ChIP-on-chip analysis of changes in the epigenetic state and retinoid receptor occupancy of HoxA and HoxB clusters during RA-induced differentiation. H3K27me3 is used as a repressive mark; H3K4me3 is used as a mark for an active chromatin state, and Pol II is used as a mark of active transcription. Tracks are configured by using windowing function as mean and smoothing windows as 0 pixels in the UCSC Genome Browser. All time points for a given antibody are normalized with the same y-axis, and the specific range of each y-axis is shown for respective uninduced samples. The schematic at the top indicates the relative positions of Hox genes, microRNAs, and noncoding transcripts. Within 4 h of RA treatment, there is a rapid gain of H3K4me3 and Pol II, whereas H3K27me3 is gradually lost over 36 h. Many major changes in Pol II occupancy and gain of H3K4me3 are related to Heater, Hotairm1, and Hobbit1 noncoding transcripts. Distinct dynamic changes in retinoic acid receptors and the NCOR corepressor is observed over HoxA and HoxB cluster.
