Evidence map›Paper›PMID 26040287›Full record

ArticleJournal of cell science2015

Rho-kinase-dependent actin turnover and actomyosin disassembly are necessary for mouse spinal neural tube closure.

Sarah Escuin, Bertrand Vernay, Dawn Savery, Christine B Gurniak, Walter Witke, Nicholas D E Greene, Andrew J Copp

Open access · hybridAbstract read
In one paragraph

Article in Journal of cell science, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed
4.1field-weighted citation impact, top 6% 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

55 citing papers in PubMed, 84 citations in OpenAlex.

  1. Article
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  9. Article
  10. Induction andbioRxiv : the preprint server for biology · 2024
    Article
  11. Article
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  13. Article
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  16. Article
  17. Review
  18. Serum exosomal coronin 1A and dynamin 2 as neural tube defect biomarkers.Journal of molecular medicine (Berlin, Germany) · 2022
    Article
  19. Review
  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

7 authors at 2 institutions in 2 countries.

Sarah EscuinNewlife Birth Defects Research Centre, Institute of Child Health, University College London, WC1N 1EH, UK.
Bertrand VernayNewlife Birth Defects Research Centre, Institute of Child Health, University College London, WC1N 1EH, UK.
Dawn SaveryNewlife Birth Defects Research Centre, Institute of Child Health, University College London, WC1N 1EH, UK.
Christine B GurniakCell Migration Unit, Institut für Genetik, Universität Bonn, 53115 Bonn, Germany.
Walter WitkeCell Migration Unit, Institut für Genetik, Universität Bonn, 53115 Bonn, Germany.
Nicholas D E GreeneNewlife Birth Defects Research Centre, Institute of Child Health, University College London, WC1N 1EH, UK.
Andrew J CoppNewlife Birth Defects Research Centre, Institute of Child Health, University College London, WC1N 1EH, UK a.copp@ucl.ac.uk.
University College London · GBUniversity of Bonn · DE

Funding

Medical Research Council G0801124Wellcome Trust 087525
6 · The paper itself

Abstract

The cytoskeleton is widely considered essential for neurulation, yet the mouse spinal neural tube can close despite genetic and non-genetic disruption of the cytoskeleton. To investigate this apparent contradiction, we applied cytoskeletal inhibitors to mouse embryos in culture. Preventing actomyosin cross-linking, F-actin assembly or myosin II contractile activity did not disrupt spinal closure. In contrast, inhibiting Rho kinase (ROCK, for which there are two isoforms ROCK1 and ROCK2) or blocking F-actin disassembly prevented closure, with apical F-actin accumulation and adherens junction disturbance in the neuroepithelium. Cofilin-1-null embryos yielded a similar phenotype, supporting the hypothesis that there is a key role for actin turnover. Co-exposure to Blebbistatin rescued the neurulation defects caused by RhoA inhibition, whereas an inhibitor of myosin light chain kinase, ML-7, had no such effect. We conclude that regulation of RhoA, Rho kinase, LIM kinase and cofilin signalling is necessary for spinal neural tube closure through precise control of neuroepithelial actin turnover and actomyosin disassembly. In contrast, actomyosin assembly and myosin ATPase activity are not limiting for closure.

Indexed as

ActinsActomyosinAnimalsCofilin 1Lim KinasesMiceMice, Mutant StrainsNeural TuberhoA GTP-Binding Proteinrho-Associated Kinasesrho GTP-Binding ProteinsActinsActomyosinCfl1 protein, mouseCofilin 1Lim KinasesrhoA GTP-Binding ProteinRhoA protein, mouserho-Associated Kinasesrho GTP-Binding ProteinsRock1 protein, mouseRock2 protein, mouseCytoskeletonEmbryoMouseNeurulation

Identifiers

PMID26040287
PMCPMC4510849
OpenAlexW2138168533

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.