Genetic Control of Ecdysone Synthesis in Drosophila

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In many organisms, growth occurs primarily during early juvenile phases. When a specific body size is reached, the organism stops growing and transitions to a sexually mature adult (at puberty in mammals and at metamorphosis in insects). Nevertheless, it is unclear how organisms sense when they are large enough for this transition. In the fruitfly, Drosophila, metamorphosis is triggered by the steroid hormone ecdysone, synthesized in an endocrine tissue called the prothoracic gland (PG). One key activator of ecdysone synthesis is the protein hormone, PTTH. Elimination of PTTH delays ecdysone synthesis and causes large and developmentally delayed adults to form. The cellular "machinery" within the PG by which PTTH triggers ecdysone synthesis has not been identified, and yet this identification is critical to understanding how the timing of metamorphosis, and hence final body size, is regulated. This research project will test the hypothesis that PTTH activates ecdysone synthesis via a regulatory pathway (MAP kinase pathway) in the PG. Transgenes inhibiting or activating the MAP kinase pathway will be expressed specifically in the PG to determine if these transgenes either block the ability of PTTH to induce ecdysone synthesis, or activate ecdysone synthesis in the absence of PTTH. In addition, transgenes will be used to increase or decrease PTTH synthesis, and the effects of changes in PTTH levels on MAP kinase activity will be determined. Successful completion of these experiments will provide essential information on the machinery used by organisms to control the timing of developmental transitions and hence final body size. In addition, this project will support the development of the next generation of scientists by training undergraduate and graduate researchers in genetic and molecular techniques.