While the primary sequence of the human genome is largely preserved in all human cell types, the epigenomic landscape of each cell can vary considerably, contributing to distinct gene expression programs and biological functions1-4. Epigenomic information, such as covalent histone modifications, DNA accessibility, and DNA methylation can be interrogated in each cell and tissue type using high-throughput molecular assays2,5-8. The resulting maps have been instrumental for annotating cis-regulatory elements and other non-coding genomic features with characteristic epigenomic signatures9-10, and for dissecting gene regulatory programs in development and disease7,9,11-14. Despite these technological advances, we still lack a systematic understanding of how the epigenomic landscape contributes to cellular circuitry, lineage specification, and the onset and progression of human disease.
