Drosophila growth disruption by Ecdysone Receptor transcriptional repression
Disciplines
Cell Biology | Developmental Biology | Molecular Biology | Molecular Genetics
Abstract (300 words maximum)
Ecdysone is a Drosophila hormone responsible for growth and development of various aspects of the fly anatomy, including their 19 imaginal discs that grow to become important structures like antenna, legs, and wings. When Ecdysone binds the Ecdysone Receptor (EcR), this complex inhibits or activates transcription of genes based on what coregulator proteins are bound. EcR is a nuclear hormone receptor with an N-terminal activation domain, a DNA binding domain, and a ligand binding domain (LBD) at the C-terminal. The LBD binds ecdysone and proteins that direct EcR activity. To study the role of EcR during development, our lab developed a genetic tool, UAS-EcRLBD (Sponge), to disrupt the interaction of EcR and coregulators that bind the LBD. A point mutation in our genetic tool, UAS-EcRLBD-A483T (Dumbr), prevents Sponge from interacting with a key corepressor called Smrter. Here we used these tools to measure EcR regulation of the growth of an organ, the adult wing. We forced the expression of our tools with Nubbin-Gal4, a wing-specific Gal4 driver, and measured the size of the adult wing to determine the effects of disrupting EcR coregulator interactions on wing growth. One-way ANOVAs showed that wing areas and vein distances of Sponge and Dumbr were significantly smaller than the controls, with Sponge showing a more severe phenotype than Dumbr. These results indicate that EcR repression is important for wing growth. Future work will focus on identifying the developmental window when EcR signaling is important for wing growth.
Academic department under which the project should be listed
CSM - Molecular and Cellular Biology
Primary Investigator (PI) Name
Dr. Joanna Wardwell-Ozgo
Drosophila growth disruption by Ecdysone Receptor transcriptional repression
Ecdysone is a Drosophila hormone responsible for growth and development of various aspects of the fly anatomy, including their 19 imaginal discs that grow to become important structures like antenna, legs, and wings. When Ecdysone binds the Ecdysone Receptor (EcR), this complex inhibits or activates transcription of genes based on what coregulator proteins are bound. EcR is a nuclear hormone receptor with an N-terminal activation domain, a DNA binding domain, and a ligand binding domain (LBD) at the C-terminal. The LBD binds ecdysone and proteins that direct EcR activity. To study the role of EcR during development, our lab developed a genetic tool, UAS-EcRLBD (Sponge), to disrupt the interaction of EcR and coregulators that bind the LBD. A point mutation in our genetic tool, UAS-EcRLBD-A483T (Dumbr), prevents Sponge from interacting with a key corepressor called Smrter. Here we used these tools to measure EcR regulation of the growth of an organ, the adult wing. We forced the expression of our tools with Nubbin-Gal4, a wing-specific Gal4 driver, and measured the size of the adult wing to determine the effects of disrupting EcR coregulator interactions on wing growth. One-way ANOVAs showed that wing areas and vein distances of Sponge and Dumbr were significantly smaller than the controls, with Sponge showing a more severe phenotype than Dumbr. These results indicate that EcR repression is important for wing growth. Future work will focus on identifying the developmental window when EcR signaling is important for wing growth.