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Transcription factors Sp8 and Sp9 regulate the development of caudal ganglionic eminence‐derived cortical interneurons
Author(s) -
Wei Song,
Du Heng,
Li Zhenmeiyu,
Tao Guangxu,
Xu Zhejun,
Song Xiaolei,
Shang Zicong,
Su Zihao,
Chen Haotian,
Wen Yan,
Liu Guoping,
You Yan,
Zhang Zhuangzhi,
Yang Zhengang
Publication year - 2019
Publication title -
journal of comparative neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.855
H-Index - 209
eISSN - 1096-9861
pISSN - 0021-9967
DOI - 10.1002/cne.24712
Subject(s) - ganglionic eminence , dlx5 , biology , calretinin , neuroscience , interneuron , neurogenesis , reelin , optogenetics , homeobox , subventricular zone , conditional gene knockout , microbiology and biotechnology , gabaergic , transcription factor , genetics , neural stem cell , receptor , inhibitory postsynaptic potential , immunohistochemistry , gene , immunology , stem cell , phenotype
Cortical interneurons are derived from the subcortical medial ganglionic eminence (MGE), caudal ganglionic eminence (CGE) and preoptic area (POA). CGE‐derived cortical interneurons, which comprise around 30% of all cortical interneurons, mainly express Htr3a, calretinin (CR), Reelin (RELN) and vasoactive intestinal polypeptide (VIP). In the present study, we show that transcription factors Sp8 and Sp9 are co‐expressed in the subventricular zone (SVZ) of the dorsal CGE. Conditional knockout of Sp8/9 using the Gsx2‐Cre transgenic line results in severe loss of CGE‐derived cortical interneurons. We observed migration defects of Sp8/9 double mutant CGE‐derived cortical interneurons as they had longer leading processes than controls and they ectopically accumulated in the CGE. Dlx5/6‐CIE conditional deletion of Sp8/9 also leads to a significant reduction in the CGE‐derived cortical interneurons. We provide evidence that Sp8 / 9 coordinately regulate CGE‐derived cortical interneuron development in part through repressing the expression of Pak3 , Robo1 , and Slit1 . Finally, we show that Cxcl14 , a member of the CXC chemokine family, is mainly expressed in CGE‐derived interneurons in cortical layers I and II, and its expression is critically dependent on SP8.