Polarization of Myosin II refines tissue material properties to buffer mechanical stress

Polarization of Myosin II refines tissue material properties to buffer mechanical stress
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肌球蛋白 II 的极化可改善组织材料特性以缓冲机械应力

DOI:
10.1101/241497
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发表时间:
2017
期刊:
--
影响因子:
--
通讯作者:
Duda M
Duda M
中科院分区:
--
文献类型:
--
作者:
Duda M

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随着组织的发育,它们会受到各种机械力的作用。其中一些力量有助于组织的发育,而另一些力量则可能导致组织损伤。尽管我们对力引导的形态发生有广泛的了解,但我们对组织如何在发育后确定形状后如何阻止进一步的形态发生的了解有限。在这里,通过开发一种组织拉伸设备,我们发现了一条机械敏感的途径,通过肌动球蛋白在组织中的极化来调节组织对机械应力的反应。我们发现,拉伸可以诱导线形多细胞肌球蛋白缆线的形成,这种线形缆线依赖于透明的成核。这会使上皮变硬,限制形状的进一步变化,并防止骨折在整个组织中传播。总体而言,这种力诱导组织力学性质变化的机制提供了一个力缓冲的通用模型,该模型用于在机械应力条件下保持组织的形状。
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.
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发表时间: 2016
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