Fragile X Syndrome, caused by mutation or malfunction of the FMR1 gene that is also implicated in autism, is the most common heritable form of cognitive impairment. Research groups at University of Pennsylvania, led by Tom Jorgens, and at Brown, led Robert Reenan, teamed up to study an analagous gene in fruit flies. In a new study that appeared Oct. 30 in Nature Neuroscience, they report evidence that the FMRP protein, which FMR1 encodes, plays a key role in RNA editing, which is part of the process that turns DNA instructions into proteins that work in the body. The team also linked FMRP and potential pitfalls in RNA editing with another protein called ADAR, particularly at the junction where muscles and nerves meet. Reenan said the findings could produce insights beyond Fragile X or autism: “It is a remarkable finding that FMRP can be linked so directly with ADAR and RNA editing activity. Deranged RNA editing has been implicated in epilepsy, suicidal depression, schizophrenia and even some neurological cancers. These data are surely pointing in the direction of deep connections between numerous distinct diseases of the brain.”