| Description |
Insect metamorphosis is a complex developmental process involving the degradation of larval tissues and the growth and differentiation of adult tissues. In the fruit fly, Drosophila melanogaster, this dramatic transformation is initiated by increases in the titer of a single hormone, the steroid 20-hydroxyecdysone. The steroid directly induces the expression of a small number of early genes which, in tum, activate a large set of late genes that directly control the events of metamorphosis. The E93 early gene is an interesting candidate for study as it exhibits a complex stage- and tissue-specific response unlike that of any other early puff gene studied to date. E93 expression is induced by only the prepupal pulse of steroid in the larval salivary gland, and expression is generally restricted to larval tissues fated to undergo histolysis and die. E93 encodes a novel protein of unknown function. Understanding the function of this gene will require mutations specific to E93. Initially, the only existing E93 mutations were large deletions spanning multiple genes. In order to generate mutations specific to E93, a series of mutageneses have been performed. Mutagenesis by local P-element transposition failed to generate any new insertions within or near the E93locus. Subsequently, an irradiation mutagenesis protocol using a Cs137 source was used to generate smaller deletions of the 93F locus. We have utilized these new lesions, in conjunction with the existing mutations in the 93F region of the genome, to screen for specific E93 mutations induced by the chemical mutagen ethylmethane sulfonate (EMS). Currently, several putative E93 mutations exist. Further characterization of these mutations will be required before functional studies of E93 can be undertaken. Such studies should provide insight into the mechanisms of the steroid regulatory hierarchy of Drosophila as well as our understanding of steroid signaling in other higher organisms. |
