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The neural tube closes as the paralleled neural folds are brought to the dorsal midline to eventually form brain and spinal cord.This eminent morphogenetic event is achieved by the coordinated action of cellular morphogenesis as well as of tissue rearrangements.During neural tube closure, cells in the neuroepithelial sheet (neural plate) undergo a drastic cell shape change, called apical constriction, which triggers the neural plate to form tubular structure, generating a force to bend the plate inward of the embryo.Yet how the apical constriction is controlled in the neural plate and how it contributes to the tissue morphogenesis are not fully understood.In this study,we show that intracellular calcium ion (Ca2+) is required for the neural tube formation,and its concentration fluctuates throughout the Xenopus neural plate at the single-cell level.The Ca2+ fluctuation preceded a remodeling of F-actin and the apical constriction at the cellular level, and repeated accelerations of the closing movement of the neural plate, suggesting that the Ca2+ fluctuation at the cellular level dynamically regulates the apical constriction for the efficient tube formation.In silico analysis predicts that the Ca2+ fluctuation accelerates apical constriction and decreases tissue size independently of its frequency.However, although the dense rather than sparse fluctuation induces rapid tissue deformation, its overall effect throughout the entire course of the simulation is not effective when the total number of the pulses is constant.We also show the spatio-temporal patterns of the Ca2+ fluctuations are differentially regulated by Ca2+ channel, inositol triphosphate receptor, and extracellular ATP.This Ca2+-dependent mechanism of the apical constriction might act coordinately with the Rho/ROCK-dependent system to ensure the primitive CNS formation.