Mio: Connecting Meiotic Progression to Metabolism in Early Oogenesis. John C Reich, Mary Lilly. CBMP, NICHD, Bethesda, MD.

   In the Drosophila ovary, oocyte specification occurs in the context of a 16-germ cell cyst, where one of the 16-germ cells is designated as the future oocyte, and the other germ cells become polyploidy nurse cells. Multiple events contribute to this process, including the localization of oocyte specific proteins and RNAs, and the maintenance of the meiotic cycle specifically in the oocyte. Previously, our lab used a forward genetics approach to identify genes involved in oocyte formation/maintenance. Through this genetic screen, our lab identified missing oocyte (mio), a gene required to maintain oocyte specification during oogenesis potentially by maintaining the oocyte-specific meiotic arrest. Here we use a combination of genetics and fluorescent microscopy to show that mio mutant egg chambers (the precursor to an embryo) grow more slowly and have an increase in the catabolic process of autophagy compared to wildtype egg chambers, implicating mio in metabolism. In addition, mio mutant egg chambers have enlarged autolysosomes that can be seen by both fluorescent microscopy and EM, suggesting that mio may be involved in stopping autophagy. Consistent with this, under fed conditions mio mutant fat bodies do not show an increase in autophagy, but show a failure to stop autophagy during fat body recovery from starvation. Given the localization Mio-eGFP at the lysosome, a hub for nutritional signaling, we believe that Mio may be involved in reactivating cell growth after cells have been subjected to stress. We are currently testing this model. Coordination of growth and metabolism are essential for proper organismal development, and our data suggest that mio is important in this process.