A conditional rescue system reveals essential functions for the ecdysone receptor (EcR) gene during molting and metamorphosis in Drosophila

In Drosophila, pulses of the steroid hormone ecdysone trigger larval moltin g and metamorphosis and coordinate aspects of embryonic development and adu lt reproduction. At each of these developmental stages, the ecdysone signal is thought to act through a heteromeric receptor composed of the EcR and U SP nuclear receptor proteins. Mutations that inactivate all EcR protein iso forms (EcR-A, EcR-B1, and EcR-B2) are embryonic lethal, hindering analysis of EcR function during later development. Using transgenes in which a heat shock promoter drives expression of an EcR cDNA, we have employed temperatu re-dependent rescue of EcR null mutants to determine EcR requirements at la ter stages of development. Our results show that EcR is required for hatchi ng, at each larval molt, and for the initiation of metamorphosis. In EcR mu tants arrested prior to metamorphosis, expression of ecdysone-responsive ge nes is blocked and normal ecdysone responses of both imaginal and larval ti ssues are blocked at an early stage. These results show that EcR mediates e cdysone signaling at multiple developmental stages and implicate EcR in the reorganization of imaginal and larval tissues at the onset of metamorphosi s. required for hatching, at each larval molt, and for the initiation of me tamorphosis. In EcR mutants arrested prior to metamorphosis, expression of ecdysone-responsive genes is blocked and normal ecdysone responses of both imaginal and larval tissues are blocked at an early stage. These results sh ow that EcR mediates ecdysone signaling at multiple developmental stages an d implicate EcR in the reorganization of imaginal and larval tissues at the onset of metamorphosis.