Investigation of FMRFamide and SCP as targets for the Juvenile Hormone Nuclear Receptor
Bielang, Rebecca E.
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Studies of insect development have played a key role in our current understanding of the neuroendocrine system of both insects and vertebrates. Mutations in the Drosophila melanogaster gene apterous (ap) result in a pleiotropic phenotype due to neuroendocrine dysfunction. Juvenile Honnone (JH) is crucial for proper development of insects such as Drosophila. Previous studies have shown that a lack of JH in ap mutants results in sterility, which can be rescued by ectopic application of JH. Another key aspect of the ap phenotype is the lack of FMRFamide, a neuropeptide, in the thoracicventral (Tv) cells. Because Tv cells are known to express Apterous protein, it has been suggested that this protein directly regulates FMRFamide gene expression. A recent study reports FMRFamide rescue through the expression of a wild-type ap cDNA from an ap central nervous system enhancer. This enhancer also showed reporter gene expression in the corpus allatum, where JH is produced. Due to these findings we hypothesize that FMRFamide is regulated in two ways: directly by Apterous protein and through JH. In this study the goal is to identify the regulatory mechanism among JH, apterous, and FMRFamide. Included in the mechanics may be the currently unidentified JH receptor. To accomplish this, flies with different mutations in the ligand binding domains which may affect FMRFa expression were immunostained with an antibody for the FMRFa peptide. Our results of 12 different mutants proved disappointing. None of the flies we stained showed similar patterns to the apterous mutants. Therefore, we were unsuccessful in identifying another piece of the puzzle to how JH is linked to the Apterous protein.