Ever so often, you stumble across a magnificent work of science. This was the case for me a few weeks ago when this work popped up in my news feed. The authors investigate how a genomic locus that is the strongest risk factor for artherosclerosis produces a regulatory non-coding gene that regulates other genes associated to the disease.
They used stable over-expression and knock-down approaches to investigate the role of distinct ANRIL (a long non-coding RNA, aka lncRNA) isoforms in several key mechanisms of atherogenesis. They show that this gene guides epigenetic effector complexes to specific genomic loci.
Through what molecular mechanism you ask? None other than via endogenous transposable elements–ALUs specifically–that have been harnessed through evolution to perform regulation of gene expression in our genomes. FYI, repetitive elements compose ~46% of the human genome, 20% of which are ALUs.