Effects of a temperature-sensitive mutation in the immediate-early gene of pseudorabies virus on class II and class III gene transcription.
Effects of a temperature-sensitive mutation in the immediate-early gene of pseudorabies virus on class II and class III gene transcription.
复制标题
伪狂犬病病毒早期基因温度敏感突变对 II 类和 III 类基因转录的影响。
DOI：
10.1128/jvi.61.4.1103-1107.1987
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发表时间：
1987
影响因子：
5.4
通讯作者：
Feldman,LT
中科院分区：
文献类型：
--
作者：
Ahlers,SE;Feldman,LT
伪狂犬病毒即时早期蛋白激活II类和III类基因的转录。目前尚不清楚II类基因的激活是通过细胞因子的激活还是通过即时早期蛋白与因子或DNA的直接相互作用发生的。II类和III类基因的激活是否通过相似或不同的机制发生也不清楚。我们利用伪狂犬病毒即时早期基因的温度敏感突变tsG，研究了RNA聚合酶II和III转录的病毒基因的激活。先前的研究表明，tsG在非允许温度下抑制野生型腺病毒共感染的早期基因转录（L. T. Feldman和S. E. Ahlers， J. Virol. 57:13-17, 1986）。使用这种混合感染系统作为试验，我们获得了一些结果，使我们能够得出关于伪狂犬病毒立即早期蛋白（IEP）作用模式的某些结论。首先，tsG突变抑制II类基因上新转录复合物的形成，但不影响在存在或不存在腺病毒E1A蛋白时形成的预先建立的转录复合物的转录。其次，tsG不抑制III类基因的转录，提示IEP激活II类和III类基因的机制不同。第三，腺病毒E1A蛋白对转录的激活并不比tsG的抑制更明显，这表明温度敏感的IEP参与了一些物理相互作用，从而积极抑制病毒基因的转录。
The pseudorabies virus immediate-early protein activates transcription of both class II and class III genes. At present it is not known whether the activation of class II genes occurs through an activation of cellular factors or by a direct interaction of the immediate-early protein with factors or DNA. It is also not known whether the activation of class II and class III genes occurs by a similar or different mechanism. We utilized tsG, a temperature-sensitive mutation in the immediate-early gene of pseudorabies virus, to study the activation of viral genes transcribed by RNA polymerases II and III. Previous studies have shown that tsG inhibits wild-type adenovirus early gene transcription in coinfections at the nonpermissive temperature (L. T. Feldman and S. E. Ahlers, J. Virol. 57:13-17, 1986). Using this system of mixed infections as an assay, we obtained several results which allowed us to draw certain conclusions about the mode of action of the pseudorabies virus immediate-early protein (IEP). First, the tsG mutation inhibits the formation of new transcription complexes on class II genes, but does not affect transcription from preestablished transcription complexes formed in the presence or absence of the adenovirus E1A protein. Second, tsG does not inhibit transcription from class III genes, suggesting that the activation by IEP of class II and class III genes occurs by different mechanisms. Third, activation of transcription by the adenovirus E1A protein is not dominant to inhibition by tsG, suggesting that the temperature-sensitive IEP is involved in some physical interaction which actively inhibits transcription of viral genes.