期刊
DEVELOPMENTAL CELL
卷 48, 期 2, 页码 245-+出版社
CELL PRESS
DOI: 10.1016/j.devcel.2018.12.020
关键词
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资金
- Marie Sklodowska-Curie Horizon 2020 Individual Fellowship (MRTGS)
- MRC
- Rosetrees Trust
- UCL Graduate School
- EPSRC
- UCL Overseas Research Scholarship
- Sir Henry Wellcome Fellowship [103095]
- CNRS
- Institut Curie
- European Research Council (MolCellTissMech) [647186]
- CRUK [17343]
- BBSRC [BB/K009001/1, BB/J008532/1]
- MRC [MR/L009056/1, MC_U12266B]
- UCL Excellence Fellowship
- NSFC International Young Scientist Fellowship [31650110472]
- BBSRC [BB/J008532/1, BB/K009001/1] Funding Source: UKRI
- MRC [MR/L009056/1] Funding Source: UKRI
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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