Calcium and actomyosin pulses drive tricellular zipping to remodel epithelial cell-cell junctions and facilitate cell packing

Epithelial morphogenesis relies on coordinated adjustments in cell shape, neighboring cell organization, and cell packing to create functional tissue structures. However, the precise regulation of signals responsible for local junction remodeling in rapidly proliferating epithelial tissues remains unknown. The authors of this study describe a novel junction remodeling process called "tricellular zipping."

This process resolves lengthy, slender cell extensions initiated by cell-division forces that terminate at temporary high-order vertices.

Tricellular zipping aids in packing epithelial cells within blastula-stage Xenopus laevis embryos by asymmetrically displacing a tricellular vertex and establishing a new bicellular interface. Similar observations of tricellular zipping are made in developing mouse embryos. Using modeling and live imaging methods, the researchers discovered that the displacement of the remodeling vertex relies on actomyosin-driven asymmetric force generation and the concentration of adaptor proteins that link actomyosin to junctions, allowing effective force transmission.

In contrast, the stationary vertex stays near mechanical equilibrium and does not undergo net displacement.

Moreover, the study reveals that calcium flashes trigger the localized, pulsatile actomyosin contractility essential for efficient tricellular zipping. Extending these findings, the authors demonstrate that interrupting transient calcium signaling also impacts cell packing in Drosophila embryos, impairing mesoderm internalization.

By integrating interdisciplinary and multisystem strategies, the researchers uncover a new form of junctional remodeling and emphasize the significance of spatiotemporally controlled calcium signaling in facilitating local junction rearrangements to promote morphogenesis.