| Formation of a functional nervous system in vertebrates requires the establishment of billions of correct axonal connections. In the developing organism, nerve axons are guided over great distances to reach their targets by the action of the nerves' growth cones. Understanding how this occurs requires the identification of molecules involved in growth cone motility. Previous work suggested a role for GAP-43 in growth cone motility. Through the use of microscale chromophore-assisted laser inactivation (micro-CALI), I demonstrated that GAP-43 is crucial for the maintenance of lamellipodial stability. Micro-CALI of GAP-43 in growth cones of cultured, embryonic chick dorsal root ganglia leads to lamellipodial retraction. Two proteins previously shown to interact in vitro with GAP-43, the heterotrimeric G protein G ao and Protein Kinase C (PKC), were investigated as possible effectors of GAP-43 in growth cones. My results support a role for PKC, but not G ao , in lamellipodial stability. The micro-CALI results of GAP-43 and PKC coupled with data from CALI of GAP-43 in vitro in a PKC kinase assay support the model that phosphorylation of GAP-43 by PKC is important for lamellipodial stability. |
