Exposure to maternal obesity in utero perturbs the organization and maturation of the neural circuitry requiredfor the development of a child’s mental health. In view of the concomitant increase in the prevalence of bothobesity and Autism spectrum disorder (ASD), we crucially need to understand the relationship between thetwo. While maternal obesity significantly increases the risk of ASD in children, how maternal obesity leads toneurodevelopmental disorders in offspring remains unknown. By combining metagenomics, metabolomics,molecular biology, genetics, electrophysiology and behavioral studies both on conventionally colonized and ongerm-free mice, we will test the hypothesis that maternal high fat diet (MHFD) induces a shift in microbialecology which perturbs social behavior and related changes in synaptic strength in offspring. In addition, wewill study the gut-brain axis and specific metabolites responsible for MHFD-mediated ASD-like behaviors inoffspring. By defining the basic molecular and cellular mechanisms underlying MHFD-induced ASD, theknowledge gained in this study may also lead to new probiotic-based non-invasive treatments for millions ofpatients suffering from ASD.