Opposing Activity at the Apical Surface: An Antagonistic Collaboration Between Crumbs and Myosin II Determines Organ Shape.

Morphogenesis, the sculpting of tissues into functional architectures, requires precise orchestration of cell shape changes and rearrangements. In the Drosophila salivary gland (SG), recent studies reveal that Crumbs (Crb) and non-muscle Myosin II (MyoII) act as collaborative antagonists to drive SG internalization. Crb, a conserved type I transmembrane protein best known as a master regulator of apical-basal polarity, stabilizes attachments by forming homophilic extracellular bridges between neighboring cells and restricting the distribution of junctional MyoII. Conversely, MyoII is a highly conserved motor protein that drives apical constriction and junctional shrinkage by generating contractile forces on apicomedial and cortical actin and promoting apical membrane removal. During SG invagination, these opposing activities are exquisitely tuned, with Crb-mediated stabilization balancing MyoII-mediated destabilization to facilitate apical constriction for internalization and neighbor exchange for tube elongation. The conserved interplay between Crb and MyoII goes beyond the shaping of organs, serving as a critical mechanism for cell extrusion and EMT-like processes in animal development.