Abstract
The steroid hormone ecdysone triggers metamorphosis m Drosophila and also controls important reproductive functions. We have carried out a mutational analysis of the ecdysone receptor (EcR) gene EcR encodes three protein isoforms (EcR-A, EcR-B1 and EcR-B2), each of which heterodimerizes with the USP protein to mediate signaling by ecdysone during development. We will present our results in three areas 1.) A ts EcR. mutation was used to construct EcR mutant adults. Female fertility is severely affected in these mutants and defects in oogenesis are observed, including loss of late vitellogenic egg chambers. 2.) We have isolated deletion mutants that lack EcR-BI and EcR-B2 expression but retain EcR-A expression and shown that these mutants ate blocked in regression of larval-specific dendrites in remodeling neurons during metamorphosis (a collaboration with M.S. and J.W.T.). These results indicate a requirement for EcR-B isoforms in neuronal remodeling. 3.) Heatshock controlled expression of EcR from transgenes results in rescue of EcR null mutants (normally embryonic lethal) through the larval period well into pupal development. We have used this conditional system to examine EcR mutant effects on ecdysone target gene expression. Supported by NIH grants #GM53681 (to IvI.B.) and #NS 29971 (to J.W.T.).