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Signalling through mechanical inputs – a coordinated process
Huimin Zhang, Michel Labouesse


There is growing awareness that mechanical forces – in parallel to electrical or chemical inputs – have a central role in driving development and influencing the outcome of many diseases. However, we still have an incomplete understanding of how such forces function in coordination with each other and with other signalling inputs in vivo. Mechanical forces, which are generated throughout the organism, can produce signals through force-sensitive processes. Here, we first explore the mechanisms through which forces can be generated and the cellular responses to forces by discussing several examples from animal development. We then go on to examine the mechanotransduction-induced signalling processes that have been identified in vivo. Finally, we discuss what is known about the specificity of the responses to different forces, the mechanisms that might stabilize cells in response to such forces, and the crosstalk between mechanical forces and chemical signalling. Where known, we mention kinetic parameters that characterize forces and their responses. The multi-layered regulatory control of force generation, force response and force adaptation should be viewed as a well-integrated aspect in the greater biological signalling systems.


  • Funding

    Work in IGBMC is supported by grants from the Agence Nationale pour la Recherche, Association pour la Recherche sur le Cancer and institutional funds from CNRS, INSERM and Université de Strasbourg.

  • Note added in proof

    Several papers of direct relevance to the issues discussed in this Commentary have been published since the final acceptance of the manuscript, and we would like to briefly mention two.

    First, Roh-Johnson, Goldstein and colleagues (Roh-Johnson et al, 2012) suggest that before the junction and apical membrane can actually move a molecular clutch should engage pre-existing actomyosin contractions. Their work identifies the Rac GTPase, one of its upstream regulators and E-cadherin as potential actors or regulators of the clutch. It refines and potentially challenges the ideas illustrated in Fig. 2D. Second, Blosveld, Bella�che and collaborators (Bosveld et al., 2012) have examined the patterns of cell proliferation and tissue deformation in the fly dorsal thorax. They report that areas where the PCP protocaderin Dachsous mediates the polarised accumulation of the atypical myosin Dachs in turn anisotropically build up tension, which leads to changes in tissue shape. This study illustrates how PCP can lead to tissue deformation (see also Fig. 2F) and nicely illustrates the power of systematic image analysis coupled with physical modelling.

  • This article is part of a Minifocus on Mechanotransduction. For further reading, please see related articles: ‘Deconstructing the third dimension – how 3D culture microenvironments alter cellular cues’ by Brendon M. Baker and Christopher S. Chen (J. Cell Sci. 125, 3015-3024). ‘Finding the weakest link – exploring integrin-mediated mechanical molecular pathways’ by Pere Roca-Cusachs et al. (J. Cell Sci. 125, 3025-3038). ‘United we stand – integrating the actin cytoskeleton and cell–matrix adhesions in cellular mechanotransduction’ by Ulrich S. Schwarz and Margaret L. Gardel (J. Cell Sci. 125, 3051-3060). ‘Mechanosensitive mechanisms in transcriptional regulation’ by Akiko Mammoto et al. (J. Cell Sci. 125, 3061-3073). ‘Molecular force transduction by ion channels – diversity and unifying principles’ by Sergei Sukharev and Frederick Sachs (J. Cell Sci. 125, 3075-3083).

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