In news more surprising than the rise of the Occupy Wall Street movement, researchers have unearthed a novel mechanism in which RNA demethylation is mediated by, of all things, the obesity related protein FTO.
FTO is a well-established target of obesity and diabetes researchers, but its function has so far been elusive. At least it was, until a scientific team from the University of Chicago learned a bit more about FTO’s regulatory abilities during some experiments. Working off information that RNAs may be substrates for FTO, the team focused on N6-methyladenosine (m6A), the most commonly methylated base in mRNA and here’s what they found:
- siRNA knockdown of FTO increased the m6A in mRNA
- Overexpression of FTO reduced m6A
- FTO efficiently demethylates m6A in vitro
- FTO seemed to colocalize with “nuclear speckles”, showing its relation to nuclear RNAS.
The team’s observations indicate that m6A RNA mods are a major substrate for the FTO protein, that functions to control processing of pre-mRNAs or other nuclear RNAs.
Could RNA methylation hold potential for a brand new epigenetic mechanism? Check out what the team suggests atNature Chemical Biology, October 2011.