LAUSR

The mechanisms controlling the dynamics of expansion of adherens junctions are significantly less understood than those controlling their static properties. Here, we report that for suspended cell aggregates, the time to form a new junction between two cells speeds up with the number of junctions that the cells are already engaged in. Upon junction formation, the activation of the Epidermal Growth Factor Receptor (EGFR) distally affects the actin turnover dynamics of the cell-free cortex. The "primed" actin cortex results in a faster expansion of the subsequent new junctions. In such aggregates, we show that this mechanism results in a cooperative acceleration of the junction expansion dynamics (kinetype) but leaves the cell contractility, and hence the final junction size (phenotype), unaltered.