For a while now, scientists have been on the trail of N6-methyladenine—methyl-A—as a possible epigenetic modification in mammals. Like methylcytosine, it's a chemically modified base that performs regulatory roles, but so far, we only knew of methyl-A operating in RNA, as well as in the DNA of just a few species. 'Till now, only modified cytosine—methyl-C—was clearly operating in mammals.

But in mouse embryos at least, methyl-A helps to suppress transposons, says this team from the Yale School of Medicine and elsewhere. Its role might even be epigenetic too.

So we can legitimately be all "new base!" even though everyone has long had strong suspicions.

I mean, here's Holger Heyn and Manel Esteller in Cell last May: "An Adenine Code for DNA: A Second Life for N6-Methyladenine."

And a group from the University of Chicago in October: "DNA N6-methyladenine: a new epigenetic mark in eukaryotes?"

In the new research published in Nature, cells deficient in the demethylase Alkbh1 experience a buildup of methyl-A, as well as transcriptional silencing. Methyl-A marks are more prevalent in young LINE transposons—those estimated to be younger than 1.5 million years old, as compared to those older than 6 million years.

Methyl-A not only shuts down these transposons, it also silences genes and enhancers nearby.

Check out methyl-A: