Explore the roles of steroid hormone signaling mediated Drosophila oogenesis
Authors: Chueh Wen Wang; Anna C.-C. Jang
Affiliation: Biotechnology and Bioindustry Sciences, National Cheng Kung University, Tainan, TW
Keywords: p. cell migration; n. hormonal control
Steroid hormone is temporal control in development process. The p160 steroid receptor coactivators (SRC) are shown being amplified and overexpressed in various cancers to promote proliferation and metastasis. However the molecular mechanism by which SRC induces dissemination of tumors has not been well established. Therefore, use border cells that are originated from follicle epithelial cells and invade through nurse cells that migrate to oocyte boundary in Drosophila oogenesis be study collective cell migration model. This migration process is also regulated by steroid hormone signaling and required SRC, named Taiman (Tai) in Drosophila. Tai interact with hormone receptor complex via LXXLL domain in a ligand dependent manner. Without any of these components, border cells fail to migrate and egg chambers will not develop. Steroid hormone in Drosophila is spatially and temporally regulated in oogenesis and this signaling is required to schedule border cell migration. Steroid hormone signaling begins to rise during stage 9 then reaches the peak at stage 10 and its level is controlled by the bHLH domain of Tai. The bHLH domain truncated Tai, Tai (ΔB), causes hyperactivation of steroid hormone signaling and precautious migration in co-expression of hyperactive Jak. To further explore the molecular mechanism by which Tai (ΔB) regulates steroid hormone signaling, we screened for genetic modifiers of tai (ΔB) by crossing with deficiency lines that include various deletions on chromosome II. In overexpression of tai (ΔB), nearly 60 % border cell failed to arrival at the oocyte and 15 % border cells did not exceed a quarter of migration journey. I have screened 209 deficiency lines to seek any of them to enhance or suppress migration defect. Currently, there are 48 lines displaying suppression phenotype and 74 lines showing enhancement. We will further analyze the top 10 enhancers and suppressors to identify which genes are responsible for the migration defect in hyperactivation of steroid hormone signaling. To figure out which gene involved in spatial regulation of cell migration.