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Abstract Neuronal microexons are a highly conserved class of alternative splicing events enriched in genes with critical functions in nervous system biology1,2. Microexon splicing is often disrupted in the brains of autistic individuals, and mice with microexon deficiencies display autism-like phenotypes1,3,4. However, the full landscape of microexons is not known, and the impact of genetic variation on these exons has not been systematically investigated.
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