Creation of EcR isoform-specific mutations in Drosophila melanogaster via local P element transposition, imprecise P element excision, and male recombination

G. E. Carney, A. Robertson, M. B. Davis, M. Bender

Research output: Contribution to journalArticle

11 Scopus citations


Collections of single P transposable-element insertion strains that currently inactivate more than 25% of essential Drosophila genes have proven to be a valuable tool for genome research in Drosophila melanogaster. For genes unrepresented in these collections, strategies including local P element transposition and transposase-induced imprecise excision can be used to inactivate or delete the gene of interest. Here we report our use of local P element transposition followed by imprecise P element excision and transposase-induced male recombination to generate two deficiencies specific for the EcR-A isoform of the ecdysone receptor (EcR) gene, and four larger deficiencies likely to affect multiple EcR functions. We also report here the determination of sequences flanking six EcR-B deficiencies generated in a previous imprecise excision screen. EcR-A encodes one of a family of three related nuclear receptor proteins that, together with the heterodimer partner USP, mediate ecdysone signaling during Drosophila development. Our results delineate sequences required in vivo for EcR-A function, as well as identifying EcR-A intron 1 sequences that are not essential for EcR function.

Original languageEnglish (US)
Pages (from-to)282-290
Number of pages9
JournalMolecular Genetics and Genomics
Issue number3
StatePublished - Apr 1 2004



  • EcR
  • Imprecise excision
  • Local transposition
  • Male recombination
  • P element

ASJC Scopus subject areas

  • Molecular Biology
  • Genetics

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