Cellular Polarity in the Ascidian Notochord
The 40 cells of the Ciona notochord develop according to a fixed and well-characterized cell lineage, making it ideally suited to studying polarity. Much of our work has centered on mechanisms operating during medio-lateral intercalation (MLI) of the notochord cells that takes place in the gastrula and neurula embryos. Here, notochord cells are polarized in a medio-lateral (M/L) plane--cell shape, lamellipodial cell protrusions and nuclear localization all show a M/L polarity. Later, during elongation taking place in the tailbud embryo, the nuclei in the notochord initially stretch across the cell, then snap to the posterior of the cell. The nuclei of notochord cells are invariably in the posterior of the cell, except for the most posterior notochord cell, where the nuclei is in the anterior. Therefore, in one tissue of Ciona, we observe polarity in different axes (medio-lateral and A/P).
The PCP pathway is active during both MLI and the subsequent A/P expansion of the notochord cells. We have identified a mutant, aimless (aim), which has a deletion creating a frame-shift and premature stop in the gene prickle (pk) (Jiang et al., 2005). pk is a key component of the planar cell polarity (PCP) pathway. Notochord cells of aim mutant animals do not move in a polarity dependent way during MLI as normal notochord cells do. In tailbud aim embryos, the nuclei do not show the posterior placement seen in wild-type embryos; the cells are not polarized normally. We have also found that pk and other PCP pathway proteins are localized to one side of the cell during MLI and/or notochord expansion in the tailbud stage embryo. We are using genetic, microscopic and molecular techniques to investigate the mechanisms responsible for setting up the polarity during MLI and how and when the shift to the A/P axis occurs. Both possible global controls (such as wnt, a possible ligand in the PCP pathway) and local controls (such as cell-to-cell communication) are being investigated.