Glial cells perform numerous functions to support neuron development and function, from regulation of axon pathfinding and synapse formation to ensheathment of neurons and maintenance of ionic homeostasis. In vertebrates defective glial cells have been linked to neurological diseases such as neuropathies and schizophrenia. Our lab is interested in genes that regulate glia-neuron interactions during development. Specifically, we have found the raw gene to be required in glia, as reducing raw levels in glial cells by RNAi results in lethality. Due to the lethality observed when raw is removed from glia we examined how glia were being affected in the developing central and peripheral nervous system. We have observed a decrease in the size of the brain and an elongated ventral nerve cord within the central nervous system. In the peripheral nervous system, reduced levels of raw affect the number of glia along the nerve extension region (NER) of the peripheral nerves. Further examination of peripheral nerve structure by transmission electron microscopy reveals significant changes in nerve morphology when raw levels are reduced. These phenotypes suggest a defect in glial specification, proliferation or survival. While glia appear to be specified normally in raw mutants, we are currently examining the levels of glial proliferation and death when raw levels are reduced. Finally, we are interested in how impaired glial function affects neuronal output. Results of a larval crawling assay reveal that larvae exhibit reduced locomotion when Raw levels are reduced in glia as compared to controls. These studies have resulted in the identification of a novel regulator of glial development, and are likely to yield novel molecular mechanisms underlying the establishment of neuron-glia interactions during development.