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Initiation and maintenance of apical compartments via differential contractility regulated by the dynamic recruitment of Rasip1. A Diagrams showing the molecular steps of de novo lumen formation. In wild-type embryos, both Myosin and its inhibitor Rasip1 are recruited to the initial contact sites (initial contact). The initial contact sites expand into junctional patches (expansion). Rasip1 induces differential contractility at the junctional patches by inhibiting NMII at the center (segregation). Thus, Cdh5 effectively relocates toward the periphery, pulled by surrounding Myosin, generating the clear apical domain (ring formation). Once the apical compartments are established, Rasip1 shuttles between junctions and apical compartments in response to local high tension, tuning contractility at both compartments. Rasip1 confines Cdh5 to junctions by suppressing apical contractility, maintaining the clear segregation of apical compartments from junctions. Conversely, the recruitment of Rasip1 to junctions, controlled by Heg1 and Krit1, is critical for moderating contractility along junctions. B In rasip1 mutants, the pre-apical Myosin fails to be inhibited, leading to ectopic radial contractility toward the center and unsustainable Cdh5 relocation toward the periphery (failed segregation and defective ring formation). The ectopic radial contractility in rasip1 mutants de-stabilizes junctional proteins at boundaries and induces ectopic aggregations of junctional clusters at both apical compartments and boundary regions (improper maintenance).
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