H3K4me3 is a mark of promoters and early transcription elongation whereas H3K36me3 marks gene bodies [ 22], which is where Chd1 localization has been observed.
For example, genome-wide location analyses of basal transcription factors have provided important information on the marking of promoter regions within a eukaryotic transcription circuit [ 24, 25].
An alternative hypothesis could be that another type of DNA modification than CpG methylation would be involved in a genome-wide marking of promoter regions in Drosophila.
Given that developmental potential is likely to be reflected in the epigenetic marking of promoters and enhancers linked to poised states, epigenomic maps should be more predictive of iPSC differentiation capacity than transcriptome profiling alone.
In the embryonic day 14.5 (E14.5) mouse brain, DNase I-hypersensitive regions align with ChIP-seq peaks from the EMCODE project [ 24] for marks of promoters (H3K4me3), enhancers (H3K4me1, H3K27ac), and poised or negatively regulated regions (H3K27me3).
However, the other domain boundary located 20 kb downstream of the Blcat gene showed a relatively stronger NFI-binding site, which corresponds to a consistently stronger histone H3K27me3 and H3K36me3 modification boundary that does not bear the H3K4me3 marks of promoters.
NFI binding to predicted sites was favored at promoters that are enriched with the H3K4me3 chromatin mark of active promoters, and notably at the promoters of genes that are up-regulated by NFI-C.
We used chromatin immunoprecipitation (ChIP) to study the occupancy of histones and histone marks on promoters of MeCP2 target genes BDNF and DLX5 in lymphocytes from RTT patients and controls.
This in turn suggests that H3K14ac, which is generally considered as a mark of active promoters along with other acetylation marks, can also mark inactive promoters, although to a lesser extent.
Incorporation of the histone variant H2A.z is a mark of active promoters in human and mouse system [ 21].
