The effects of the glucocorticoid, dexamethasone, on the development of the Drosophila embryo

We have investigated the effects of the glucocorticoid, dexamethasone, and five structural analogs on Drosophila development in an effort to identify steroid ligands that may play a role in the embryogenesis of this organism. Embryos were exposed to glucocorticoids either by direct culture in supplemented medium, or by examining embryos from adult flies raised on supplemented fly food. After exposure, embryos were examined for developmental defects. At a morphological level, exposure to dexamethasone disrupts the dorsolateral folding of the amnioserosa during germ band extension. In addition, germ band retraction and dorsal closure is also disrupted. The phenocritical period of these effects is within the first 4 h of embryogenesis. This response is dosage sensitive, with embryos responding to concentrations of dexamethasone ranging from 10^(−6) to 10^(−3)M. Furthermore, glucocorticoids which are closely related structural analogs of dexamethasone also disrupt germ band retraction and dorsal closure, while other tested steroids had no effect on embryonic development. At a molecular level, expression of the gene, Krüppel, is absent from the amnioserosa of dexamethasone-treated embryos. The cuticular phenocopy resulting from exposure to dexamethasone and related glucocorticoids is morphologically similar to the mutant phenotype associated with four genes required for germ band retraction, namely hindsight, serpent, tail-up and u-shaped. The results of this study represent the first association of a glucocorticoid with dose, stage and tissue specific effects on Drosophila development at both morphological and molecular levels