Strain-Tension Feedback Leads to Sustained Pulsing Activity in Epithelial Tissues

Tissue morphogenesis is the result of coordinated deformations of the underlying cells. In vivo, this occurs through the recruitment of myosin motors along cell junctions, which produce contractile forces. Previous work has found that to undergo the permanent deformations required for structure-altering transitions, repeated pulses of myosin activity are necessary. The mechanistic basis of this tissue-wide pulsing activity remains unknown. To capture this phenomenon, we have developed a vertex model of epithelial tissues with mechanochemical feedback, where junctional active tension is controlled by junction strain. In our model, a junction is activated when it is stretched beyond a threshold strain, and deactivated when it is contracted beyond a minimum strain or an activation lifetime is reached due to actomyosin turnover. These feedback rules reflect mechanosensitive rates of actomyosin assembly and disassembly. This mechanochemical model produces tissues which can remodel through self-sustaining tension pulses that cause junction length ratcheting. Without the need for externally controlled junction activation, our model is capable of generating spontaneous pulsing activities in tissues.