Fig. 7

An integrated working model for the cross-talk between Hippo and Hedgehog signaling. Activation of Hippo signaling (e.g. high cell density) induces the phosphorylation of Lats1/2, which in turn phosphorylate Taz, resulting in the cytosolic retention and alternatively proteasomal degradation of Taz. However, inactivation of Hippo signaling (e.g. low cell density) stabilizes cytosolic Taz, which binds to and drives the PKA to phosphorylate Gli3 at six conserved serine sites, causing the processing of full-length of Gli3 (Gli3F) into C-terminal truncation form of Gli3 (Gli3R) and thereby negating the Hedgehog signaling