H3K27me3

The genomic DNA of eukaryotic cells is wrapped around special protein molecules known as histones.

[2][3] The placement of a repressive mark on lysine 27 requires the recruitment of chromatin regulators by transcription factors.

This occurs through polycomb mediated gene silencing via histone methylation and chromodomain interactions.

[9] H3K27me2 is broadly distributed within the core histone H3 and is believed to play a protective role by inhibiting non-cell-type specific enhancers.

[16] The current understanding and interpretation of histones comes from two large scale projects: ENCODE and the Epigenomic roadmap.

This led to chromatin states which define genomic regions by grouping the interactions of different proteins and/or histone modifications together.

Chromatin states were investigated in Drosophila cells by looking at the binding location of proteins in the genome.

[19] A look in to the data obtained led to the definition of chromatin states based on histone modifications.

This additional level of annotation allows for a deeper understanding of cell specific gene regulation.

[21] Cause-and-effect relationship between sperm-transmitted histone marks and gene expression and development is in offspring and grandoffspring.

Cohen–Gibson syndrome is a disorder linked to overgrowth and is characterised by dysmorphic facial features and variable intellectual disability.

In some cases, a de novo missense mutation in EED was associated with decreased levels of H3K27me3 in comparison to wild type.

All DMGs exhibit loss of H3K27me3, in about 80% of cases due to a genetic mutation receplacing lysine with methionine (M), known as H3K27M.

It results in good optimization and is used in vivo to reveal DNA-protein binding occurring in cells.

ChIP-Seq can be used to identify and quantify various DNA fragments for different histone modifications along a genomic region.

Micrococcal Nuclease sequencing (MNase-seq) is used to investigate regions that are bound by well positioned nucleosomes.