Analysis of the cell cycle regulatory protein (E2F1) after infection of cultured cells with bovine herpesvirus 1 (BHV-1) or herpes simplex virus type 1 (HSV-1).
Analysis of the cell cycle regulatory protein (E2F1) after infection of cultured cells with bovine herpesvirus 1 (BHV-1) or herpes simplex virus type 1 (HSV-1).
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DOI：
10.1016/j.virusres.2011.05.009
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发表时间：
2011-09
期刊：
影响因子：
5
通讯作者：
Jones, Clinton
中科院分区：
文献类型：
--
作者：
Workman, Aspen;Jones, Clinton
细胞转录因子 E2F 家族控制细胞周期进程和细胞死亡。在细胞周期进程中，激活的细胞周期蛋白依赖性激酶磷酸化视网膜母细胞瘤 (Rb) 蛋白，导致 E2F 家族成员的释放和激活。先前的研究表明，牛疱疹病毒1（BHV-1）生产性感染会增加E2F1蛋白水平，bICP0早期启动子被E2F1或E2F2激活超过100倍，沉默E2F1会降低生产性感染的效率。在本研究中，在相同的允许细胞系、兔皮肤（RS）细胞中，将 HSV-1 有效感染对 E2F 蛋白水平和 E2F 依赖性转录调节的影响与 BHV-1 感染进行了比较。使用特定的 siRNA 沉默 E2F1，可使 RS 细胞中单纯疱疹病毒 1 型 (HSV-1) 的有效感染减少约 10 倍，并且在有效感染期间总 E2F1 蛋白水平增加。与感染 BHV-1 的 RS 细胞相比，总 E2F1 蛋白水平的一部分位于 HSV-1 感染的 RS 细胞的细胞质中。此外，E2F1 不能有效地反式激活 HSV-1 ICP0 或 ICP4 启动子。当RS细胞用E2F报告构建体或细胞周期蛋白D1启动子转染，然后用BHV-1感染时，启动子活性在感染后增加。相反，RS细胞的HSV-1感染对E2F依赖性转录影响不大，并且细胞周期蛋白D1启动子活性降低。总之，这些研究表明沉默 E2F1 降低了 HSV-1 和 BHV-1 生产性感染的效率。然而，只有 BHV-1 有效感染诱导 E2F 依赖性转录。
The E2F family of cellular transcription factors controls cell cycle progression and cell death. During cell cycle progression, activated cyclin-dependent kinases phosphorylate the retinoblastoma (Rb) protein, causing the release and activation of E2F family members. Previous studies demonstrated that bovine herpes virus 1 (BHV-1) productive infection increases E2F1 protein levels, the bICP0 early promoter is activated more than 100 fold by E2F1 or E2F2, and silencing E2F1 reduced the efficiency of productive infection. In this study, the effect of HSV-1 productive infection on E2F protein levels and regulation of E2F dependent transcription was compared to BHV-1 infection in the same permissive cell line, rabbit skin (RS) cells. Silencing E2F1 with a specific siRNA reduced herpes simplex virus type 1 (HSV-1) productive infection approximately 10 fold in RS cells, and total E2F1 protein levels increased during productive infection. In contrast to RS cells infected with BHV-1, a fraction of total E2F1 protein levels was localized to the cytoplasm in HSV-1 infected RS cells. Furthermore, E2F1 did not efficiently trans-activate the HSV-1 ICP0 or ICP4 promoter. When RS cells were transfected with an E2F reporter construct or the cyclin D1 promoter and then infected with BHV-1, promoter activity increased after infection. In contrast, HSV-1 infection of RS cells had little effect on E2F dependent transcription and cyclin D1 promoter activity was reduced. In summary, these studies indicated that silencing E2F1 reduced the efficiency of HSV-1 and BHV-1 productive infection. However, only BHV-1 productive infection induced E2F dependent transcription.
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