Tubular organs support the uptake and exchange of nutrition, metabolites, and gases that are essential for the normal physiology of animals.The notochord of ascidian Ciona forms a tube consisting of only 40 cells, and serves as a hydrostatic "skeleton" essential for swimming.Using molecular markers and confocal imaging, for the first time, we reveal the cellular processes of notochord tubulogenesis in marine ascidians, Ciona and utilize it as a model to an assortment of common and fundamental cellular processes including cell shape change, apical membrane biogenesis, cell/cell adhesion remodeling, dynamic cell crawling, and lumen matrix secretion.We focus our interests on the dynamics and roles of cytoskeleton in notochord tubulogenesis and find a previously undescribed dynamic actin-and non-muscle myosin II-containing constriction midway along the anterior/posterior aspect of each notochord cell during notochord elongation.We further demonstrate that the actomyosin ring is assembled by bi-directional actin flow, during which actin binding proteins a-actinin, tropomyosin and cofilin are required for this process.Intriguingly,the position of contractile ring is regulated by the interaction of contractility and PCP signaling.Using drug and genetic manipulations, we uncover a tug-of-war between contractility and PCP.We develop a simple model of the physical forces underlying this tug-of-war, which reproduces quantitatively our results.Furthermore, the model predicts a scaling between ring width and cell size, which we could verify experimentally.Our results suggests a quantitative framework for how contractility and PCP can self-assemble and modulate the localization of cytoskeletal structures in non-dividing cells, which should be applicable to other morphogenetic events.