The adult cuticular wing of Drosophila is covered by an array of distally pointing hairs that reveals the planar polarity of the wing. We report here that mutations in dachsous (ds) disrupt this regular pattern, and do so by affecting frizzled (fz) signaling. ds encodes a large membrane protein that contains many cadherin domains and ds mutations cause deformed body parts. We found that mutations in ds also result in a tissue polarity phenotype that at the cellular level is similar to frizzled (fz), dishevelled (dsh) and prickle (pk), as many cells form a single hair of abnormal polarity. Although their cellular phenotype is similar to fz, dsh and pk, ds mutant wings display a unique and distinctive abnormal hair polarity pattern including regions of reversed polarity. The development of this pattern requires the function of fz pathway genes suggesting that in a ds mutant the fz pathway is functioning - but in an abnormal way. Genetic experiments indicated that ds was not required for the intracellular transduction of the fz signal. However, we found that ds clones disrupted the polarity of neighboring wild type cells suggesting the possibility that ds affected the intercellular signaling function of fz. Consistent with this hypothesis we found that fz clones in a ds mutant background displayed enhanced domineering non-autonomy, and that the anatomical direction of this domineering non-autonomy was altered in regions of ds wings that have abnormal hair polarity. The direction of this domineering nonautonomy was coincident with the direction of the abnormal hair polarity. We conclude that ds causes a tissue polarity phenotype because it alters the direction of fz signaling.