Planar cell polarity (PCP) is the coordinated polarization of a field of cells in the plane of an epithelium. PCP is manifested in different biological systems, such as the oriented arrangement of hairs and bristles in insects, feathers in birds and fur in mammals. The core Frizzled (Fz)/PCP factors is evolutionary conserved and is required not only to establish the planar polarity in epithelia, but also it is required to regulate convergent extension of mesenchymal cells in vertebrates. The Fz/PCP core consists of two molecular complexes associated with the plasma membrane, which interact antagonistically to establish the polarity of the cell: the Fz complex and the Strabismus (Stbm) complex. The downstream effects of Fz/PCP signaling are different depending on the tissue, ranging from cell-fate specification in the eye, to the orientation of cytoskeletal elements and cell division in the wing and thorax, respectively. Although many regulators and effectors of the pathway had been discovered, there are many unknown factors required for the pathway activation, the interaction between components of both complexes and with other signaling pathways. In order to find new regulators and downstream effectors of the Fz/PCP signaling we are carrying out a genome-wide genetic screening for modifiers of Fz/PCP signaling in the Drosophila eye. In brief, the screening approach is based in dominant genetic interactions between mild Fz or Stbm gain of function genotypes and large molecularly mapped chromosome deletions. I have identified three candidates loci based on this criteria and which suppress the gain of function phenotype of dishevelled, a major component of the Fz/PCP pathway. Currently, I am mapping the genes associated with the genetic interactions and characterizing the role of two additional genes in PCP establishment.