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Quantitative Comparison of cis-Regulatory Element (CRE) Activities in Transgenic Drosophila melanogaster
Published on: December 19, 2011
Drosophila ecdysone receptor mutations reveal functional differences among receptor isoforms
M Bender1, F B Imam, W S Talbot
1Department of Developmental Biology, Stanford University Medical Center, California 94305, USA.
Cell
|December 31, 1997
Summary
Ecdysone receptor (EcR) isoforms direct fruit fly metamorphosis. Mutations in EcR-B1 disrupt metamorphosis and gene activation, while other EcR mutations cause embryonic lethality, revealing isoform-specific functions.
Area of Science:
- Developmental Biology
- Molecular Endocrinology
- Genetics
Background:
- The steroid hormone ecdysone regulates Drosophila metamorphosis.
- This process involves heterodimeric receptors formed by ecdysone receptor (EcR) isoforms and the USP protein.
- Three EcR isoforms (EcR-A, EcR-B1, EcR-B2) exist, encoded by the EcR gene.
Purpose of the Study:
- To identify and characterize mutations in the Drosophila EcR gene.
- To understand the specific roles of different EcR isoforms in metamorphosis and gene regulation.
Main Methods:
- Molecular mapping of EcR mutations.
- Analysis of gene expression in larval salivary glands.
- Transgenic expression of EcR isoforms in mutant backgrounds.
Main Results:
- Two classes of EcR mutations were identified: EcR-B1-specific mutations affecting metamorphosis and embryonic-lethal mutations in common DNA/ligand-binding domains.
- Loss of EcR-B1 function in salivary glands abolished ecdysone-induced gene activation.
- Transgenic expression demonstrated EcR-B1 mediated full repair, EcR-B2 partial repair, and EcR-A no repair of gene activation defects.
Conclusions:
- EcR-B1 plays a critical role in ecdysone-mediated gene activation during Drosophila metamorphosis.
- Different EcR isoforms exhibit distinct functions in regulating developmental processes.
- Understanding EcR isoform function is crucial for deciphering the molecular mechanisms of insect metamorphosis.
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