[Show abstract][Hide abstract] ABSTRACT: Spatially restricted epidermal growth factor receptor (EGFR) activity plays a central role in patterning the follicular epithelium of the Drosophila ovary. In midoogenesis, localized EGFR activation is achieved by the graded dorsal anterior localization of its ligand, Gurken. Graded EGFR activity determines multiple dorsal anterior fates along the dorsal-ventral axis but cannot explain the sharp posterior limit of this domain. Here, we show that posterior follicle cells express the T-box transcription factors Midline and H15, which render cells unable to adopt a dorsal anterior fate in response to EGFR activation. The posterior expression of Midline and H15 is itself induced in early oogenesis by posteriorly localized EGFR signaling, defining a feedback loop in which early induction of Mid and H15 confers a molecular memory that fundamentally alters the outcome of later EGFR signaling. Spatial regulation of the EGFR pathway thus occurs both through localization of the ligand and through localized regulation of the cellular response.
[Show abstract][Hide abstract] ABSTRACT: The pattern of the Drosophila eggshell is determined by the establishment of a complex and stereotyped pattern of cell fates in the follicular epithelium of the ovary. Localized activation of the Epidermal growth factor receptor (Egfr) is essential for this patterning. Modulation of Egfr pathway activity in time and space determines distinct fates at their appropriate locations, but the details of how Egfr signaling is regulated and how the profile of Egfr activity corresponds to cell fate remain unclear. Here we analyze the effect of loss of various Egfr regulators and targets on follicle cell patterning, using a marker for follicle cell fate, and on the mature eggshell phenotype, using a novel eggshell marker. We show, contrary to current patterning models, that feedback regulation of Egfr activity by the autocrine ligand Spitz and the inhibitor Argos is not necessary for patterning. Given the cell-autonomous nature of the mutant phenotypes we observed, we propose instead that the pattern of cell fates is generated by spatial information derived directly from the germline ligand Gurken, without a requirement for subsequent patterning by diffusible Egfr regulators in the follicular epithelium.