Abstract
Mutations in Chromodomain Helicase DNA Binding Protein 8 (CHD8) are among the most common de novo mutations associated with autism spectrum disorder (ASD). CHD8 is a chromatin modifier that affects expression of many other ASD-risk genes. Mutations in CHD8 define an ASD subtype characterized by macrocephaly and gastro-intestinal (GI) problems. The field is currently interested in investigating the bidirectional communication between the gut microbiome and brain (the gut-brain-axis) in ASD. Our goal is to elucidate the role of CHD8 and the gut-brain axis in ASD by determining neural and GI phenotypes caused by loss-of-function mutations in kismet (kis), the Drosophila ortholog of CHD8. Our previous work has shown that CHD8/kis heterozygous mutants exhibit axon pathfinding defects & behavioral impairments. Here, we provide data demonstrating that CHD8/kismet heterozygous mutant flies exhibit: (1) a significant increase in GI transit time, and (2) differences in the composition of their gut microbiome.