![]() ![]() Abnormal heart looping causes abnormal connections between the heart chambers and great vessels 1, 3.ĭirectional heart looping is regulated by the secreted TGF-β family protein Nodal, which is known to be an evolutionarily conserved left determinant in vertebrates. ![]() Subsequently, the heart tube undergoes rapid elongation and directional looping, during which it is remodeled into the characteristic configuration required for efficient blood circulation. The left and right primordia fuse at the midline to form the heart tube, which is initially short and almost bilaterally symmetric 1, 2. The vertebrate heart originates from the bilateral anterior fields of lateral plate mesoderm (LPM). Collectively, our results demonstrate that Nodal signaling regulates the magnitude of morphological changes by acting on basic cellular behaviors underlying heart tube formation, driving asymmetric deformation and rotation of the heart tube. ![]() Loss of Nodal signaling abolished the asymmetric cell behaviors as well as the asymmetric convergence of the left and right heart primordia. Interestingly, left cells were more active in these behaviors than right cells, driving more rapid convergence of the left primordium, and thereby rotating the heart tube. Here, using high-resolution live imaging of zebrafish embryos, we simultaneously visualized cellular dynamics underlying early heart morphogenesis and resulting changes in tissue shape, to identify two key cell behaviors: cell rearrangement and cell shape change, which convert initially flat heart primordia into a tube through convergent extension. How Nodal regulates cell behaviors to drive asymmetric morphogenesis remains poorly understood. Clockwise rotation of the primitive heart tube, a process regulated by restricted left-sided Nodal signaling, is the first morphological manifestation of left-right asymmetry. ![]()
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