Role of Myosin Va in trafficking of neuronal vesicles

Neurons (brain cells) are separated by gaps called synapses and communicate via mechanisms which enable them to send and receive signals across these gaps. Inadequate development and maintenance of synapses is associated with a number of neurological and psychiatric conditions, from epilepsy to anxiety disorders, autism and mental retardation. Neurons use axons and dendrites to communicate across synapses. Axons are long fibers that transmit impulses to other neurons. Dendrites form a network of branches that receive signals from other nerve cells. Newly-made proteins within neurons must be transported to appropriate sites in axons or dendrites for proper communication to occur. However, little is known about how these proteins are accurately relocated. Frederick Dobie is studying one of the molecules thought to be involved in protein transport (Myosin Va), which is widespread in the brain, to clarify its role in pre and post-synaptic communication. Research has shown that a mutation in Myosin Va leads to Griscelli Syndrome, a disorder which causes severe motor and neurological impairment in humans. Other CNS disorders may also result from malfunctions in intracellular transportation of the proteins that facilitate communication between neurons. A better understanding of the action of transport molecules may lead to better methods of treatment for neurological disorders.