Aging Related Oogenesis Defects of Upd3 Mutants. Michelle Giedt¹, Liqun Wang², Travis Sexton³, Claire Venard¹, Douglas Harrison¹. 1) Biology Department, University of Kentucky, Lexington, KY; 2) Department of Pathology, Brigham & Woman's Hospital, Harvard Medical School, Harvard New Research Building, Room 652, 77 Avenue Louis Pasteur, Boston, MA; 3) University of Kentucky College of Medicine, Cardiovascular Research Center, 741 S. Limestone St., Lexington, KY.

   In Drosophila, Jak/Stat signaling has many developmental roles including several in oogenesis. In one, a gradient of activity patterns the A/P axis of the follicular epithelium, with the highest levels specifying terminal cell fates. The Upd ligand is secreted from the anterior and posterior polar cells, and reduction of Upd reduces terminal fates. Another ligand, Upd3, is also expressed in the polar cells, raising the question of whether Upd and Upd3 act redundantly or have distinct functions in oogenesis. To address this, mutants of upd3 were generated. Young upd3 mutant females are fertile but exhibit increasing frequency of unfertilized eggs and defective egg chambers as they age. Defects include egg chamber fusions and degenerating chambers that are also observed in Jak/Stat pathway mutants. To determine if the role of Upd3 is additive in follicular fate specification, terminal cells were examined. Mutants had a slight reduction in border cell numbers, but the biological significance of this is unknown. Because border cells are important in micropyle formation, examination of unhatched eggs was performed to determine if the decrease in fertility was due to morphological defects. Some eggs from mutants had micropyles lacking a clear channel, but these occurred at a frequency too low to account for the decrease in fertility. The possibility of more subtle micropyle defects responsible for the low rate of fertilization is currently being investigated. Defects in posterior terminal cells were also examined. These cells give rise to the aeropyle, a respiratory structure located at the posterior. Loss of upd3 resulted in loss, reduction, or changes in shape of the cells in the aeropyle. This evidence suggests Upd and Upd3 act in an additive manner to specify follicle cell fates, with Upd3 increasing in importance as the female ages.