Drosophila ecdysone receptor mutations reveal functional differences among receptor isoforms

Cell. 1997 Dec 12;91(6):777-88. doi: 10.1016/s0092-8674(00)80466-3.


The steroid hormone ecdysone directs Drosophila metamorphosis via three heterodimeric receptors that differ according to which of three ecdysone receptor isoforms encoded by the EcR gene (EcR-A, EcR-B1, or EcR-B2) is activated by the orphan nuclear receptor USP. We have identified and molecularly mapped two classes of EcR mutations: those specific to EcR-B1 that uncouple metamorphosis, and embryonic-lethal mutations that map to common sequences encoding the DNA- and ligand-binding domains. In the larval salivary gland, loss of EcR-B1 results in loss of activation of ecdysone-induced genes. Comparable transgenic expression of EcR-B1, EcR-B2, and EcR-A in these mutant glands results, respectively, in full, partial, and no repair of that loss.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, Non-P.H.S.
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Chromosome Mapping*
  • Drosophila melanogaster / genetics*
  • Drosophila melanogaster / growth & development
  • Drosophila melanogaster / physiology
  • Ecdysone / physiology
  • Exons
  • Female
  • Genes, Insect
  • Genes, Lethal
  • Genetic Complementation Test
  • Male
  • Metamorphosis, Biological
  • Mutagenesis
  • Receptors, Steroid / genetics*
  • Receptors, Steroid / physiology


  • Receptors, Steroid
  • ecdysone receptor
  • Ecdysone