Accepted_test

The transcriptional activation by 20-hydroxyecdysone (20H) in Drosophila is an excellent model for studying tissue-specific response to steroids. An increase in 20H titer controls degradation of larval and proliferation of adult tissues during metamorphosis. To study 20H-dependent transcription, we used the natural system for controlling the 20H titer – E23 membrane transporter exporting 20H out of the cell. We artificially expressed the E23 in tissues to suppress the first wave of 20H-inducible transcription in metamorphosis.  Expression of E23 revealed plenty of 20H target genes in salivary glands, but not affected transcriptional pattern in brain/eye-antennal discs (a tissue resistant to 20H at this stage). We described the mechanism of 20H-dependent transcription induction in salivary glands. 20H affects promoters of its targets differently - by stimulating the chromatin decompaction and the RNA polymerase II recruitment, or promoting the RNA polymerase II elongation. We observed the formation of enhancers within 20H target loci, where increase in 20H titer promotes chromatin decompaction, recruitment of EcR ecdysone receptor and CBP/Nejire acetyltransferase. We believe that the emergence of these enhancers leads to a change in the status of 20H targets in the salivary glands of the wandering larvae.