Polarity cascade initiated by aPKC in the periderm is transduced by adherens junction component E-cadherin to the basal epidermis during the development of zebrafish bilayered epidermis.
A combined experimental and computational approach was developed to understand lateral interactions between membrane-bound proteins and used to quantify the contributions of specific and non-specific interactions to cadherin cis-binding kinetics.
Two critical events initiate and promote efficient desmosome assembly: stable binding of opposing E-cadherin cell-cell adhesion proteins; and direct interaction of E-cadherin and Desmoglein.
Pathological vessel leakage in mouse retinopathy models depends on VE-cadherin Y685 phosphorylation status, which in turn is regulated by a signaling cascade originating with VEGFR2 Y949 phosphorylation.
FGFRs regulate multipolar cortical neuron orientation and the morphological change into bipolar cells in vivo under the control of N-Cadherin and the extracellular matrix protein Reelin.
N-cadherin at heterotypic contacts controls the level and asymmetric localisation of Myosin-II motor, thereby influencing cell shapes and cell packing.
Endothelial YAP/TAZ shape the developing vasculature by orchestrating mechanical inputs with BMP signalling to promote junctional VE-Cadherin turnover and cellular rearrangements.
The primary molecular mechanosensor involved in a physiological process of mechanically induced cell fate differentiation is revealed here for the first time in vivo, highly sensitive and potentially shared by all metazoan epithelia.
