Our research uses Drosophila as a model to study the evolutionarily conserved Wnt/Wingless signal transduction pathway, with a focus on one component in this pathway, Adenomatous polyposis coli (APC). Wnt/Wingless signaling directs cell proliferation, cell fate, and apoptotic cell death during development and is inappropriately activated in several types of cancer. The majority of colorectal carcinomas have truncating mutations in APC, a negative regulator in Wnt signaling. APC functions in a protein complex that targets the key transcriptional activator in the pathway, beta-catenin, for proteasomal degradation. Thus inactivation of APC results in ectopic Wnt signaling, and the aberrant activation of target genes. The primary goals of our research are to determine the molecular mechanisms by which APC regulates Wnt signaling, and the molecular consequences of APC loss.