Evidence map›Paper›PMID 30695698›Full record

ArticleDevelopmental cell2019

Polarization of Myosin II Refines Tissue Material Properties to Buffer Mechanical Stress.

Maria Duda, Natalie J Kirkland, Nargess Khalilgharibi, Melda Tozluoglu, Alice C Yuen, Nicolas Carpi, Anna Bove, Matthieu Piel, Guillaume Charras, Buzz Baum and 1 more

Abstract read
In one paragraph

Article in Developmental cell, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.

0numbers the graph read from it
0cells of the map it votes in
52citing 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

52 citing papers in PubMed.

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  14. The Geometric Basis of Epithelial Convergent Extension.bioRxiv : the preprint server for biology · 2024
    Article
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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

11 authors.

Maria DudaMRC Laboratory for Molecular Cell Biology, University College London, London WC1E 6BT, UK.
Natalie J KirklandMRC Laboratory for Molecular Cell Biology, University College London, London WC1E 6BT, UK.
Nargess KhalilgharibiMRC Laboratory for Molecular Cell Biology, University College London, London WC1E 6BT, UK; London Centre for Nanotechnology, University College London, London WC1E 6BT, UK; Centre for Computation, Mathematics and Physics in the Life Sciences and Experimental Biology (CoMPLEX), University College London, London WC1E 6BT, UK.
Melda TozluogluMRC Laboratory for Molecular Cell Biology, University College London, London WC1E 6BT, UK.
Alice C YuenMRC Laboratory for Molecular Cell Biology, University College London, London WC1E 6BT, UK.
Nicolas CarpiInstitut Curie, PSL Research University, CNRS, UMR 144, Paris 75005, France.
Anna BoveLondon Centre for Nanotechnology, University College London, London WC1E 6BT, UK; Cell and Developmental Biology, University College London, Gower Street, London WC1E 6BT, UK.
Matthieu PielInstitut Curie, PSL Research University, CNRS, UMR 144, Paris 75005, France.
Guillaume CharrasLondon Centre for Nanotechnology, University College London, London WC1E 6BT, UK; Institute for the Physics of Living Systems, University College London, London WC1E 6BT, UK; Cell and Developmental Biology, University College London, Gower Street, London WC1E 6BT, UK.
Buzz BaumMRC Laboratory for Molecular Cell Biology, University College London, London WC1E 6BT, UK; Institute for the Physics of Living Systems, University College London, London WC1E 6BT, UK.
Yanlan MaoMRC Laboratory for Molecular Cell Biology, University College London, London WC1E 6BT, UK; Institute for the Physics of Living Systems, University College London, London WC1E 6BT, UK; College of Information and Control, Nanjing University of Information Science and Technology, Nanjing, Jiangsu 210044, China. Electronic address: y.mao@ucl.ac.uk.

Funding

Biotechnology and Biological Sciences Research Council BB/J008532/1Biotechnology and Biological Sciences Research Council BB/K009001/1Cancer Research UK 17343Cancer Research UK 23335Medical Research Council MC_U12266BMedical Research Council MR/L009056/1
6 · The paper itself

Abstract

As tissues develop, they are subjected to a variety of mechanical forces. Some of these forces are instrumental in the development of tissues, while others can result in tissue damage. Despite our extensive understanding of force-guided morphogenesis, we have only a limited understanding of how tissues prevent further morphogenesis once the shape is determined after development. Here, through the development of a tissue-stretching device, we uncover a mechanosensitive pathway that regulates tissue responses to mechanical stress through the polarization of actomyosin across the tissue. We show that stretch induces the formation of linear multicellular actomyosin cables, which depend on Diaphanous for their nucleation. These stiffen the epithelium, limiting further changes in shape, and prevent fractures from propagating across the tissue. Overall, this mechanism of force-induced changes in tissue mechanical properties provides a general model of force buffering that serves to preserve the shape of tissues under conditions of mechanical stress.

Indexed as

Stress, MechanicalActomyosinAnimalsCell ShapeCytoskeletal ProteinsEpitheliumMorphogenesisMyosin Type IIActomyosinCytoskeletal ProteinsMyosin Type IIDiaphanouselasticityforce bufferingMyoII polarityshape maintenancestiffnesstissue mechanics

Identifiers

PMID30695698
PMCPMC6353629

What OpenQuestion holds

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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.