Graduate School of Sciences and Technology for Innovation, Yamaguchi University, Yamaguchi 753-8511, Japan.
Institute of Food and Radiation Biology, AERE, Bangladesh Atomic Energy Commission, Savar, Dhaka 3787, Bangladesh.
Cells. 2022 Oct 9;11(19):3166. doi: 10.3390/cells11193166.
The repair of wounded cell membranes is essential for cell survival. Upon wounding, actin transiently accumulates at the wound site. The loss of actin accumulation leads to cell death. The mechanism by which actin accumulates at the wound site, the types of actin-related proteins participating in the actin remodeling, and their signaling pathways are unclear. We firstly examined how actin accumulates at a wound site in cells. Actin assembled de novo at the wound site, independent of cortical flow. Next, we searched for actin- and signal-related proteins targeting the wound site. Fourteen of the examined proteins transiently accumulated at different times. Thirdly, we performed functional analyses using gene knockout mutants or specific inhibitors. Rac, WASP, formin, the Arp2/3 complex, profilin, and coronin contribute to the actin dynamics. Finally, we found that multiple signaling pathways related to TORC2, the Elmo/Doc complex, PIP2-derived products, PLA2, and calmodulin are involved in the actin dynamics for wound repair.
细胞膜的修复对于细胞存活至关重要。在受伤时，肌动蛋白会在伤口部位短暂积累。肌动蛋白积累的丧失会导致细胞死亡。肌动蛋白在伤口部位积累的机制、参与肌动蛋白重塑的肌动蛋白相关蛋白的类型及其信号通路尚不清楚。我们首先研究了 细胞中肌动蛋白如何在伤口部位积累。肌动蛋白在伤口部位从头组装，不依赖于皮质流。接下来，我们搜索了针对伤口部位的肌动蛋白和信号相关蛋白。在不同时间，有 14 种被检查的蛋白会短暂积累。第三，我们使用基因敲除突变体或特定抑制剂进行功能分析。 Rac、WASP、formin、Arp2/3 复合物、丝氨酸/苏氨酸蛋白激酶和 coronin 有助于肌动蛋白动态变化。最后，我们发现与 TORC2、Elmo/Doc 复合物、PIP2 衍生产物、PLA2 和钙调蛋白相关的多个信号通路参与了伤口修复的肌动蛋白动态变化。
