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Polymicrogyria is a neurodevelopmental condition defined by excessive folding of the neocortex due to disruptions in neural migration which led to malformed sulci and gyri. The condition has an array of clinical presentations including impaired intellectual development, seizures, and cerebral palsy. Whole genome sequencing of a patient with polymicrogyria revealed a likely pathogenic variant in the X-linked gene bromodomain and WD-repeat domain containing 3 (BRWD3). Bromodomains are regions on histone acetyltransferases that are involved in epigenetic regulation and gene activation. Malformations in the human neocortex such as macrocephaly and microcephaly have previously been associated with pathogenic variants in bromodomain coding regions. Here, we created the mouse model of Brwd3 recapitulating the human variant (S1320L). In situ RNA hybridization revealed Brwd3 is differentially expressed in the neocortex at various points in embryonic development, as well as the basal ganglia, hippocampus, and neural tube. Brwd3 mRNA is also expressed in intermediate progenitors and radial glia cells. Brwd3S1320L/Y hemizygous male mice survive at normal rates. Immunohistochemistry revealed an abnormal distribution of known neocortical layer markers, CTIP2, SATB2, and CUX1 in Brwd3S1320L/Y males. Neuronal migration was more directly observed through tracking proliferating neurons in the neocortex through an EdU pulse chase experiment suggesting compromised migration of upper-layer cortical neurons. Whole genome RNA-sequencing revealed differential expression of many genes known for their roles in cell adhesion such as laminin. Cre-dependent stochastic labeling of neocortical neurons revealed a decrease in multipolar neurons in the cortical plate suggesting reduced neuronal complexity during cortical circuit formation. Here, we demonstrate BRWD3 is involved in neocortical development.