在单纯疱疹病毒 1 感染过程中，使核糖体生物发生调节与 RNA 聚合酶 I 活性解耦。
Uncoupling ribosome biogenesis regulation from RNA polymerase I activity during herpes simplex virus type 1 infection.
机构信息
Centre National de la Recherche Scientifique (CNRS), Université de Lyon, Lyon F-69003, France.
出版信息
RNA. 2010 Jan;16(1):131-40. doi: 10.1261/rna.1935610. Epub 2009 Nov 24.
Abstract
The ribosome is the central effector of protein synthesis, and its synthesis is intimately coordinated with that of proteins. At present, the most documented way to modulate ribosome biogenesis involves control of rDNA transcription by RNA polymerase I (RNA Pol I). Here we show that after infection of human cells with herpes simplex virus type 1 (HSV-1) the rate of ribosome biogenesis is modulated independently of RNA Pol I activity by a dramatic change in the rRNA maturation pathway. This process permits control of the ribosome biogenesis rate, giving the possibility of escaping ribosomal stress and eventually allowing assembly of specialized kinds of ribosomes.
摘要
核糖体是蛋白质合成的核心效应器，其合成与蛋白质的合成密切协调。目前，调节核糖体生物发生的最有文献记载的方法涉及 RNA 聚合酶 I（RNA Pol I）对 rDNA 转录的控制。在这里，我们表明，在人类细胞感染单纯疱疹病毒 1 型（HSV-1）后，核糖体生物发生的速度通过 rRNA 成熟途径的显著变化而独立于 RNA Pol I 活性进行调节。这个过程允许控制核糖体生物发生的速度，有可能逃避核糖体压力，并最终允许专门类型的核糖体的组装。
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