Loss of the ecdysteroid-inducible E75A orphan nuclear receptor uncouples molting from metamorphosis in Drosophila

Michael Bialecki, Alycia Shilton, Caroline Fichtenberg, William A. Segraves, Carl S. Thummel

Research output: Contribution to journalArticle

Abstract

Isoform-specific null mutations were used to define the functions of three orphan members of the nuclear receptor superfamily, E75A, E75B, and E75C, encoded by the E75 early ecdysteroid-inducible gene. E75B mutants are viable and fertile, while E75C mutants die as adults. In contrast, E75A mutants have a reduced ecdysteroid titer during larval development, resulting in developmental delays, developmental arrests, and molting defects. Remarkably, some E75A mutant second instar larvae display a heterochronic phenotype in which they induce genes specific to the third instar and pupariate without undergoing a molt. We propose that ecdysteroid-induced E75A expression defines a feed-forward pathway that amplifies or maintains the ecdysteroid titer during larval development, ensuring proper temporal progression through the life cycle.

Original languageEnglish (US)
Pages (from-to)209-220
Number of pages12
JournalDevelopmental Cell
Volume3
Issue number2
DOIs
StatePublished - Aug 2002
Externally publishedYes

ASJC Scopus subject areas

  • Developmental Biology

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