Autism spectrum disorder (ASD) is a highly heterogeneous neurodevelopmental condition associated with substantial lifelong disability and healthcare burden. Although genetic studies have implicated hundreds of ASD-associated genes, the mechanisms by which these disruptions give rise to diverse behavioral and cognitive phenotypes remain poorly understood. Traditional gene-by-gene approaches are limited, particularly because many ASD genes are pleiotropic and distinct genes often produce overlapping developmental phenotypes, suggesting convergence on shared biological pathways. To address this, I propose a genome- and phenome-wide framework to identify the developmental convergence points- where, when, and how ASD risk genes disrupt neurodevelopment. A major barrier to this effort is the lack of a comprehensive reference map of the cell lineages, developmental trajectories, and regulatory transcription factors that govern neuronal lineage specification during embryonic brain development. Leveraging comparative genomics and the deep homology between mouse and human development, I will generate a high-resolution mouse developmental atlas to define neuroectoderm and neurogenic trajectories as the foundation for this work. This includes a whole-embryo single-cell atlas comprising 12.4 million nuclei from 83 precisely staged mouse embryos spanning embryonic day 8 to birth, with 2–6 hour temporal resolution, representing the deepest and highest-resolution atlas of its kind to date. Using this reference together with new genetic and environmental perturbation datasets, I will systematically pinpoint the cell lineages, developmental timepoints, and gene regulatory programs that serve as shared convergence points across ASD-associated genes during early neurogenesis. This approach will provide a foundation for more precise, pathway-informed therapeutic strategies for ASD.