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Mutations in the gene encoding the chromatin remodeler  CHD8  are strongly associated with autism spectrum disorder (ASD).  CHD8  haploinsufficiency also results in autistic phenotypes in humans and mice. Although myelination defects have been observed in individuals with ASD, whether oligodendrocyte dysfunction is responsible for autistic phenotypes has remained unknown. Here we show that reduced expression of  CHD8  in oligodendrocytes gives rise to abnormal behavioral phenotypes in mice.  CHD8  was found to regulate the expression of many myelination-related genes and to be required for oligodendrocyte maturation and myelination. Ablation of  Chd8  specifically in oligodendrocytes of mice impaired myelination, slowed action potential propagation and resulted in behavioral deficits including increased social interaction and anxiety-like behavior, with similar effects being apparent in  Chd8  heterozygous mutant mice. Our results thus indicate that  CHD8  is essential for myelination and that dysfunction of oligodendrocytes as a result of  CHD8  haploinsufficiency gives rise to several neuropsychiatric phenotypes.

Oligodendrocyte dysfunction due to Chd8 mutation gives rise to behavioral deficits in mice