In conclusion, we have further characterized the phenotype of cells deleted for the Sz. pombe orthologue of the human Batten disease gene CLN3, btn1. We identified a failure to correctly polarize F-actin patches and the endocytic machinery, leading to the loss of polarity of Myo1p and sterol-rich membrane domains. The gene discussed is CLN3; the disease is juvenile neuronal ceroid lipofuscinosis.