Abstract Mutations in the Van Gogh gene result in the altered polarity of adult Drosophila cuticular structures. On the wing, Van Gogh mutations cause an altered polarity pattern that is typical of mutations that inactivate the frizzled signaling/signal transduction pathway. The phenotype however, differs from those seen previously, as the number of wing cells forming more than one hair is intermediate between that seen previously for typical frizzled-like or inturned-like mutations. Consistent with Van Gogh being involved in the function of the frizzled signaling/signal transduction pathway, Van Gogh mutations show strong interactions with mutations in frizzled and prickle. Mitotic clones of Van Gogh display domineering cell nonautonomy. In contrast to frizzled clones, Van Gogh clones alter the polarity of cells proximal (and in part anterior and posterior) but not distal to the clone. In further contrast to frizzled clones, Van Gogh clones cause neighboring wild-type hairs to point away from rather than toward the clone. This anti-frizzled type of domineering nonautonomy and the strong genetic interactions seen between frizzled and Van Gogh suggested the possibility that Van Gogh was required for the noncell autonomous function of frizzled. As a test of this possibility we induced frizzled clones in a Van Gogh mutant background and Van Gogh clones in a frizzled mutant background. In both cases the domineering nonautonomy was suppressed consistent with Van Gogh being essential for frizzled signaling.