Institute of Biomaterials and Biomedical Engineering, University of Toronto, Toronto, ON M5S 3G9, Canada.
Ted Rogers Centre for Heart Research, University of Toronto, Toronto, ON M5G 1M1, Canada.
Mol Biol Cell. 2019 Nov 1;30(23):2901-2912. doi: 10.1091/mbc.E18-11-0703. Epub 2019 Sep 25.
Collective cell movements play a central role in embryonic development, tissue repair, and metastatic disease. Cell movements are often coordinated by supracellular networks formed by the cytoskeletal protein actin and the molecular motor nonmuscle myosin II. During wound closure in the embryonic epidermis, the cells around the wound migrate collectively into the damaged region. In embryos, mechanical tension stabilizes myosin at the wound edge, facilitating the assembly of a supracellular myosin cable around the wound that coordinates cell migration. Here, we show that actin is also stabilized at the wound edge. However, loss of tension or myosin activity does not affect the dynamics of actin at the wound margin. Conversely, pharmacological stabilization of actin does not affect myosin levels or dynamics around the wound. Together, our data suggest that actin and myosin are independently regulated during embryonic wound closure, thus conferring robustness to the embryonic wound healing response.
细胞集体运动在胚胎发育、组织修复和转移性疾病中起着核心作用。细胞运动通常通过细胞骨架蛋白肌动蛋白和非肌肉肌球蛋白 II 形成的细胞超网络来协调。在胚胎表皮的伤口闭合过程中，伤口周围的细胞集体迁移到受损区域。在胚胎中，机械张力稳定了伤口边缘的肌球蛋白，有助于在伤口周围组装一个协调细胞迁移的细胞超网络肌球蛋白缆绳。在这里，我们表明肌动蛋白也在伤口边缘稳定。然而，张力或肌球蛋白活性的丧失并不影响伤口边缘处肌动蛋白的动力学。相反，肌动蛋白的药理学稳定并不影响伤口周围的肌球蛋白水平或动力学。总之，我们的数据表明，在胚胎伤口闭合过程中，肌动蛋白和肌球蛋白是独立调控的，从而使胚胎伤口愈合反应具有稳健性。
