ABSTRACT
Crawling migration plays an essential role in a range of biological phenomena, including development, wound healing, and immune system function. The current consensus is that in the typical mechanism of crawling cell migration, actin polymerization pushes the cell front, and actomyosin contraction pulls the rear, although there is a high degree of variability in the details according to cell type. These forces are translated into traction forces on the substratum, and, simultaneously, appear to regulate the tension of the actin cytoskeleton. Cells can generate anterior-posterior polarity to drive migration by mechanical interaction between the cells and the substratum. In relation to this polarity generation, it has been shown that cofilin and myosin II change their affinity to actin filaments dependent on their tension. How cell migration is regulated by mechanical signals via cofilin and myosin II-related processes remains an interesting future area of study.
