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Mice with Impaired Met Tyrosine Kinase Signaling Demonstrate Characteristics Relevant to Autism

Jacob M. Smith, Elizabeth M. Powell

Variants of MET, a receptor tyrosine kinase which binds the ligand Hepatocyte growth factor (HGF), have been linked to elevated risk for developing autism spectrum disorders (ASD) in humans. Though best known as a proto-oncogene, MET also plays important roles during normal development, including the development of the central nervous system. Recent studies in several mouse lines have shown that mice with reduced HGF-Met signaling have altered profiles of interneurons in the cortex, striatum, and hippocampus. Alterations in neuronal development, particularly in the cerebral cortex, may contribute to the pathology of developmental disorders, including autism. Other studies have shown changes in excitatory signaling in the Met-deficient cortex. Interestingly, mice with deficient Met signaling also show behavioral alterations characteristic of autism. Here we review anatomical and behavioral findings in mice with altered HGF - Met signaling.