Wnt signals are one of the five signal transduction pathways that shape virtually all cell fates and which are inappropriately activated in most solid tumors.  The key regulated effector of Wnt signaling is the protein ß-catenin.  Wnt signaling acts by regulating its stability.  In the absence of Wnt signaling, ß-catenin is targeted for proteasomal destruction by a multi-protein complex called the destruction complex.  In the presence of Wnt signals, the destruction complex is

inactivated, and ß-catenin levels rise, allowing it to enter the nucleus and work with TCF proteins to regulate Wnt target genes.  In our lab, we seek to determine how the tumor suppressor APC, a key component of the destruction complex, regulates both Wnt signaling and the cytoskeleton.  We use both the fruit fly Drosophila and cultured human colon culture cells to unravel the mechanisms by which APC works.  We combine powerful