Mesenchymal cells can perform diverse modes of contact-dependent collective cell migration.(A) Diverse modes by which cell–cell contact gives rise to specific swarm behaviors. Architectural transitions are depicted using the conceptual map from Fig. 1. (A1) Cells can align with respect to migration trajectories either passively, due to their shape, or actively through collision guidance, which involves contact-dependent downregulation of actomyosin contractility. (A2) In contact-stimulated migration, as observed in Drosophila testis myotubes, all cells remain protrusive but downregulate matrix adhesion at cell–cell interfaces. This allows individual cells to spread, while the entire sheet expands collectively—resulting in space-filling behavior without cell dissociation. (A3) In epithelial collective cell migration, cells exhibit apical–basal polarity, where cell–cell contact induces epithelial junctions and free edges become protrusive, enabling division of labor and coordinated space filling. (A4) In CIL, cells migrate individually but undergo transformation upon contact, resulting in either repolarization or cessation of migration. (A5) In contact-following migration, as seen in the Drosophila follicle cell epithelium (left), each cell must autonomously polarize, but this needs to be synchronized in the collective. Each cell becomes directionally protrusive, using PCP without a polarizing free edge. In contrast, in systems like Dictyostelium fruiting body development (right), contact following can be extrinsically polarized due to the presence of a defined front (the first cell in a strand). (A6) Cells may also use other cells as migratory substrates, as observed in the Drosophila border cell cluster. (A7) During mesenchymal intercalation, such as in frog mesoderm, cells use interface-guided protrusiveness not for migration but for tissue deformation. As in contact following, this requires internal polarization to differentially respond at different interfaces. (B) Comparison of CIL, contact following, and mesenchymal intercalation, deconstructing these modes into local effects on protrusion—either induction (+) or repression (−) (using the color code of the map in Fig. 1 A). (B1) In CIL, both cells respond symmetrically by retracting upon contact. The contact site itself induces a new polarity, overwriting the cell’s previous orientation. (B2) In contrast, during contact following, one cell at the interface induces protrusion, while the other retracts. This asymmetric response requires synchronization and preestablished polarity, enabling cells to react differently at specific interfaces—for example, via PCP signaling modules. (B3) In mesenchymal intercalation, protrusions are repressed at junctions along one axis and induced along the perpendicular axis. This necessitates two predefined polarity axes, often established through PCP signaling. PCP, planar cell polarity.
Figure 2.

Mesenchymal cells can perform diverse modes of contact-dependent collective cell migration. (A) Diverse modes by which cell–cell contact gives rise to specific swarm behaviors. Architectural transitions are depicted using the conceptual map from Fig. 1. (A1) Cells can align with respect to migration trajectories either passively, due to their shape, or actively through collision guidance, which involves contact-dependent downregulation of actomyosin contractility. (A2) In contact-stimulated migration, as observed in Drosophila testis myotubes, all cells remain protrusive but downregulate matrix adhesion at cell–cell interfaces. This allows individual cells to spread, while the entire sheet expands collectively—resulting in space-filling behavior without cell dissociation. (A3) In epithelial collective cell migration, cells exhibit apical–basal polarity, where cell–cell contact induces epithelial junctions and free edges become protrusive, enabling division of labor and coordinated space filling. (A4) In CIL, cells migrate individually but undergo transformation upon contact, resulting in either repolarization or cessation of migration. (A5) In contact-following migration, as seen in the Drosophila follicle cell epithelium (left), each cell must autonomously polarize, but this needs to be synchronized in the collective. Each cell becomes directionally protrusive, using PCP without a polarizing free edge. In contrast, in systems like Dictyostelium fruiting body development (right), contact following can be extrinsically polarized due to the presence of a defined front (the first cell in a strand). (A6) Cells may also use other cells as migratory substrates, as observed in the Drosophila border cell cluster. (A7) During mesenchymal intercalation, such as in frog mesoderm, cells use interface-guided protrusiveness not for migration but for tissue deformation. As in contact following, this requires internal polarization to differentially respond at different interfaces. (B) Comparison of CIL, contact following, and mesenchymal intercalation, deconstructing these modes into local effects on protrusion—either induction (+) or repression (−) (using the color code of the map in Fig. 1 A). (B1) In CIL, both cells respond symmetrically by retracting upon contact. The contact site itself induces a new polarity, overwriting the cell’s previous orientation. (B2) In contrast, during contact following, one cell at the interface induces protrusion, while the other retracts. This asymmetric response requires synchronization and preestablished polarity, enabling cells to react differently at specific interfaces—for example, via PCP signaling modules. (B3) In mesenchymal intercalation, protrusions are repressed at junctions along one axis and induced along the perpendicular axis. This necessitates two predefined polarity axes, often established through PCP signaling. PCP, planar cell polarity.

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