Abstract: Signaling between Gurken, a TGF-alpha like molecule, and the Drosophila Epidermal Growth Factor (EGF) receptor sets up both the anterior-posterior and the dorsal-ventral axes of the egg and the embryo. My thesis describes two different approaches to study the regulation of this pathway. I performed a follicle cell mosaic screen on the X chromosome to uncover genes functioning in the follicle cell layer that may regulate the EGF receptor pathway. From the screen, we identified a mutation that is essential for dorsal appendage formation. Absence of this gene leads to an expansion of the operculum fates at the expense of dorsal appendage fates. I determined that the mutation is in brinker (brk) gene, a repressor of Dpp signaling. In brk mutant follicle cell clones at the dorsal anterior region, Broad Complex (BR-C) expression is down-regulated in a larger domain than in wild type. I showed that BR-C is required for dorsal appendage development. In addition, I showed that EGF receptor signaling represses TGFβ signaling in oogenesis by up-regulating brk expression. From our results and previously published data, it appears that anterior follicle cells integrate the levels of EGF receptor activation and TGFβ receptor activation. Operculum fate results when the sum of the level of activation of both pathways reaches a threshold level. I also cloned and characterized a female sterile mutation, cutoff (cuff), functioning in the germline to regulate the production of Gurken. Cuff mutations lead to eggshell ventralization and reduced fecundity. We found that there is a marked increase in the transcript levels of two retro-transposable elements, Het-A and Tart in cuff mutant ovaries. Tagged Cuff protein shows a peri-nuclear localization in the nurse cells, similar to components of the RNAi machinery. These results indicate that Cuff is likely to be involved in the rasiRNA pathway. The eggshell and egg laying defects of cuff mutants are suppressed by a mutation in chk2. We propose that mutants in rasiRNA pathways lead to elevated transposition incidents in the germline, which activates a checkpoint that causes a loss of germ cells and a reduction of Gurken protein in the remaining egg chambers.