Side view model of mechanoresponsive collective migration of MCF10A cells. To achieve coordination in cell movements, cells at the wound edge respond to directional cue by front-rear polarization (P) in the direction of wound healing. The establishment and maintenance of cell polarity require actomyosin contractility (M), and they are influenced by cell–cell adhesions (C). Actomyosin contractility is governed by focal adhesions (FA) and cell–cell adhesion signaling. At the same time, actomyosin contractility promotes the formation and maturation of both focal adhesions and cell–cell adhesions (double-headed arrows). Actomyosin contractility can also be a negative regulator of cell–cell adhesions (flat-end arrow). The feedback coupling between actomyosin contractility and focal adhesions is stronger on stiff substrates and at the wound edge compared with >500 µm into the sheet, whereas within the sheet, the coupling between actomyosin contractility and cell–cell adhesions is stronger than between actomyosin contractility and focal adhesions. Forces generated by actomyosin contractility are transmitted to neighboring cells across cell–cell adhesions (blue dots connected by a line), where they activate actomyosin contractility and promote front-rear polarization in the follower cells. Propagation of front-rear polarization beyond the wound edge into the monolayer leads to cell–cell coordination. Various perturbations studied in this work affect focal adhesions, actomyosin contractility, and cell–cell adhesions, which in turn affect force transmission and front-rear polarization, leading to different levels of motion coordination. The sizes of the letters reflect relative magnitudes, and letters with asterisks indicate a parameter that is inferred and not directly measured in this study. All arrows are inferred, and the widths of the arrows reflect the relative strengths of interactions compared across the scenarios.