{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,13]],"date-time":"2026-09-13T20:40:11Z","timestamp":1789332011409,"version":"build-2803163510"},"reference-count":75,"publisher":"Oxford University Press (OUP)","issue":"9","license":[{"start":{"date-parts":[[2026,2,3]],"date-time":"2026-02-03T00:00:00Z","timestamp":1770076800000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/100000065","name":"National Institute of Neurological Disorders and Stroke","doi-asserted-by":"publisher","award":["R01 NS100007"],"award-info":[{"award-number":["R01 NS100007"]}],"id":[{"id":"10.13039\/100000065","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000065","name":"National Institute of Neurological Disorders and Stroke","doi-asserted-by":"publisher","award":["R01 NS113516"],"award-info":[{"award-number":["R01 NS113516"]}],"id":[{"id":"10.13039\/100000065","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2026,9,7]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>Cortical interneuron (cIN) dysfunction is associated with various neurodevelopmental and neurological disorders, including developmental epilepsies, autism spectrum disorders and intellectual disabilities. Mutations in ARX (aristaless-related homeobox) are linked to these conditions, with or without accompanying structural brain anomalies. We previously demonstrated that the loss of Arx in the mouse ganglionic eminence, the birthplace of cINs, is associated with seizures, whereas its loss in cortical excitatory neuron progenitor cells results in structural anomalies but no seizures.<\/jats:p>\n                  <jats:p>To elucidate the pathophysiological role of ARX in cINs and its relationship to seizure phenotype, Arx conditional mutant mouse lines were investigated using Gad2- and Nkx2.1-Cre drivers to target distinct populations in the cIN lineage.<\/jats:p>\n                  <jats:p>Our data demonstrate that ARX abrogation results in defects in cIN density and distribution, as well as perinatal lethality. In these mice, we observed defects in cell cycle exit, a biased loss of the marginal zone migration stream of cINs, shifts in cell fate from caudal ganglionic eminence to medial ganglionic eminence identity, and a reduced number of parvalbumin\u207a and somatostatin\u207a cINs, with parvalbumin\u207a cINs being more severely affected. Single-cell RNA sequencing combined with chromatin immunoprecipitation and sequencing revealed that ARX regulates key processes involved in cell cycle progression, cIN subtype differentiation and cIN migration.<\/jats:p>\n                  <jats:p>Investigation of one downregulated target gene, Lmo1, uncovered a potential mechanism by which ARX regulates the number and distribution of cINs in the cortex. Cortical slice cultures demonstrate that LMO1 inhibits cIN migration by repressing Cxcr4 expression, which encodes a key receptor involved in cortical guidance. These data indicate that ARX positively regulates cIN migration by derepressing LMO1's repressive role. Consistent with our mouse model, we observed a significant loss of parvalbumin+ and somatostatin+ cINs in the brain of a patient carrying a pathogenic variant of ARX, who was diagnosed with developmental epileptic encephalopathy.<\/jats:p>\n                  <jats:p>Together, our data provide novel insights into how ARX and its target genes regulate cIN development and migration and into the pathogenic mechanisms underlying a spectrum of neurodevelopmental disorders linked to loss of ARX.<\/jats:p>","DOI":"10.1093\/brain\/awag036","type":"journal-article","created":{"date-parts":[[2026,1,30]],"date-time":"2026-01-30T12:45:55Z","timestamp":1769777155000},"page":"3197-3213","source":"Crossref","is-referenced-by-count":2,"title":["<i>ARX<\/i>\n                    mutation-associated interneuron defects provide insights into mechanisms underlying developmental epilepsies"],"prefix":"10.1093","volume":"149","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-7842-3244","authenticated-orcid":false,"given":"Youngshin","family":"Lim","sequence":"first","affiliation":[{"name":"Department of Pathology and Laboratory Medicine, Cedars-Sinai Medical Center , Los Angeles, CA 90048 ,","place":["USA"]},{"name":"Department of Biomedical Science Education, Charles R Drew University of Medicine and Science , Los Angeles, CA 90059 ,","place":["USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shyam K","family":"Akula","sequence":"additional","affiliation":[{"name":"Division of Genetics and Genomics, Manton Center for Orphan Disease Research, Boston Children\u2019s Hospital , Boston, MA 02115 ,","place":["USA"]},{"name":"Departments of Pediatrics and Neurology, Harvard Medical School , Boston, MA 02115 ,","place":["USA"]},{"name":"Howard Hughes Medical Institute , Chevy Chase, MD 20815 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