从应力纤维到粘着斑：肌动蛋白交联剂在力传递中的作用。
From stress fiber to focal adhesion: a role of actin crosslinkers in force transmission.
发表日期：2024
作者：
Hiroki Katsuta, Masahiro Sokabe, Hiroaki Hirata
来源：
Frontiers in Cell and Developmental Biology
摘要：
收缩装置、应力纤维 (SF) 在 SF 末端与细胞粘附机制、粘着斑 (FA) 连接。 SF-FA 复合物对于细胞的各种机械活动至关重要，包括细胞粘附到细胞外基质 (ECM)、ECM 刚性感应和细胞迁移。这篇小评论强调了 SF 力学在这些细胞活动中的重要性。肌动蛋白交联蛋白通过减弱 SF 内肌球蛋白驱动的肌动蛋白和肌球蛋白丝的流动来固化 SF。在固化的 SF 中，SF 中肌动蛋白丝之间以及丝与周围细胞质之间的粘性滑移减少，导致肌球蛋白产生的收缩力沿着 SF 有效传递。因此，通过肌动蛋白交联的 SF 固化确保对 FA 施加很大的力，从而实现 FA 成熟、ECM 刚性传感和细胞迁移。我们进一步讨论了调节交联剂调节 SF 力学的细胞内机制，以及 SF 力学异常与包括癌症在内的病理学之间的潜在关系。版权所有 © 2024 Katsuta、Sokabe 和 Hirata。
The contractile apparatus, stress fiber (SF), is connected to the cell adhesion machinery, focal adhesion (FA), at the termini of SF. The SF-FA complex is essential for various mechanical activities of cells, including cell adhesion to the extracellular matrix (ECM), ECM rigidity sensing, and cell migration. This mini-review highlights the importance of SF mechanics in these cellular activities. Actin-crosslinking proteins solidify SFs by attenuating myosin-driven flows of actin and myosin filaments within the SF. In the solidified SFs, viscous slippage between actin filaments in SFs and between the filaments and the surrounding cytosol is reduced, leading to efficient transmission of myosin-generated contractile force along the SFs. Hence, SF solidification via actin crosslinking ensures exertion of a large force to FAs, enabling FA maturation, ECM rigidity sensing and cell migration. We further discuss intracellular mechanisms for tuning crosslinker-modulated SF mechanics and the potential relationship between the aberrance of SF mechanics and pathology including cancer.Copyright © 2024 Katsuta, Sokabe and Hirata.