Transposable elements are a common mover and shaker in our genomes. Much like your obnoxious friend that you have to keep close tabs on at dinner parties, they’re usually kept under wraps by fancy host silencing mechanisms like DNA methylation. There’s been some evidence that suggests that the DNA methylation that silences transposable elements can spread to neighboring genes.
A team of researchers in Vancouver previously showed that DNA methylation and histone methylation spreads from one particular mouse endogenous retrovirus (ERV) to a certain gene promoter. That led the team to wonder just how often this really happens and how transposons and nearby genes interact.
The Canadian crew found that this spreading is rare (at least in mice), and it can actually go the other way sometimes—euchromatin can spread to the transposons.
They studied two ERVs in mice: IAPs and ETn/MusDs, which are repressed by DNA methylation. It turns out that there’s likely a negative selection pressure on ERVs that are close to gene termini, as the transposons were underrepresented in these regions. ETn/MusDs were generally less methylated when they were near expressed genes’ TSSs, but IAPs were heavily methylated, no matter where they were. Interestingly, in three ERVs that had two LTRs, the LTR closer to a gene TSS was less methylated than the one that was farther away.
The researchers also found that DNA methylation didn’t spread from the ERVs they studied into gene promoters. In fact, H3K4me3 and CTCF in the region between promoters and transposons may protect unmethylated promoters from the potential spreading. And, in an interesting twist, they found evidence suggesting that host gene euchromatin can spread the other way—from genes to ERVs.
“We have shown that spreading of DNA methylation from ERV copies toward active gene promoters is rare,” they conclude.
Get the full story at Genome Biology October 2012.