Olig1 Function Is Required to Repress Dlx1/2 and Interneuron Production in Mammalian Brain

J.C. Silbereis, H. Nobuta, H.H. Tsai, V.M. Heine, G.L. McKinsey, D.H. Meijer, M.A. Howard, M.A. Petryniak, G.B. Potter, J.A. Alberta, S.C. Baraban, C.D. Stiles, J.L.R. Rubenstein, D.H. Rowitch

    Research output: Contribution to JournalArticleAcademicpeer-review

    Abstract

    Abnormal GABAergic interneuron density, and imbalance of excitatory versus inhibitory tone, is thought to result in epilepsy, neurodevelopmental disorders, and psychiatric disease. Recent studies indicate that interneuron cortical density is determined primarily by the size of the precursor pool inthe embryonic telencephalon. However, factors essential for regulating interneuron allocation from telencephalic multipotent precursors are poorly understood. Here we report that Olig1 represses production of GABAergic interneurons throughout the mouse brain. Olig1 deletion in mutant mice results in ectopic expression and upregulation of Dlx1/2 genes in the ventral medial ganglionic eminences and adjacent regions of the septum, resulting in an ~30% increase in adult cortical interneuron numbers. We show that Olig1 directly represses the. Dlx1/2 I12b intergenic enhancer and that Dlx1/2 functions genetically downstream of Olig1. These findings establish Olig1 as an essential repressor of. Dlx1/2 and interneuron production in developing mammalian brain. © 2014 Elsevier Inc.
    Original languageEnglish
    Pages (from-to)574-587
    JournalNeuron
    Volume81
    Issue number3
    DOIs
    Publication statusPublished - 2014

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