Genes disrupted in schizophrenia may be revealed by de novo mutations in affected persons from otherwise healthy families. Furthermore, during normal brain development, genes are expressed in patterns specific to developmental stage and neuroanatomical structure. We identified de novo mutations in persons with schizophrenia and then mapped the responsible genes onto transcriptome profiles of normal human brain tissues from age 13 weeks gestation to adulthood. In the dorsolateral and ventrolateral prefrontal cortex during fetal development, genes harboring damaging de novo mutations in schizophrenia formed a network significantly enriched for transcriptional coexpression and protein interaction. The 50 genes in the network function in neuronal migration, synaptic transmission, signaling, transcriptional regulation, and transport. These results suggest that disruptions of fetal prefrontal cortical neurogenesis are critical to the pathophysiology of schizophrenia. These results also support the feasibility of integrating genomic and transcriptome analyses to map critical neurodevelopmental processes in time and space in the brain. Display omitted •De novo damaging mutations are enriched in schizophrenia•Schizophrenia genes are highly coexpressed in fetal prefrontal cortex•Schizophrenia genes operate in pathways important for brain development•Disruptions of fetal prefrontal cortical neurogenesis are critical to schizophrenia Integrating sequencing data from persons with schizophrenia and their healthy siblings with transcript data from human brain samples at different points in development reveals a network of genes coexpressed specifically in the prefrontal cortex during fetal development. The findings contextualize disease-related mutations and implicate cortical neurogenesis defects in schizophrenia.