Epilepsy is a common neurological disorder (3.4 million adults and 470,000 children) defined by recurrent seizures. Medically intractable (drug resistant) epilepsy affects approximately one-third of adults and 20-25% of children. Intractable epilepsy is often the result of germline gene mutations e.g., ion channels, kinases, neurotransmitter receptor subunits, identified in patient blood. Interestingly, recent studies have revealed somatic mosaicism associated with epilepsy in which variants are focally present in a subset of brain cells and cause epilepsy-associated focal malformations of cortical development (MCD). SLC35A2, was recently identified in a substantial fraction focal cortical dysplasia type 1a specimens. SLC35A2 encodes UGT-1, a transmembrane UDP-galactose transporter that facilitates movement of UDP-galactose from the cytosol to the lumen of the Golgi apparatus. Further, the variant allele frequency (VAF) in somatic SLC35A2 patients appears to correlate with severity in phenotype i.e., higher allelic burden is associated with greater morbidity. Patients exhibit a range of phenotypes including MRI confirmed FCD, intractable seizures, and intellectual disability. Germline variants in SLC35A2 are categorized under congenital disorders of glycosylation (CDG) and are implicated in an X-linked developmental and epileptic encephalopathy. All pathogenic variants, both somatic and germline, prevent UDP-galactose from being transported across the Golgi membrane and thus lead to aberrant glycosylated proteoglycans. Solute carrier families (SLCs) are the largest family of transmembrane transporters of sugars and a portion of these genes are implicated in epilepsy, neurodegenerative diseases, and autism spectrum disorder. To date, no study has addressed the effects of SLC35A2 knockout (KO) on neuronal morphology, protein glycosylation, or cortical lamination in a mouse model despite SLC35A2 mutations being recognized as a common cause of drug resistant epilepsy. I hypothesize that Slc35a2 KO results in disrupted neuronal Golgi structure, aberrant dendritic arborization, altered glycosylation profiles, aberrant cortical lamination, and disrupted network integrity. I will test this hypothesis under 4 specific aims: 1) To define the consequences of Slc35a2 KO in vitro on Golgi structure and dendritic arborization, 2) To demonstrate that Slc35a2 KO results in aberrant glycosylation profiles in mouse neurons, 3) To demonstrate that Slc35a2 KO in vivo alters cortical lamination and network integrity in mice using in utero electroporation, and 4) To establish 2 conditional KO (cKO) mouse lines of Slc35a2 and demonstrate that they alter cortical architecture and network integrity.