Newly published research has found that variations in the MET tyrosine kinase receptor are significantly associated with autism. It is estimated that presence of a specific allele may almost double the risk of developing the disorder. Parallel to human genetic studies, MET signaling has been studied in animal models to determine the role of MET on brain development. MET has been shown to be responsible for normal migration of neurons by interacting with a molecule called hepatocyte growth factor/scatter factor (HGF/SF). Loss of this molecule (HGF/SF) leads to a reduction in the number of neurons which release GABA as a neurotransmitter, specifically a class of neurons called “interneurons”. These interneurons connect with cells both within and outside specific brain regions to monitor and modulate normal activity levels. In this way, brain cells can integrate information from several different sources. The current research program proposes to examine the role of HGF/SF and MET on the development of GABAergic inhibitory interneurons in the developing mouse embryo. The experiments will artificially eliminate HCF/SF-MET function where these interneurons are generated and link this back to impairments in proper migration of GABAergic interneurons. The fellow on this project has a background in psychology and cognition, and will be trained on advanced molecular biology techniques to further examine if rescue of MET function can reverse these deficits. What this means for people with autism: This work is relevant to the growing body of evidence suggesting altered GABAergic signaling in the brains of individuals with autism and will specifically advance the understanding about embryonic perturbations in the development of GABAergic interneurons in the brain.