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首页> 外文期刊>Molecular and Cellular Biology >Effect of adenovirus on metabolism of specific host mRNAs: transport control and specific translational discrimination.
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Effect of adenovirus on metabolism of specific host mRNAs: transport control and specific translational discrimination.

机译：腺病毒对特定宿主mRNA代谢的影响：转运控制和特异性翻译区分。

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We have studied the adenovirus-induced inhibition of host cell protein synthesis and the effect of infection on the overall metabolism of host cell mRNA during the late phase of adenovirus infection by following the fate of a number of cellular mRNAs complementary to specific cloned DNA segments. At a time in infection when the rate of total cellular protein synthesis is drastically (greater than 90%) reduced, transcription of specific cellular genes is undiminished. However, the transport of newly synthesized cellular mRNA to the cytoplasm is greatly decreased. This decreased appearance of new mRNA in the cytoplasm cannot account for the observed cessation of cell specific protein synthesis, however, since the concentration of several preexisting cellular mRNAs, including the mRNA for actin, remains unchanged throughout the course of infection. The preexisting mRNA is intact, capped, and functional as judged by its ability to direct protein synthesis in vitro in a cap-dependent fashion. The interruption in host translation appears to operate at the level of initiation directly, since we find that fewer ribosomes are associated with a given cellular mRNA after infection than before infection. Furthermore, the in vivo inhibition of cellular protein synthesis does not appear to be the result of competition with viral mRNA, since conditions which prevent the efficient initiation of translation of viral mRNA (infection with a viral mutant) do not result in the recovery of cell translation. Thus, it appears that a late adenovirus gene product directly mediates a shutoff of host protein synthesis.
机译：我们已经研究了腺病毒诱导的宿主细胞蛋白合成的抑制作用以及在腺病毒感染后期感染对宿主细胞mRNA总体代谢的影响的作用，方法是追踪许多与特定克隆的DNA片段互补的细胞mRNA的命运。在感染期间，当细胞总蛋白的合成速率急剧下降（大于90％）时，特定细胞基因的转录不会降低。但是，大大减少了新合成的细胞mRNA向细胞质的转运。然而，由于在感染过程中几种先前存在的细胞mRNA（包括肌动蛋白的mRNA）的浓度保持不变，因此细胞质中新mRNA的这种减少的出现不能解释观察到的细胞特异性蛋白质合成的停止。预先存在的mRNA通过以帽依赖方式体外指导蛋白质合成的能力来判断是完整的，有帽的和有功能的。宿主翻译的中断似乎直接在起始水平上起作用，因为我们发现感染后与给定细胞mRNA相关的核糖体少于感染前。此外，体内抑制细胞蛋白质合成似乎不是与病毒mRNA竞争的结果，因为阻止病毒mRNA翻译有效启动的条件（感染病毒突变体）不会导致细胞恢复。翻译。因此，似乎晚期腺病毒基因产物直接介导了宿主蛋白合成的关闭。

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