Analysis of transcriptional activity mediated by Drosophila melanogaster ecdysone receptor isoforms in a heterologous cell culture system

UNCG Author/Contributor (non-UNCG co-authors, if there are any, appear on document)
Jenna L. Callender (Creator)
Vincent C. Henrich, Professor (Creator)
The University of North Carolina at Greensboro (UNCG )
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Abstract: Ecdysteroid regulation of gene transcription in Drosophila melanogaster and other insects is mediated by a heterodimer comprised of Ultraspiracle (USP) and one of three ecdysone receptor (EcR) isoforms (A, B1 and B2). This study revealed that the EcR/USP heterodimer displays isoform-specific capabilities. EcRB1 is normally induced with a form of USP that is missing its DNA-binding domain (DBD), although potentiation by juvenile hormone (JH) III is reduced. The EcRA and B2 isoforms, however, display almost no response to ecdysteroids with the DBD- USP. A mutation, K497E, in the shared ligand-binding domain of the EcR isoforms caused elevated EcRB2-specific affinity for a canonical ecdysone response element. The effects of directed modification and mutagenesis offer a strategy for developing hypotheses and considerations for studying in vivo function.

Additional Information

Insect Mol. Biol., 15, 785-795.
Language: English
Date: 2006
Juvenile hormone, Mutagenesis, Ultraspiracle, Retinoid X receptor, Repression

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