Diverse autism mutations converge on a shared chromatin-regulation network in stem-cell–derived human cortex

A large hiPSC-based study generated cortical organoids from eight ASD-risk mutations, idiopathic ASD, and controls, profiling gene expression across 25–100 days. Early mutation-specific changes give way to convergent transcriptional and chromatin-regulatory disruptions enriched for ASD risk genes, including SWI–SNF components. CRISPRi validation supports key regulators driving this convergent network, suggesting that diverse genetic risks in ASD propagate through shared transcriptional pathways that affect early neurodevelopment, while idiopathic cases show less convergence.