Differential Expression of a Classic Cadherin Directs Tissue-Level Contractile Asymmetry during Neural Tube Closure.

Embryos control force generation at tissue boundaries, but how they do so remains poorly understood. Here we show how tissue-specific expression of the type II cadherin, Cadherin2, patterns actomyosin contractility along tissue boundaries to control zippering and neural tube closure in the basal chordate, Ciona robusta. Cadherin2 is differentially expressed and homotypically enriched in neural cells along the neural/epidermal (Ne/Epi) boundary, where RhoA and myosin are activated during zipper progression. Homotypically enriched Cadherin2 sequesters the Rho GTPase-activating protein, Gap21/23, to homotypic junctions. Gap21/23 in turn redirects RhoA/myosin activity to heterotypic Ne/Epi junctions. By activating myosin II along Ne/Epi junctions ahead of the zipper and inhibiting myosin II along newly formed Ne/Ne junctions behind the zipper, Cadherin2 promotes tissue-level contractile asymmetry to drive zipper progression. We propose that dynamic coupling of junction exchange to local changes in contractility may control fusion and separation of epithelia in many other contexts.