Distinct Apical and Basolateral Mechanisms Drive Planar Cell Polarity-Dependent Convergent Extension of the Mouse Neural Plate

• Mouse neural plate undergoes convergent extension by mediolateral cell intercalation
• Distinct apical and basolateral mechanisms drive neuroepithelial cell intercalation
• Planar polarity of neural cell motility and intercalation requires Ptk7 function
• Apical boundary rearrangement is inhibited in Vangl2 mutant neural epithelium

SummaryThe mechanisms of tissue convergence and extension (CE) driving axial elongation in mammalian embryos, and in particular, the cellular behaviors underlying CE in the epithelial neural tissue, have not been identified. Here we show that mouse neural cells undergo mediolaterally biased cell intercalation and exhibit both apical boundary rearrangement and polarized basolateral protrusive activity. Planar polarization and coordination of these two cell behaviors are essential for neural CE, as shown by failure of mediolateral intercalation in embryos mutant for two proteins associated with planar cell polarity signaling: Vangl2 and Ptk7. Embryos with mutations in Ptk7 fail to polarize cell behaviors within the plane of the tissue, whereas Vangl2 mutant embryos maintain tissue polarity and basal protrusive activity but are deficient in apical neighbor exchange. Neuroepithelial cells in both mutants fail to apically constrict, leading to craniorachischisis. These results reveal a cooperative mechanism for cell rearrangement during epithelial morphogenesis.