In female Aedes aegypti mosquitoes, a neuropeptide, ovary ecdysteroidogenic hormone (OEH) is released from neurosecretory cells shortly after a blood meal and stimulates ovaries to secrete ecdysteroids. The rising titer of ecdysteroids activates the fat body to synthesize yolk proteins, which are stored in eggs and used during post-embryonic development. Both OEH and bovine insulin stimulate ovary steroidogenesis in vitro through the activation of a receptor tyrosine kinase (RTK) and the phosphotidylinositol 3-kinase (PI3-K)/protein kinase B (PKB) pathway, as indicated by the effects of selected inhibitors and activators. A mosquito RTK related to the insulin receptor has been characterized and localized on ovary follicle cells. This receptor likely is involved in the binding of radiolabeled insulin to ovaries and its displacement by both unlabeled OEH and insulin. The gene for the catalytic subunit of PI3-K has been partially elucidated in the mosquito and shares sequence similarity to the Drosophila and vertebrate PI3-Ks. The complete sequence of the gene encoding the mosquito PKB has been determined and closely resembles the Drosophila PKB. The characterization of the mosquito PKB gene and protein during a reproductive cycle is in progress. The function and signal transduction of OEH, along with its limited similarity to the insulin superfamily, support the concept developed from recent studies of mammals and invertebrates that insulins and the RTK/PI3-K/PKB pathway are an important nexus for the regulation of reproduction, nutrient stores, growth, and immunity. Supported by a grant (AI33108) from NIH to M. R. Brown
Species 1: Diptera Culicidae Aedes aegypti (yellow fever mosquito)
Keywords: Mosquito Insulin Receptor, Protein Kinase B
The ESA 2001 Annual Meeting - 2001: An Entomological Odyssey of ESA