Our analysis of chromatin in this work differs from our previous analysis of chromatin data7 in three ways. First, we use a larger range of marks and tissues/cell types: every track available from the Roadmap Epigenomics website (see URLs) for any of six activating marks, H3K27ac, H3K4me1, H3K4me3, H3K9ac, H3K36me3, and DHS, in any of the 88 primary tissues and cell types available, in addition to recent EN-TEx data. Second, for our analysis of Roadmap data, we used narrow peaks from Roadmap for all of the marks. Previously, we analyzed H3K27ac data from one source6 and H3K4me1, H3K4me3, and H3K9ac data from another source5,12; now that there is a single standard source with uniformly processed data for all Roadmap data, we have switched to using this data. Finally, we controlled more strictly for confounders by including the average across cell types of the cell-type-specific annotations for a given mark as an annotation in the model, so that annotations that tend to fall in areas that are more active overall are not falsely interpreted as cell-type-specific signal.
