NG2 expression in NG2 glia is regulated by binding of SoxE and bHLH transcription factors to a Cspg4 intronic enhancer.
NG2 expression in NG2 glia is regulated by binding of SoxE and bHLH transcription factors to a Cspg4 intronic enhancer.
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NG2 神经胶质细胞中的 NG2 表达通过 SoxE 和 bHLH 转录因子与 Cspg4 内含子增强子的结合来调节。
作者：
Gotoh H;Wood WM;Patel KD;Factor DC;Boshans LL;Nomura T;Tesar PJ;Ono K;Nishiyama A
NG2是一种由Cspg4基因编码的1型完整膜糖蛋白。它在被称为NG2胶质细胞或少突胶质细胞的胶质前体细胞上表达，这些细胞广泛存在于发育和成熟的中枢神经系统和血管壁细胞中，但不在成熟的少突胶质细胞、星形胶质细胞、小胶质细胞、神经元或神经干细胞上表达。因此，NG2在啮齿类动物和人类中被广泛用作NG2胶质细胞的标记物。小鼠Cspg4基因的调控元件及其侧翼序列已成功地将转基因小鼠的报告基因和Cre重组酶靶向到NG2胶质细胞上，并应用于中心含有38千碱基Cspg4基因的200千碱基细菌人工染色体盒中。尽管NG2在脑和脊髓中的细胞类型和阶段特异性表达受到严格调控，但调控其转录的机制仍不清楚。在这里，我们描述了一个1.45 kb的小鼠Cspg4基因内含子增强子，该内含子在体外和转基因小鼠中指导EGFP报告基因转录到NG2胶质细胞而不是周细胞。1.45 kb的增强子包含SoxE和基本螺旋-环-螺旋转录因子的结合位点，这些因子的结合元件相互靠近，从而增强子的活性。当在出生后的小鼠大脑中进行测试时，这些结合元素的突变会消除增强子的活性。
NG2 is a type 1 integral membrane glycoprotein encoded by the Cspg4 gene. It is expressed on glial progenitor cells known as NG2 glial cells or oligodendrocyte precursor cells that exist widely throughout the developing and mature central nervous system and vascular mural cells but not on mature oligodendrocytes, astrocytes, microglia, neurons, or neural stem cells. Hence NG2 is widely used as a marker for NG2 glia in the rodent and human. The regulatory elements of the mouse Cspg4 gene and its flanking sequences have been used successfully to target reporter and Cre recombinase to NG2 glia in transgenic mice when used in a large 200-kilobase bacterial artificial chromosome cassette that contained the 38-kilobase Cspg4 gene in the center. Despite the tightly regulated cell type- and stage-specific expression of NG2 in the brain and spinal cord, the mechanisms that regulate its transcription have remained unknown. Here, we describe a 1.45-kb intronic enhancer of the mouse Cspg4 gene that directed transcription of EGFP reporter to NG2 glia but not to pericytes in vitro and in transgenic mice. The 1.45-kb enhancer contained binding sites for SoxE and basic helix-loop-helix transcription factors, and its enhancer activity was augmented cooperatively by these factors, whose respective binding elements were found in close proximity to each other. Mutations in these binding elements abrogated the enhancer activity when tested in the postnatal mouse brain.
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影响因子：
64.8
作者：
Muroyama, Y;Fujiwara, Y;Rowitch, DH
通讯作者：
Rowitch, DH
影响因子：
25
作者：
Hill, Robert A.;Patel, Kiran D.;Goncalves, Christopher M.;Grutzendler, Jaime;Nishiyama, Akiko
通讯作者：
Nishiyama, Akiko
影响因子：
64.8
作者：
Heintzman, Nathaniel D.;Hon, Gary C.;Hawkins, R. David;Kheradpour, Pouya;Stark, Alexander;Harp, Lindsey F.;Ye, Zhen;Lee, Leonard K.;Stuart, Rhona K.;Ching, Christina W.;Ching, Keith A.;Antosiewicz-Bourget, Jessica E.;Liu, Hui;Zhang, Xinmin;Green, Roland D.;Lobanenkov, Victor V.;Stewart, Ron;Thomson, James A.;Crawford, Gregory E.;Kellis, Manolis;Ren, Bing
通讯作者：
Ren, Bing
影响因子：
4.6
作者：
Budde, Holger;Schmitt, Sebastian;Simons, Mikael
通讯作者：
Simons, Mikael
DOI：
10.1523/jneurosci.0805-13.2013
发表时间：
2013-06-05
期刊：
The Journal of neuroscience : the official journal of the Society for Neuroscience
影响因子：
--
作者：
Nakatani H;Martin E;Hassani H;Clavairoly A;Maire CL;Viadieu A;Kerninon C;Delmasure A;Frah M;Weber M;Nakafuku M;Zalc B;Thomas JL;Guillemot F;Nait-Oumesmar B;Parras C
通讯作者：
Parras C