Restricted Scope for REU Supplement: Does the Nuclear Receptor USP Integrate Methyl Farnesoate Signaling During Metamorphosis?

This is a request for an REU supplement to support an undergraduate student in research training as a part of the funded parent project on a new ligand/receptor axis involving methyl farnesoate binding to the receptor ultraspiracle. Description of the form and nature of the student's involvement in the PI's NSF research project The overall objective of this proposal is to determine whether a hormone receptor that is central to metamorphosis of all insects and crustaceans (Ultraspiracle/RXR) actually requires its own ligand for its endogenous function, and if so, what is that endogenous ligand? The Specific Aims that contribute toward accomplishing this objective are: Specific Aim 1: Challenge the Endogenous Methyl Farnesoate with Mutated Exogenous USP Specific Aim 2: Challenge the Endogenous USP with Altered Exogenous Methyl Farnesoate Structures Specific Aim 3: Challenge the Endogenous USP with Altered Endogenous Concentrations of Methyl Farnesoate The student will participate in experiments that serve Specific Aim 1, in which the natural endogenous level of methyl farnesoate is challenged with various mutant exogenous nuclear receptor Ultraspiracle. The developing transgenic larvae are assessed for the developmental disruption arising from the different mutations to the ligand binding pocket. These assessments include analysis of misprogrammings of the larval tissues and imaginal discs (that are to form adult structures) that result in particular (and interesting) kinds of developmental aberration. Another researcher who will be joining the project in June will be performing complementary physical studies on the effect of each ligand pocket mutation to reduce the binding of that mutant pocket to the methyl farnesoate ligand. Part of the training activities of the student will be to interact with this second researcher in making inferences about the reduction in physical binding of methyl farnesoate for the receptor in relation to the strength of the mutation in causing developmental aberrations.