Ebert P J, Campbell D B, Levitt P
Department of Pharmacology, Vanderbilt University School of Medicine, 465 21st Ave South, MRB III, Room 8114, Nashville, TN 37232, USA.
Neuroscience. 2006 Nov 3;142(4):1163-81. doi: 10.1016/j.neuroscience.2006.08.012. Epub 2006 Sep 20.
A large family of regulator of G protein signaling (RGS) proteins modulates signaling through G-protein-coupled receptors. Previous studies have implicated RGS4 as a vulnerability gene in schizophrenia. To begin to understand structure-function relationships, we have utilized bacterial artificial chromosome (BAC) methods to create transgenic mice that express green fluorescent protein (GFP) under the control of endogenous RGS4 enhancer elements, circumventing the lack of suitable antibodies for analysis of dynamic patterns of expression. This report follows from the accompanying mapping paper in cerebral cortex, with a focus on developmental and mature expression patterns in subcortical telencephalic, diencephalic and brainstem areas. Based on reporter distribution, the data suggest that alterations in RGS4 function will engender a complex phenotype of increased and decreased neuronal output, with developmental, regional, and cellular specificity.
G蛋白信号调节（RGS）蛋白的一个大家族通过G蛋白偶联受体调节信号传导。先前的研究表明RGS4是精神分裂症的一个易损基因。为了开始理解结构-功能关系，我们利用细菌人工染色体（BAC）方法创建了转基因小鼠，这些小鼠在内源性RGS4增强子元件的控制下表达绿色荧光蛋白（GFP），从而避免了缺乏合适抗体来分析动态表达模式的问题。本报告基于随附的大脑皮质定位论文，重点关注皮质下端脑、间脑和脑干区域的发育和成熟表达模式。根据报告基因的分布，数据表明RGS4功能的改变将导致神经元输出增加和减少的复杂表型，具有发育、区域和细胞特异性。
