The ascidian notochord follows a morphogenetic program that includes convergent extension (C/E), followed by anterior-posterior (A/P) elongation [1-4]. As described here, developing notochord cells show polarity first in the mediolateral (M/L) axis during C/E, and subsequently in the A/P axis during elongation. Previous embryological studies [3] have shown that contact with neighboring tissues is essential for directing M/L polarity of ascidian notochord cells. During C/E, the planar cell polarity (PCP) gene products prickle (pk) and dishevelled (dsh) show M/L polarization. pk and dsh colocalize at the notochord cell membranes, with the exception of those in contact with neighboring muscle cells. In the mutant aimless (aim), which carries a deletion in pk, notochord morphogenesis is disrupted, and cell polarization is lost. After C/E, there is a dynamic relocalization of PCP proteins in the notochord cells with dsh localized to the lateral edges of the membrane, and pk and strabismus (stbm) at the anterior edges. An A/P polarity is present in the extending notochord cells and is evident by the position of the nuclei, which in normal embryos are invariably found at the posterior edge of each cell. In the aim mutant, all appearances of A/P polarity in the notochord are lost.