Fig. 5: NSL complex-mediated acetylation leads to dBRD4 recruitment.
a Heatmaps and profile plots of ΔdBRD4-S-Biotin ChIP signal, ΔH4K16ac ChIP signal and ΔPol2 ChIP signal in control (GST) RNAi versus NSL1 RNAi13, as well as ChIP-seq profiles of MOF, NSL3 and MBDR213. All genes are plotted, clustered into two groups (clustering by k-means based on MOF, NSL3 and MBDR2 ChIP profiles). Order of genes is maintained for all other heatmaps in this panel. Signal of two merged replicates for ΔdBRD4-S-Biotin, ΔH4K16ac and ΔPol2 is shown. ΔdBRD4-S-Biotin was calculated as ChIP control-ChIP RNAi, ΔH4K16ac and ΔPol2 were calculated as log2 fold change (ChIP control over input) − log2 fold change (ChIP RNAi over input). b ChIP-qPCR of dBRD4-S-Biotin ChIP and H4K16ac ChIP after treatment with DMSO or HDAC inhibitor panobinostat (4 h, 200 nM) in control RNAi (GST) or NSL1 RNAi cells. Primers target the promoters and ends of dBRD4 and NSL complex-bound genes. Data are presented as mean value of n = 2 biological replicates. Source data are provided as a Source Data file.
