The eyes are the most important sensory organs for most vertebrates. Their structure and development is conserved between several vertebrate species. The development is regulated by several signalling pathways, including the Wnt/β-catenin signalling pathway. It is required for several aspects of retinal development and it is known to regulate the proliferation of neuro-epithelial stem cells. In Xenopus laevis the intracellular Wnt/β-catenin signalling pathway is activated in the retina by the Wnt receptor Fz5. Fz5 function in the eye was shown to regulate tissue specific gene expression and neuron versus Müller glial cell differentiation. However, no candidate Wnt ligand that could act through the Fz5 receptor in this tissue had been described. Wnt6 was recently found to be expressed in the developing retina, indicating that Wnt6 and Fz5 share temporal and spatial expression. Here, I tested the hypothesis that Wnt6 might function as ligand for Fz5 in the retina. In this thesis I show that a knock down of Wnt6 led to the same eye phenotype seen in Fz5 morphants, including reduced eye size, changed marker gene expression and altered neuron/Müller glia ratio. Rescue experiments show that the observed phenotype is specific and is mediated by altered Wnt/β-catenin signalling pathway function. These findings support a linear model, in which Wnt6 signal interacts with the Fz5 receptor to activate the Wnt/β-catenin pathway to regulate neural and Müller glia cell differentiation in retinal tissue. These results make Wnt6 a candidate for Fz5 ligand.