Planar cell polarity (PCP) describes the coordinated polarization of cells or cell structures within the plane of a tissue and is an essential process of embryogenesis. For zebrafish gastrula cells engaged in directed cell migration, PCP is defined as the elongation and mediolateral alignment of each cell with respect to the dorsal embryonic axis. Loss of PCP protein function disrupts membrane protrusive activity, cell elongation and orientation resulting in misshapen embryos. Mutations in the Wnt co-receptor glypican4/knypek cause embryos to have a pronounced convergence and extension phenotype characterized by a shortened and broadened body axes. For many types of collective or group cell migration events, it has become clear that the movement of polarized cells requires regulation of cell-cell adhesion. Rapid remodeling of cadherin-mediated cell adhesion allows dynamic changes in cell coupling while maintaining coherent movement of cell populations. However, though cadherins are often required for collective cell migration, their molecular relationship with the PCP pathway is not well understood. Previous research by the Jessen laboratory showed that glypican4/knypek mutant embryos have increased cell surface expression of cadherin. Moreover, glypican4/knypek mutant embryos have increased cell-cell adhesion and increased fibronectin fibrillogenesis. We have now shown that loss of Glypican4 function affects the cell surface level of both E-cadherin (Cdh1) and N-cadherin (Cdh2). We hypothesize that Glypican4 function and Wnt/Frizzled PCP signaling regulate the endocytosis of Cdh1 and Cdh2. Indeed, we find that glypican4/knypek mutant embryos are sensitive to rab5c knockdown. Current efforts are aimed at further understanding the molecular mechanism connecting Glypican4 function and cell surface cadherin levels and determining the role of cadherin-mediated cell adhesion in establishing planar cell polarity.