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肌球蛋白 II 的极化使组织材料特性精细化,以缓冲机械应力。

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

机构信息

MRC Laboratory for Molecular Cell Biology, University College London, London WC1E 6BT, UK.

MRC 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.

出版信息

Dev Cell. 2019 Jan 28;48(2):245-260.e7. doi: 10.1016/j.devcel.2018.12.020.

DOI:10.1016/j.devcel.2018.12.020
PMID:30695698
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6353629/
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.

摘要

随着组织的发育,它们会受到各种机械力的作用。其中一些力在组织发育中起重要作用,而另一些力则可能导致组织损伤。尽管我们对力引导的形态发生有了广泛的了解,但对于组织在发育后确定形状后如何防止进一步的形态发生,我们的了解还很有限。在这里,通过开发一种组织拉伸装置,我们揭示了一种机械敏感途径,该途径通过跨组织肌动球蛋白的极化来调节组织对机械应激的反应。我们表明,拉伸诱导了线性多细胞肌动球蛋白电缆的形成,该电缆的形成依赖于 Dia 来起始。这些电缆使上皮变硬,限制了形状的进一步变化,并防止骨折在组织中传播。总的来说,这种力诱导的组织力学性质变化的机制提供了一个力缓冲的一般模型,有助于在机械应力条件下保持组织的形状。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7303/6353629/421ff4f58620/gr7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7303/6353629/1bac065ef018/fx1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7303/6353629/1dc151e64b74/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7303/6353629/435f302ae757/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7303/6353629/2ae8e16183c9/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7303/6353629/3168514ae220/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7303/6353629/c37fc10e9791/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7303/6353629/257d8be6628a/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7303/6353629/421ff4f58620/gr7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7303/6353629/1bac065ef018/fx1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7303/6353629/1dc151e64b74/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7303/6353629/435f302ae757/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7303/6353629/2ae8e16183c9/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7303/6353629/3168514ae220/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7303/6353629/c37fc10e9791/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7303/6353629/257d8be6628a/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7303/6353629/421ff4f58620/gr7.jpg

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