Activation of early adenovirus transcription by the herpesvirus immediate early gene: evidence for a common cellular control factor.
Activation of early adenovirus transcription by the herpesvirus immediate early gene: evidence for a common cellular control factor.
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疱疹病毒立即早期基因激活早期腺病毒转录：常见细胞控制因子的证据。
DOI：
10.1073/pnas.79.16.4952
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发表时间：
1982
影响因子：
11.1
通讯作者：
Nevins,JR
中科院分区：
文献类型：
--
作者：
Feldman,LT;Imperiale,MJ;Nevins,JR
携带缺陷型E1A基因的腺病毒突变体，如dl312，在感染HeLa细胞后不能表达任何早期病毒基因。然而，当dl312感染的HeLa细胞与伪狂犬病病毒（一种疱疹病毒）共感染时，获得了其他早期腺病毒基因的有效表达。通过使用温度敏感的伪狂犬病突变体（tsG 1），证明负责诱导腺病毒转录的疱疹病毒功能是立即早期基因，这是激活疱疹病毒早期基因表达和维持早期和晚期疱疹病毒转录所需的基因。具体而言，共感染dl312和tsG1的HeLa细胞，当转移到非允许温度时，失去了表达早期腺病毒基因的能力。此外，激活早期腺病毒基因表达疱疹病毒合并感染发生更早，在一个更高的水平比野生型腺病毒感染。因此，疱疹病毒立即早期蛋白不仅激活早期腺病毒转录单位，而且显然比腺病毒E1A基因产物更有效。由于这一事实，我们认为，激活，无论是由E1A蛋白或疱疹病毒立即早期蛋白，最有可能间接发生通过与细胞蛋白的相互作用，而不是通过在腺病毒启动子的调节序列的直接识别。
Adenovirus mutants carrying a defective E1A gene, such as dl312, are unable to express any of the early viral genes upon infection of HeLa cells. However, efficient expression of the other early adenovirus genes was obtained when dl312-infected HeLa cells were coinfected with pseudorabies virus, a herpesvirus. By employing a temperature-sensitive pseudorabies mutant (tsG1) it was demonstrated that the herpesvirus function responsible for the induction of adenovirus transcription was the immediate early gene, a gene required for the activation of herpesvirus early gene expression and the maintenance of early and late herpesvirus transcription. Specifically, HeLa cells coinfected with dl312 and tsG1, when shifted to the nonpermissive temperature, lost their capacity to express the early adenovirus genes. Furthermore, activation of early adenovirus gene expression in herpesvirus coinfection occurred earlier and at a higher level than in wild-type adenovirus infection. Therefore, the herpesvirus immediate early protein not only activates the early adenovirus transcription units but apparently does so more efficiently than the adenovirus E1A gene product. Because of this fact, we argue that the activation, either by the E1A protein or the herpesvirus immediately early protein, most likely occurs indirectly through interaction with a cellular protein rather than by a direct recognition of regulatory sequences at the adenovirus promoters.