For at least 100 genes, only one of its alleles can be expressed right from the get-go while the other allele is shut down. This imprinted pattern remains throughout development. While cis-acting epigenetic elements have been implicated in the process, the research community doesn’t have enough evidence to conclusively pin the blame on any one. After all, this isn’t politics!
Researchers in Texas looked at clusters of genes known to be imprinted in mice, comparing the DNA and chromatin methylation profiles of sperm with somatic tissues. The usual suspects – hypermethylated CpG islands, post-translationally modified histones, etc., were all rounded up, and queried separately. All had leaky alibis, but taken together, a story begins to take shape.
It looks like the areas that control imprinting can be identified by a combination of overlapping histone tri-methylation patterns at H3K4 and H3K9, along with DNA that’s differentially methylated in sperm relative to heart and brain.
Find out what else the “triple hit” analysis uncovered about genomic imprinting at Genome Research, June 2009.