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首页> 美国卫生研究院文献>The Journal of Neuroscience >Connexin 47 (Cx47)-Deficient Mice with Enhanced Green Fluorescent Protein Reporter Gene Reveal Predominant Oligodendrocytic Expression of Cx47 and Display Vacuolized Myelin in the CNS
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Connexin 47 (Cx47)-Deficient Mice with Enhanced Green Fluorescent Protein Reporter Gene Reveal Predominant Oligodendrocytic Expression of Cx47 and Display Vacuolized Myelin in the CNS

机译：具有增强的绿色荧光蛋白报道基因的连接蛋白47（Cx47）缺陷小鼠揭示Cx47的主要少突胶质细胞表达并在CNS中显示空化的髓磷脂

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To further characterize the recently described gap junction gene connexin 47 (Cx47), we generated Cx47-null mice by replacing the Cx47 coding DNA with an enhanced green fluorescent protein (EGFP) reporter gene, which was thus placed under control of the endogenous Cx47 promoter. Homozygous mutant mice were fertile and showed no obvious morphological or behavioral abnormalities. Colocalization of EGFP fluorescence and immunofluorescence of cell marker proteins revealed that Cx47 was mainly expressed in oligodendrocytes in highly myelinated CNS tissues and in few calcium-binding protein S100β subunit-positive cells but not in neurons or peripheral sciatic nerve. This corrects our previous conclusion that Cx47 mRNA is expressed in brain and spinal cord neurons (). Cx47 protein was detected by Western blot analysis after immunoprecipitation in CNS tissues of wild-type mice but not in heart or Cx47-deficient tissues. Electron microscopic analysis of CNS white matter in Cx47-deficient mice revealed a conspicuous vacuolation of nerve fibers, particularly at the site of the optic nerve where axons are first contacted by oligodendrocytes and myelination starts. Initial analyses of Cx32/Cx47-double-deficient mice showed that these mice developed an action tremor and died on average at 51 d after birth. The central white matter of these double-deficient mice exhibited much more abundant vacuolation in nerve fibers than mice deficient only in Cx47.
机译：为了进一步表征最近描述的间隙连接基因连接蛋白47（Cx47），我们用增强的绿色荧光蛋白（EGFP）报告基因替换了编码Cx47的DNA，从而产生了Cx47无小鼠，从而将其置于内源性Cx47启动子的控制之下。纯合突变小鼠能育，没有明显的形态或行为异常。 EGFP荧光和细胞标记蛋白的免疫荧光共定位显示，Cx47主要在高度髓鞘化的CNS组织中少突胶质细胞中表达，在钙结合蛋白S100β亚基阳性细胞中很少表达，而在神经元或周围坐骨神经中则不表达。这纠正了我们先前的结论，即Cx47 mRNA在脑和脊髓神经元中表达（）。在野生型小鼠的CNS组织中进行免疫沉淀后，通过Western blot分析检测到Cx47蛋白，而在心脏或Cx47缺陷组织中则没有。在Cx47缺陷小鼠中对中枢神经系统白质进行电子显微镜分析后，发现神经纤维明显空泡，特别是在视神经的轴突首先与少突胶质细胞接触并开始髓鞘形成的部位。对Cx32 / Cx47-双缺陷小鼠的初步分析表明，这些小鼠在出生后平均51 d出现动作震颤并死亡。与仅缺乏Cx47的小鼠相比，这些双重缺陷的小鼠的中央白质在神经纤维中显示出更多的空泡。

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