NIH HHS R01 GM33860
6 · The paper itself

Abstract

We demonstrate that ion channels contribute to the regulation of dorsal closure in Drosophila, a model system for cell sheet morphogenesis. We find that Ca(2+) is sufficient to cause cell contraction in dorsal closure tissues, as UV-mediated release of caged Ca(2+) leads to cell contraction. Furthermore, endogenous Ca(2+) fluxes correlate with cell contraction in the amnioserosa during closure, whereas the chelation of Ca(2+) slows closure. Microinjection of high concentrations of the peptide GsMTx4, which is a specific modulator of mechanically gated ion channel function, causes increases in cytoplasmic free Ca(2+) and actomyosin contractility and, in the long term, blocks closure in a dose-dependent manner. We identify two channel subunits, ripped pocket and dtrpA1 (TrpA1), that play a role in closure and other morphogenetic events. Blocking channels leads to defects in force generation via failure of actomyosin structures, and impairs the ability of tissues to regulate forces in response to laser microsurgery. Our results point to a key role for ion channels in closure, and suggest a mechanism for the coordination of force-producing cell behaviors across the embryo.

Indexed as

ActomyosinAnimalsAnimals, Genetically ModifiedBiomechanical PhenomenaCalciumChelating AgentsDrosophila melanogasterDrosophila ProteinsIntercellular Signaling Peptides and ProteinsIon ChannelsMorphogenesisMutationPeptidesSodium ChannelsSpider VenomsTRPA1 Cation ChannelActomyosinCalciumChelating AgentsDrosophila ProteinsIntercellular Signaling Peptides and ProteinsIon ChannelsMTx4 protein, Grammostola spatulataPeptidesrpk protein, DrosophilaSodium ChannelsSpider VenomsTRPA1 Cation ChannelTrpA1 protein, DrosophilaTRPC Cation ChannelsDorsal closureIon channelsMorphogenesis

Identifiers

PMID24306105
PMCPMC3879814
OpenAlexW2167737829

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.