Epigenomics generally refers to regulatory features of the genome that can be passed from one generation to another -- either from mother to daughter cells or from parent to child -- without altering the actual DNA coding sequences of genes. The epigenentic regulatory features most commonly studied are chemical modifications of DNA (such as methylation) or histone proteins (the proteins that help pack down chromosomal DNA in the nucleus). From our published studies, we have examined roles for histone function during ESC exist from the pluripotent state (Schaniel et al., Stem Cells 2009) and roles for particular histone marks (e.g., H3K9me2) during hematopoietic stem/progenitor cells lineage commitment (Chen et al., 2012 Genes and Dev.). From our hematopoietic stem cell (HSC) studies, HSCs are developmentally "reprogrammed" to have little or no histone H3 lysine 9 methylation in the primitive state. Upon lineage commitment, H3K9me2 marks are nucleated at specific sites in the genome and then spread across the entire genome (Chen et al., 2012 Genes and Dev.). Increase in this mark coincides with global changes in chromatin structure during differentiation (Schones et al., Epigenetics and Chromatin 2014). One possibility is that the absence of this histone mark promotes developmental plasticity in uncommitted stem and progenitor populations.
Epitranscriptomics generally pertains to chemical modifications of mRNA occurring during or after gene transcription. We are currently performing broad genomic surveys of the impact of mRNA methylation (i.e., N6-methyladenosine) on regulation of key gene mRNAs required for progenitor cell lineage commitment and stem cell self-renewal (Kuppers et al., in preparation).