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Trans-kingdom mimicry underlies ribosome customization by a poxvirus kinase

机译：跨王国模仿是痘病毒激酶对核糖体定制的基础

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摘要

Ribosomes have the capacity to selectively control translation through changes in their composition that enable recognition of specific RNA elements(1). However, beyond differential subunit expression during development(2,3), evidence for regulated ribosome specification within individual cells has remained elusive(1). Here we report that a poxvirus kinase phosphorylates serine/threonine residues in the human small ribosomal subunit protein, receptor for activated C kinase (RACK1), that are not phosphorylated in uninfected cells or cells infected by other viruses. These modified residues cluster in an extended loop in RACK1, phosphorylation of which selects for translation of viral or reporter mRNAs with 5' untranslated regions that contain adenosine repeats, so-called polyA-leaders. Structural and phylogenetic analyses revealed that although RACK1 is highly conserved, this loop is variable and contains negatively charged amino acids in plants, in which these leaders act as translational enhancers. Phosphomimetics and interspecies chimaeras have shown that negative charge in the RACK1 loop dictates ribosome selectivity towards viral RNAs. By converting human RACK1 to a charged, plant-like state, poxviruses remodel host ribosomes so that adenosine repeats erroneously generated by slippage of the viral RNA polymerase(4) confer a translational advantage. Our findings provide insight into ribosome customization through trans-kingdom mimicry and the mechanics of species-specific leader activity that underlie poxvirus polyA-leaders(4).
机译：核糖体有能力通过其组成的变化选择性地控制翻译，从而能够识别特定的RNA元素（1）。然而，除了发育过程中亚基的差异表达外（2,3），单个细胞内核糖体规范的证据仍然难以捉摸（1）。在这里，我们报告痘病毒激酶使人小核糖体亚基蛋白（激活的C激酶（RACK1）的受体）中的丝氨酸/苏氨酸残基磷酸化，在未感染的细胞或被其他病毒感染的细胞中未被磷酸化。这些修饰的残基聚集在RACK1的一个延伸环中，其磷酸化作用选择带有腺苷重复序列的5'非翻译区的病毒或报告基因mRNA进行翻译，即所谓的polyA-leaders。结构和系统发育分析表明，尽管RACK1是高度保守的，但该环是可变的，并且在植物中包含带负电荷的氨基酸，其中这些前导序列充当翻译增强子。拟膦化合物和种间嵌合体已显示，RACK1环中的负电荷指示核糖体对病毒RNA的选择性。通过将人RACK1转变为带电的植物样状态，痘病毒可重塑宿主核糖体，从而使腺苷重复错误地由病毒RNA聚合酶的滑动产生（4），从而赋予翻译优势。我们的发现提供了通过跨王国模仿和核糖体polyA-leaders（4）基础的特定物种的leader活动机制对核糖体定制的见解。

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  • 来源
    《Nature》 |2017年第7660期|651-655|共5页
  • 作者

    Jha Sujata; Rollins Madeline G.; Fuchs Gabriele; Procter Dean J.; Hall Elizabeth A.; Cozzolino Kira; Sarnow Peter; Savas Jeffrey N.; Walsh Derek;

  • 作者单位

    Northwestern Univ, Feinberg Sch Med, Dept Microbiol Immunol, Chicago, IL 60611 USA;

    Northwestern Univ, Feinberg Sch Med, Dept Microbiol Immunol, Chicago, IL 60611 USA;

    SUNY Albany, Dept Biol Sci, RNA Inst, Albany, NY 12222 USA;

    Northwestern Univ, Feinberg Sch Med, Dept Microbiol Immunol, Chicago, IL 60611 USA;

    Northwestern Univ, Feinberg Sch Med, Dept Neurol, Chicago, IL 60611 USA;

    Northwestern Univ, Feinberg Sch Med, Dept Neurol, Chicago, IL 60611 USA;

    Stanford Univ, Sch Med, Dept Microbiol & Immunol, Stanford, CA 94305 USA;

    Northwestern Univ, Feinberg Sch Med, Dept Neurol, Chicago, IL 60611 USA;

    Northwestern Univ, Feinberg Sch Med, Dept Microbiol Immunol, Chicago, IL 60611 USA;

  • 收录信息 美国《科学引文索引》(SCI);美国《工程索引》(EI);美国《生物学医学文摘》(MEDLINE);美国《化学文摘》(CA);
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