Sp9 Regulates Medial Ganglionic Eminence-Derived Cortical Interneuron Development. (13th May 2018)

• Record Type: Journal Article
• Authors: Liu, Zhidong; Zhang, Zhuangzhi; Lindtner, Susan; Li, Zhenmeiyu; Xu, Zhejun; Wei, Song; Liang, Qifei; Wen, Yan; Tao, Guangxu; You, Yan; Chen, Bin; Wang, Yanling; Rubenstein, John L; Yang, Zhengang
• Is Part Of: Cerebral cortex. Volume 29:Number 6(2019)
• Page Start: 2653
• Page End: 2667
• Publication Date: 2018-05-13
• Subjects: interneurons -- Lhx6 -- Lhx8 -- medial ganglionic eminence -- Nkx2-1 -- parvalbumin -- somatostatin -- Sp9 -- tangential migration; Cerebral cortex -- Periodicals; Brain -- Periodicals; 612.825
• DOI: 10.1093/cercor/bhy133
• Languages: English
• ISSNs: 1047-3211

Abstract

Abstract: Immature neurons generated by the subpallial MGE tangentially migrate to the cortex where they become parvalbumin-expressing (PV + ) and somatostatin (SST + ) interneurons. Here, we show that the Sp9 transcription factor controls the development of MGE-derived cortical interneurons. SP9 is expressed in the MGE subventricular zone and in MGE-derived migrating interneurons. Sp9 null and conditional mutant mice have approximately 50% reduction of MGE-derived cortical interneurons, an ectopic aggregation of MGE-derived neurons in the embryonic ventral telencephalon, and an increased ratio of SST + /PV + cortical interneurons. RNA-Seq and SP9 ChIP-Seq reveal that SP9 regulates MGE-derived cortical interneuron development through controlling the expression of key transcription factors Arx, Lhx6, Lhx8, Nkx2-1, and Zeb2 involved in interneuron development, as well as genes implicated in regulating interneuron migration Ackr3, Epha3, and St18. Thus, Sp9 has a central transcriptional role in MGE-derived cortical interneuron development.