The Conventional Kinesin-1/UNC-116 Acts in PHB Phasmid Neurons to Mediate Proper Cell Body Position

Cell migration in the nervous system is vital for developing proper nervous tissue structure. This active process begins with a migration promoting signal that leads to cell polarization and extension of membrane protrusions at the leading edge. Many pathways have been found to play a role in this process, but the downstream molecular mechanisms have yet to be thoroughly characterized. UNC-116/Kinesin-1 has been previously shown to be required for many processes including trafficking of synaptic vesicle components and axonal growth cone migration. We have found that UNC-116/Kinesin-1 also plays a role in maintaining neuronal cell body position. To understand the role of UNC-116/Kinesin-1 and its potential pathway members in this process, we study PHB phasmid neurons in the genetic model Caenorhabditis elegans. Using a combination of dye filling and cell-specific expression of the mCherry fluorophore, we have found that UNC-116/Kinesin-1 is required to maintain the anterior-posterior position of the PHB cell body throughout development. Cell specific rescue experiments indicate that UNC-116/Kinesin-1 functions cell autonomously to mediate this process. Our preliminary results suggest that this process occurs partially through an UNC-6/Netrin attractive signal and that KLC-2, one of two kinesin-light-chains, plays a role in this process. Interestingly, OSM-3/Kinesin-2 and other kinesin-like proteins including KLP-11, ZEN-4, VAB-8, and UNC-104 show no defects in this process. We believe that these results suggest a novel role for UNC-116/Kinesin-1 in maintenance of PHB cell body position. To further elucidate the function of UNC-116/kinesin-1 in this process, we will continue to test additional potential pathway members.