Our Recent Research on FOXP2
Two examples of recent work illustrate the broad scope of our research:
Functional genetic links between language disorders
In November 2008 we published a new research article in the world-leading medical journal New England Journal of Medicine. In this study we used functional genomics to search for genes regulated by the FOXP2 
transcription factor in a human neuronal cell model. We thereby identified the CNTNAP2 neurexin gene as a novel target. In collaboration with Prof. Anthony Monaco's team, also at the Wellcome Trust Centre, we went on to test CNTNAP2 gene variants in children with typical forms of language impairment, and identified a cluster of variants that were significantly associated with poor language performance. This work represented the first identification of a gene associated with common cases of specific language impairment. It also provided intriguing links to other neurodevelopmental disorders; previous work by our collaborators at UCLA, Prof. Daniel Geschwind and colleagues, showed that similar CNTNAP2 variants are associated with language delays in autism.
Reference: Vernes et al. (2008) A functional genetic link between distinct developmental language disorders. N. Engl. J. Med. 359: 2337-2345. [free pdf]
More information can be found in these news articles from the Wellcome Trust, the Times newspaper, Science magazine, and Reuters.
Synaptic plasticity, motor-skill learning and speech
In March 2008 we reported in Current Biology our novel discovery of abnormal functioning of brain circuits in mice that carry mutant forms of the Foxp2 gene. We generated mice with the equivalent mutation to the one which disrupts human FOXP2 in the KE family, the most well-studied example of an inherited speech and language disorder. Mice that carried one normal copy and one mutant copy of Foxp2 (matching the situation for the affected humans) showed overtly normal development. However, these mice displayed deficits when learning to make rapid coordinated sequences of movements. We examined the brain circuits where Foxp2 is normally switched on, which are already suspected to be important for this kind of learning. Crucially, we uncovered abnormalities in the way that the connections between nerve cells are strengthened or weakened (synaptic plasticity) in these circuits.
Reference: Groszer et al. (2008) Impaired synaptic plasticity and motor learning in mice with a point mutation implicated in human speech deficits. Curr. Biol. 18: 354-362. [free pdf]
More information can be found in this news report from the Wellcome Trust, a feature article published in New Scientist magazine in August 2008, and the Nature Neuroscience podcast from June 2008.