Several lines of evidence suggest that neurofibroma formation involves hyperactivation of PI3K within the glial layer that surrounds the motor neurons, and yet the signals within gliby which PI3K activity is regulated remain incompletely understood. Following our recent discovery that the Drosophila group II metabotropic glutamate receptor (DmGluRA) activates PI3K in motor neuron, we hypothesized that activation of DmGluRA might similarly activate PI3K in glia. In task #1, we proposed to test if inhibition of DmGluRA-PI3K activity in motor neurons is sufficient to activate PI3K in the analogue of the Schwann cell called the peripheral glia (as monitored by perineurial glial growth). We found that inhibiting PI3K activity by introducing the DmGluRA112b null mutation or by expressing the PI3KDN transgenin motor neurons did significantly increase perineurial glial growth. In task #2, we proposed to determine if DmGluRA activity in peripheral glia is required for PI3K activation The stock construction required to address this task are almost complete and experiments aranticipated to begin within the next few weeks.