@article {2454,
	title = {The RXR ortholog USP suppresses early metamorphic processes in Drosophila in the absence of ecdysteroids.},
	journal = {Development},
	volume = {127},
	year = {2000},
	month = {2000 Mar 15},
	pages = {1151-9},
	abstract = {<p>The steroid hormone 20-hydroxyecdysone (20E) initiates metamorphosis in insects by signaling through the ecdysone receptor complex, a heterodimer of the ecdysone receptor (EcR) and ultraspiracle (USP). Analysis of usp mutant clones in the wing disc of Drosophila shows that in the absence of USP, early hormone responsive genes such as EcR, DHR3 and E75B fail to up-regulate in response to 20E, but other genes that are normally expressed later, such as (\&amp;bgr;)-Ftz-F1 and the Z1 isoform of the Broad-Complex (BRC-Z1), are expressed precociously. Sensory neuron formation and axonal outgrowth, two early metamorphic events, also occur prematurely. In vitro experiments with cultured wing discs showed that BRC-Z1 expression and early metamorphic development are rendered steroid-independent in the usp mutant clones. These results are consistent with a model in which these latter processes are induced by a signal arising during the middle of the last larval stage but suppressed by the unliganded EcR/USP complex. Our observations suggest that silencing by the unliganded EcR/USP receptor and the subsequent release of silencing by moderate steroid levels may play an important role in coordinating early phases of steroid driven development.</p>
},
	keywords = {Afferent, Animals, Biological, Developmental, DNA-Binding Proteins, Drosophila, Ecdysteroids, Ecdysterone, Female, Gene Expression Regulation, Gene Targeting, Genes, Insect, Male, Metamorphosis, Models, Neurons, Receptors, Signal Transduction, Steroid, Steroids, Transcription Factors, Up-Regulation, Wing},
	issn = {0950-1991},
	author = {Schubiger, M and Truman, J W}
}
@article {2456,
	title = {Drosophila EcR-B ecdysone receptor isoforms are required for larval molting and for neuron remodeling during metamorphosis.},
	journal = {Development},
	volume = {125},
	year = {1998},
	month = {1998 Jun},
	pages = {2053-62},
	abstract = {<p>During the metamorphic reorganization of the insect central nervous system, the steroid hormone 20-hydroxyecdysone induces a wide spectrum of cellular responses including neuronal proliferation, maturation, cell death and the remodeling of larval neurons into their adult forms. In Drosophila, expression of specific ecdysone receptor (EcR) isoforms has been correlated with particular responses, suggesting that different EcR isoforms may govern distinct steroid-induced responses in these cells. We have used imprecise excision of a P element to create EcR deletion mutants that remove the EcR-B promoter and therefore should lack EcR-B1 and EcR-B2 expression but retain EcR-A expression. Most of these EcR-B mutant animals show defects in larval molting, arresting at the boundaries between the three larval stages, while a smaller percentage of EcR-B mutants survive into the early stages of metamorphosis. Remodeling of larval neurons at metamorphosis begins with the pruning back of larval-specific dendrites and occurs as these cells are expressing high levels of EcR-B1 and little EcR-A. This pruning response is blocked in the EcR-B mutants despite the fact that adult-specific neurons, which normally express only EcR-A, can progress in their development. These observations support the hypothesis that different EcR isoforms control cell-type-specific responses during remodeling of the nervous system at metamorphosis.</p>
},
	keywords = {Animals, Biological, Drosophila, Genes, Insect, Insertional, Larva, Lethal, Metamorphosis, Molting, Mutagenesis, Nervous System, Neurons, Receptors, Sequence Deletion, Steroid},
	issn = {0950-1991},
	author = {Schubiger, M and Wade, A A and Carney, G E and Truman, J W and Bender, M}
}
