In an issue of Genome Biology in January 2018, Van Baak and colleagues analyzed the epigenome of monozygotic versus dizygotic twins. As you can see from the figure which was copied from the OpenAccess journal, dizygotic twins expose divergent methylation patterns in several genes (in red). Most remarkably is this for the DUSP22 gene which codes for a “dual specificity phosphatase”. On the other hand, monozygotic twins (in blue) showed almost no divergence, methylation rate ratio were very close to one, which would be on the diagonal line.
This lead van Baak et el. to look for the origin of this invariable methylation between two individuals. They found this supersimilarity between pairs of monozygotic twins is established at or before the stage when the twins become twins. This was fairly unexpected.
During their search the authors noted that subtelomeric regions are not only important targets for methylations, but at the origin of diseases e.g. tumour later in life.
Since the paper is very technical, it is difficult to read. The fact that monozygotic twins are not only identical in the genome, but extremely similar in their epigenome, too, is worth some labour with the text.
A nice analysis of the trimethylation of histon 3 at lysine 4 (H3K4me3) appears in Cell this week (http://dx.doi.org/10.1016/j.cell.2014.06.027). Benayoun and Pollina et al. claim that this marker labels preferentially those proteins that are essential for the cell’s function. The marker has been found at the start of most transcribed genes, but Benayoun and Pollina argue that not its mere presence, but the intensity of its presence is a sign that this protein is relevant for lineage specifity. If this intensity is disturbed, that function is not maintained.
This is a metaanalysis of a very broad range including human, mammalian, protostomes, plants and fungi. Nicely done!
Epigenetic modification of DNA, mostly methylation, is the way which ensures lineage specity in mammalian organization and propagation of cell types. It is inherited while cells multiply.
In Nature this week (doi:10.1038/nature13648) Reik and Kelsey describe two article (et al. Nature 511, 606–610 (2014) and et al. Nature 511, 611–615 (2014)) where the methylation patterns in egg, sperm, fertilized eggs and blastocysts are analyzed. As has been found in mice before, blastocysts lose most of their methylation. Later in development the DNA gets remethylated again. This has been suggested but formal proof was lacking. The imprinting – methylated gene regions due to maternal or paternal origin – is not as much removed for maternal genes, but for paternal ones.
Whether these papers will improve human stem cell research is to be seen.