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NIK1-mediated translation suppression functions as a plant antiviral immunity mechanism

机译:NIK1介导的翻译抑制功能起植物抗病毒免疫机制的作用

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摘要

Plants and plant pathogens are subject to continuous co-evolutionary pressure for dominance, and the outcomes of these interactions can substantially impact agriculture and food security'. In virusplant interactions, one of the major mechanisms for plant antiviral immunity relies on RNA silencing, which is often suppressed by co-evolving virus suppressors, thus enhancing viral pathogenicity in susceptible hosts'. In addition, plants use the nucleotide-binding and leucine-rich repeat (NB-LRR) domain-containing resistance proteins, which recognize viral effectors to activate effector-triggered immunity in a defence mechanism similar to that employed in nonviral infections'''. Unlike most eukaryotic organisms, plants are not known to activate mechanisms of host global translation suppression to fight viruses'''. Here we demonstrate in Arabidopsis that the constitutive activation of NIK1, a leucine-rich repeat receptor-like kinase (LRR-RLK) identified as a virulence target of the begomovirus nuclear shuttle protein (NSP)(4-6), leads to global translation suppression and translocation of the downstream component RPL 10 to the nucleus, where it interacts with a newly identified MYB-like protein, Lb-INTERACTING MYB DOMAIN-CONTAINING PROTEIN (LIMYB), to downregulate translational machinery genes fully. LIMYB overexpression represses ribosomal protein genes at the transcriptional level, resulting in protein synthesis inhibition, decreased viral messenger RNA association with polysome fractions and enhanced tolerance to begomovirus. By contrast, the loss of LIMYB function releases the repression of translation-related genes and increases susceptibility to virus infection. Therefore, LIMYB links immune receptor LRR-RLK activation to global translation suppression as an antiviral immunity strategy in plants.
机译:植物和植物病原体一直处于持续的共同进化压力之下,而这种相互作用的结果会极大地影响农业和粮食安全。在病毒植物相互作用中,植物抗病毒免疫的主要机制之一是依赖于RNA沉默,RNA沉默通常被共同进化的病毒抑制剂抑制,从而增强了易感宿主的病毒致病性。此外,植物使用含有核苷酸结合和富含亮氨酸的重复序列(NB-LRR)的抗性蛋白,该蛋白识别病毒效应子以激活效应子触发的免疫,其防御机制类似于非病毒感染中的防御机制。与大多数真核生物不同,尚不知道植物会激活宿主整体翻译抑制机制来对抗病毒。在这里,我们在拟南芥中证明NIK1的组成型激活是富含亮氨酸的重复受体样激酶(LRR-RLK),被确定为begomovirus核穿梭蛋白(NSP)的毒力靶标(4-6),导致整体翻译下游成分RPL 10的抑制和易位到细胞核,并与新鉴定的MYB样蛋白Lb相互作用MYB含域蛋白(LIMYB)相互作用,从而完全下调翻译机制基因。 LIMYB的过表达在转录水平上抑制核糖体蛋白基因,从而导致蛋白质合成受到抑制,病毒信使RNA与多核糖体组分的缔合减少,并增强了对begomovirus的耐受性。相比之下,LIMYB功能的丧失释放了翻译相关基因的抑制,并增加了对病毒感染的敏感性。因此,LIMYB将免疫受体LRR-RLK激活与整体翻译抑制联系起来,作为植物中的抗病毒免疫策略。

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  • 来源
    《Nature》 |2015年第7549期|679-682|共4页
  • 作者单位

    Univ Fed Vicosa, Bioagro, Natl Inst Sci & Technol Plant Pest Interact, Dept Bioquim & Biol Mol, BR-36570000 Vicosa, MG, Brazil|Univ Fed Vicosa, Bioagro, Natl Inst Sci & Technol Plant Pest Interact, BR-36570000 Vicosa, MG, Brazil;

    Univ Fed Vicosa, Bioagro, Natl Inst Sci & Technol Plant Pest Interact, Dept Bioquim & Biol Mol, BR-36570000 Vicosa, MG, Brazil|Univ Fed Vicosa, Bioagro, Natl Inst Sci & Technol Plant Pest Interact, BR-36570000 Vicosa, MG, Brazil;

    Univ Fed Vicosa, Bioagro, Natl Inst Sci & Technol Plant Pest Interact, Dept Bioquim & Biol Mol, BR-36570000 Vicosa, MG, Brazil|Univ Fed Vicosa, Bioagro, Natl Inst Sci & Technol Plant Pest Interact, BR-36570000 Vicosa, MG, Brazil;

    Univ Fed Vicosa, Bioagro, Natl Inst Sci & Technol Plant Pest Interact, Dept Bioquim & Biol Mol, BR-36570000 Vicosa, MG, Brazil|Univ Fed Vicosa, Bioagro, Natl Inst Sci & Technol Plant Pest Interact, BR-36570000 Vicosa, MG, Brazil;

    Univ Fed Vicosa, Bioagro, Natl Inst Sci & Technol Plant Pest Interact, Dept Bioquim & Biol Mol, BR-36570000 Vicosa, MG, Brazil|Univ Fed Vicosa, Bioagro, Natl Inst Sci & Technol Plant Pest Interact, BR-36570000 Vicosa, MG, Brazil;

    Univ Fed Vicosa, Bioagro, Natl Inst Sci & Technol Plant Pest Interact, Dept Bioquim & Biol Mol, BR-36570000 Vicosa, MG, Brazil|Univ Fed Vicosa, Bioagro, Natl Inst Sci & Technol Plant Pest Interact, BR-36570000 Vicosa, MG, Brazil;

    Univ Fed Vicosa, Bioagro, Natl Inst Sci & Technol Plant Pest Interact, Dept Bioquim & Biol Mol, BR-36570000 Vicosa, MG, Brazil|Univ Fed Vicosa, Bioagro, Natl Inst Sci & Technol Plant Pest Interact, BR-36570000 Vicosa, MG, Brazil;

    Univ Fed Vicosa, Bioagro, Natl Inst Sci & Technol Plant Pest Interact, Dept Bioquim & Biol Mol, BR-36570000 Vicosa, MG, Brazil|Univ Fed Vicosa, Bioagro, Natl Inst Sci & Technol Plant Pest Interact, BR-36570000 Vicosa, MG, Brazil;

    Univ Fed Vicosa, Bioagro, Natl Inst Sci & Technol Plant Pest Interact, Dept Bioquim & Biol Mol, BR-36570000 Vicosa, MG, Brazil|Univ Fed Vicosa, Bioagro, Natl Inst Sci & Technol Plant Pest Interact, BR-36570000 Vicosa, MG, Brazil;

    Univ Fed Vicosa, Bioagro, Natl Inst Sci & Technol Plant Pest Interact, BR-36570000 Vicosa, MG, Brazil|Univ Fed Rio de Janeiro, Dept Genet, BR-21944970 Rio De Janeiro, Brazil;

    Univ Fed Vicosa, Bioagro, Natl Inst Sci & Technol Plant Pest Interact, Dept Bioquim & Biol Mol, BR-36570000 Vicosa, MG, Brazil|Univ Fed Vicosa, Bioagro, Natl Inst Sci & Technol Plant Pest Interact, BR-36570000 Vicosa, MG, Brazil;

    Univ Fed Vicosa, Bioagro, Natl Inst Sci & Technol Plant Pest Interact, Dept Bioquim & Biol Mol, BR-36570000 Vicosa, MG, Brazil|Univ Fed Vicosa, Bioagro, Natl Inst Sci & Technol Plant Pest Interact, BR-36570000 Vicosa, MG, Brazil;

    Univ Fed Vicosa, Bioagro, Natl Inst Sci & Technol Plant Pest Interact, BR-36570000 Vicosa, MG, Brazil;

    Univ Fed Vicosa, Dept Zootecnia, BR-36570000 Vicosa, MG, Brazil;

    Univ Fed Vicosa, Bioagro, Natl Inst Sci & Technol Plant Pest Interact, BR-36570000 Vicosa, MG, Brazil;

    Univ Fed Vicosa, Bioagro, Natl Inst Sci & Technol Plant Pest Interact, BR-36570000 Vicosa, MG, Brazil|Salk Inst Biol Studies, Howard Hughes Med Inst, La Jolla, CA 92037 USA|Salk Inst Biol Studies, Plant Biol Lab, La Jolla, CA 92037 USA;

    Univ Fed Vicosa, Bioagro, Natl Inst Sci & Technol Plant Pest Interact, Dept Bioquim & Biol Mol, BR-36570000 Vicosa, MG, Brazil|Univ Fed Vicosa, Bioagro, Natl Inst Sci & Technol Plant Pest Interact, BR-36570000 Vicosa, MG, Brazil;

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