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. 2023 Jul 24;24(14):11844. doi: 10.3390/ijms241411844

Figure 2.

Figure 2

Binding profiles of Brm, KisL, and CHD1 at the regulatory regions of the ecdysone-responsive loci in Drosophila S2 cells. The figure shows the average distribution of Brm, KisL, and CHD1 at the TSSs (transcription start sites, N = 86) (A) and FLAG-EcR peaks (N = 284) (B) of the genomic loci, whose transcription is induced by a 1 h treatment of Drosophila S2 cells with 20-hydroxyecdysone. ChIP-Seqs were performed on Drosophila S2 cells treated with 20-hydroxyecdysone (0.3 µM) for 1 h “1h 20E” (red graph) or on the sham-treated cells “DMSO” (blue graph). The protein binding levels were calculated as an enrichment (ratio of the corresponding ChIP-Seq signal to the input DNA). The average profiles were calculated as the mean of the protein binding level. The standard error appears on the graphs as a lighter area around the main line of the profiles. The background binding level for the ChIP-Seqs was estimated using the set of 500 randomly chosen regions of the Drosophila genome and was provided as a grey transparent area at the averaged plots. (C) The figure shows the binding profiles of Brm, KisL, CHD1, FLAG-EcR, and CP190 at the eip74ef ecdysone-inducible locus. The grey line indicates an inducible TSS and the blue line indicates a non-inducible one. The protein binding levels were estimated by ChIP-Seq. ChIP-Seq experiments were performed using 1 h 20E- or DMSO-treated Drosophila S2 cells. ChIP-Seq data on FLAG-EcR (GSE139316) and CP190 (GSE156847) binding were loaded from GEO and described previously. ChIP-Seq data on Brm, KisL, and CHD1 are described here for the first time and provided in GSE102520. (D) The figure shows a schematic model describing changes in the protein binding level of Brm, KisL, CHD1, FLAG-EcR, and H3K27Ac with regulatory regions of the ecdysone-inducible loci in Drosophila S2 cells be-fore and after their treatment with 20-hydroxyecdysone. The sizes of the depicted coactivators, histone modification, and RNA polymerase II reflect changes in the level of their binding to the regulatory element.