Asp Linnéa, Nellåker Christoffer, Karlsson Håkan
Department of Neuroscience, Karolinska Institutet, Stockholm, Sweden.
J Neurovirol. 2007;13(1):29-37. doi: 10.1080/13550280601103125.
Recently, two candidate analogs for human syncytin, denoted syncytins A and B, were identified in the murine genome. These were found to have expression patterns and functions similar to human syncytin. In addition, the identification of glial cells missing (GCM)-binding motifs in putative promoter regions of the mouse syncytins imply analogous regulation. Transcriptional modulation of syncytin by exogenous agents was recently suggested by studies reporting transactivation of syncytin in human cell lines following virus infections. The authors report that influenza A virus infection increased the levels of transcripts encoding Gcm1 and syncytin B, but not syncytin A, in NIH-3T3 cells as well as in mouse primary neurons or glia. Overexpression of human GCM1 in NIH-3T3 cells resulted in increased levels of transcripts encoding syncytin B but not syncytin A. Systemic administration of neurotropic influenza A virus resulted in a neuronal infection and increased levels of Gcm1-encoding transcripts in brains of young mice. The mouse may therefore be useful for studies on the expression and function of endogenous retroviral envelope genes and transcription factors regulating their expression in the placenta and brain during physiological or pathological conditions.
最近，在小鼠基因组中鉴定出了两种人类合胞素的候选类似物，分别称为合胞素A和合胞素B。发现它们具有与人类合胞素相似的表达模式和功能。此外，在小鼠合胞素假定的启动子区域中鉴定出胶质细胞缺失（GCM）结合基序，这意味着存在类似的调控。最近的研究表明，病毒感染后人细胞系中合胞素的反式激活，提示外源性因子对合胞素的转录调控作用。作者报告称，甲型流感病毒感染会增加NIH-3T3细胞以及小鼠原代神经元或神经胶质细胞中编码Gcm1和合胞素B的转录本水平，但不会增加合胞素A的转录本水平。在NIH-3T3细胞中过表达人类GCM1会导致编码合胞素B的转录本水平升高，但不会导致合胞素A的转录本水平升高。向幼鼠脑内注射嗜神经性甲型流感病毒会导致神经元感染，并增加脑中编码Gcm1的转录本水平。因此，小鼠可能有助于研究内源性逆转录病毒包膜基因在生理或病理条件下在胎盘和脑中的表达、功能以及调控其表达的转录因子。
