Identification of me31B from an in vivo RNAi screen as a potential regulator of Notch Signaling. Muhammed Soylemez, Dongyu Jia, Wu-Min Deng. Department of Biological Science, Florida State University, Tallahassee, FL. Muhammed Soylemez, Dongyu Jia, Wu Min Deng. BIOLOGICAL SCIENCE , FLORIDA STATE UNIVERSITY, TALLAHASSEE , FL.

   The Drosophila somatic follicle cells are excellent for the study of cell-cycle regulation and cell differentiation. During oogenesis, the follicle cells sequentially undergo three variations of cell cycle programs, the mitotic cycle, the endocycle and gene amplification. Notch signaling activation is required for the switch from the mitotic cycle to the endocycle (the M/E switch) and its downregulation is necessary for the switch from the endocycle to gene amplification (the E/A switch) in these cells. Recently, we have found that Broad, a zinc-finger transcription factor, is directly up-regulated by Notch signaling during the M/E switch in the follicle cells (Jia and Deng, unpublished data). During late oogenesis, Broad is also regulated by EGFR and Dpp pathways for chorionic appendage formation. To explore how these different signaling pathways regulate follicle cell differentiation and cell cycle switches, we performed an in vivo RNAi screen to examine the effect of induced knockdown of gene expression on Br expression during oogenesis. So far, 350 different RNAi lines have been screened and about 20 of them showed defects in either early or late Br expression in follicle cells. Knockdown of Me31B, a putative RNA helicase belonging to the DEAD-box family, resulted in disruption of the Br early expression pattern during the endocycle stages. In addition, we found that Hindsight and Cut, both of which are Notch targets in follicle cells, are also regulated by Me31B, suggesting a potential role of Me31B in Notch signaling. Further studies are being conducted to gain more insight into the relationship between Notch signaling and Me31B and their effects on cell cycle regulation, differentiation and growth.