Inhibition of host cell RNA polymerase III-mediated transcription by poliovirus: inactivation of specific transcription factors.
Inhibition of host cell RNA polymerase III-mediated transcription by poliovirus: inactivation of specific transcription factors.
复制标题
脊髓灰质炎病毒对宿主细胞 RNA 聚合酶 III 介导的转录的抑制：特定转录因子的失活。
DOI：
10.1128/mcb.7.11.3880-3887.1987
复制
发表时间：
1987
影响因子：
5.3
通讯作者：
Dasgupta,A
中科院分区：
文献类型：
--
作者：
Fradkin,LG;Yoshinaga,SK;Berk,AJ;Dasgupta,A
研究了脊髓灰质炎病毒感染细胞中 RNA 聚合酶 III 对转录的抑制。利用两种不同细胞系的实验表明，RNA 聚合酶 III 的转录起始步骤因这些细胞被病毒感染而受到损害。观察到的转录抑制并不是由于脊髓灰质炎病毒关闭宿主细胞蛋白质合成所致。在克隆 DNA 模板体外准确转录所需的四种不同成分中，RNA 聚合酶 III 和转录因子 TFIIIA 的活性并未受到病毒感染的显着影响。转录因子 TFIIIC（RNA 聚合酶 III 基因转录所需的限制成分）的活性在受感染的细胞中受到严重抑制，而转录因子 TFIIIB 的活性受到较小程度的抑制。然而，TFIIIC 与腺病毒 VA1 基因内部启动子的序列特异性 DNA 结合不会因病毒感染细胞而改变。我们得出的结论是：（i）至少有两种转录因子 TFIIIB 和 TFIIIC 受到脊髓灰质炎病毒感染细胞的抑制，（ii）TFIIIC 的失活并不涉及其 DNA 结合结构域的破坏，（iii）TFIIIC 的序列特异性 DNA 结合可能是必要的，但不足以形成有效的转录复合物。
The inhibition of transcription by RNA polymerase III in poliovirus-infected cells was studied. Experiments utilizing two different cell lines showed that the initiation step of transcription by RNA polymerase III was impaired by infection of these cells with the virus. The observed inhibition of transcription was not due to shut-off of host cell protein synthesis by poliovirus. Among four distinct components required for accurate transcription in vitro from cloned DNA templates, activities of RNA polymerase III and transcription factor TFIIIA were not significantly affected by virus infection. The activity of transcription factor TFIIIC, the limiting component required for transcription of RNA polymerase III genes, was severely inhibited in infected cells, whereas that of transcription factor TFIIIB was inhibited to a lesser extent. The sequence-specific DNA-binding of TFIIIC to the adenovirus VA1 gene internal promoter, however, was not altered by infection of cells with the virus. We conclude that (i) at least two transcription factors, TFIIIB and TFIIIC, are inhibited by infection of cells with poliovirus, (ii) inactivation of TFIIIC does not involve destruction of its DNA-binding domain, and (iii) sequence-specific DNA binding by TFIIIC may be necessary but is not sufficient for the formation of productive transcription complexes.