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Fig. 7 Schematic Illustration of how BEC-ECM Interactions Influence Periderm Architecture and Wound Repair. We propose that the interaction between basal epidermal stem cells (BECs) and laminin influences the junctional organization and injury response of the periderm, via the regulation of interlayer junction dynamics. The developing bilayered skin appendage is organized as collagen-enriched areas, where BECs exhibit increased adherens junction (AJ) actomyosin signaling and desmosome formation. Superficial epidermal cells (SECs) layer (the periderm) above these BECs display reduced motility, characterized by stronger desmosomal junctions and less actomyosin signaling. In laminin-rich areas, BECs show decreased actomyosin activity and reduced AJ and desmosome formation within the intralayer, but they unexpectedly maintain interlayer AJ and repress desmosome formation. SECs above these BECs have faster motility during wound closure. Partial removal of laminin matrices further reduces BEC actomyosin activity, AJ and desmosome formation while increasing desmosome connections at the interfaced membrane with SECs. SECs, connected to these BECs, exhibit increased desmosome overall, and slow wound closure.