Overexpression of the Adaptor Protein, Dreadlocks (Dock), during Drosophila Oogenesis

Indianapolis, IN

Intercellular communication is critical for the function of any multicellular organism. Communication is often facilitated by chemical transfers between cells through connections such as gap junctions, plasmodesmata, and intercellular bridges. Many medical conditions can be attributed to errors in cellular connections such as heart disease, neurological disorders, and infertility. Intercellular communication is especially important during gamete formation, and an excellent model to study intercellular bridges is the developing Drosophila egg. Mature eggs are derived from egg chambers, which contain one egg (oocyte) and fifteen nurse cells, all of which are connected by intercellular bridges called ring canals. Ring canal stability is critical in the dramatic process of nurse cell dumping, a necessary step in the formation of fertile eggs. Our lab has identified a novel role for the conserved adaptor protein, Dreadlocks (Dock), in regulating ring canal size and germ cell stability. Depletion of Dock has a modest effect on ring canal size, but Dock overexpression induces a dramatic phenotype in the egg chamber; the nurse cell membranes become unstable, causing nurse cell fusion. In order to determine the domains of the Dock protein necessary for the overexpression phenotype, I have made point mutations in three of the four domains of the Dock protein (SH3-1, SH3-3, and SH2). Preliminary investigation of these lines suggest that the SH2 domain is necessary for the over-expression phenotype. Further examination of the overexpression lines will provide insight to the mechanism behind the dramatic Dock overexpression phenotype as well as point to possible Dock-interacting proteins.