Regulated nuclear trafficking of rpL10A mediated by NIK1 represents a defense strategy of plant cells against virus.
Regulated nuclear trafficking of rpL10A mediated by NIK1 represents a defense strategy of plant cells against virus.
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DOI：
10.1371/journal.ppat.1000247
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发表时间：
2008-12
期刊：
影响因子：
6.7
通讯作者：
Fontes EP
中科院分区：
文献类型：
--
作者：
Carvalho CM;Santos AA;Pires SR;Rocha CS;Saraiva DI;Machado JP;Mattos EC;Fietto LG;Fontes EP
NSP相互作用激酶（NIK）受体介导的防御途径最近被确定为双病毒核穿梭蛋白（NSP）的毒力靶点。然而，NIK1-NSP的相互作用并不符合激发剂-受体的耐药模型，因此将这种抗病毒反应与受体激活联系起来的分子机制仍然不清楚。在这里，我们确定了一种核糖体蛋白rpL10A，作为NIK1的特定伴侣和底物，作为NIK1介导的反应的直接下游效应物。细胞质rpL10A被NIK1磷酸化后，该蛋白被重定向到细胞核，在那里它可能调节病毒感染。正常NIK1的异位表达或过度活跃的NIK1突变体促进了磷酸化rpL10A在细胞核内的积累，而不活跃的NIK1突变体不能将蛋白质重定向到共转染细胞的细胞核中。同样，NIK1磷酸化缺陷的突变体rpL10A不会被重定向到细胞核。此外，rpL10A功能的缺失增加了对双病毒感染的易感性，类似于nik1零等位基因的表型。我们还提供证据表明，双病毒感染直接干扰nik1介导的rpL10A的核再定位作为一种防御措施。然而，nik1介导的防御信号既不激活RNA沉默，也不促进超敏反应，而是抑制植物的生长发育。虽然本文研究的特殊双病毒NSP的毒力功能在拟南芥中克服了这层防御，但nik1介导的信号反应可能参与限制其他病毒的宿主范围。植物经常暴露在微生物中，像动物一样，它们发展出先天免疫系统来防止感染。尽管这些免疫系统保护植物免受大多数潜在病原体的侵害，但非宿主免疫的分子机制仍然不清楚。在这里，我们描述了一种新的植物防御策略，该策略被确定为双病毒核穿梭蛋白（NSP）的靶标，可以抑制跨膜受体NIK （NSP相互作用激酶）的活性。此外，我们确定了一种核糖体蛋白rpL10A作为该途径的直接下游组分。基于我们的研究结果，我们提出这一途径是由受体NIK1的激活引发的，这导致rpL10A磷酸化并易位到细胞核。我们还提供了遗传和生化证据，证明这种rpL10A的调控贩运可能有效地建立一种防御策略，对双病毒的增殖或运动产生负面影响。然而，来自两节双病毒CaLCuV（白菜卷曲病毒）的NSP的毒力功能能够克服nik1介导的防御，从而增强CaLCuV在拟南芥中的致病性。nik1介导的信号反应可能参与限制其他病毒的宿主范围。
The NSP-interacting kinase (NIK) receptor-mediated defense pathway has been identified recently as a virulence target of the geminivirus nuclear shuttle protein (NSP). However, the NIK1–NSP interaction does not fit into the elicitor–receptor model of resistance, and hence the molecular mechanism that links this antiviral response to receptor activation remains obscure. Here, we identified a ribosomal protein, rpL10A, as a specific partner and substrate of NIK1 that functions as an immediate downstream effector of NIK1-mediated response. Phosphorylation of cytosolic rpL10A by NIK1 redirects the protein to the nucleus where it may act to modulate viral infection. While ectopic expression of normal NIK1 or a hyperactive NIK1 mutant promotes the accumulation of phosphorylated rpL10A within the nuclei, an inactive NIK1 mutant fails to redirect the protein to the nuclei of co-transfected cells. Likewise, a mutant rpL10A defective for NIK1 phosphorylation is not redirected to the nucleus. Furthermore, loss of rpL10A function enhances susceptibility to geminivirus infection, resembling the phenotype of nik1 null alleles. We also provide evidence that geminivirus infection directly interferes with NIK1-mediated nuclear relocalization of rpL10A as a counterdefensive measure. However, the NIK1-mediated defense signaling neither activates RNA silencing nor promotes a hypersensitive response but inhibits plant growth and development. Although the virulence function of the particular geminivirus NSP studied here overcomes this layer of defense in Arabidopsis, the NIK1-mediated signaling response may be involved in restricting the host range of other viruses. Plants are constantly exposed to microorganisms and, like animals, developed innate immune systems to prevent infections. Although these immune systems protect plants against most potential pathogens, the molecular mechanisms underlying nonhost immunity remain obscure. Here, we describe a novel strategy of plant defenses identified as a target of the geminivirus nuclear shuttle protein (NSP) that suppresses the activity of the transmembrane receptor NIK (NSP-interacting kinase). In addition, we identified a ribosomal protein, rpL10A, as the immediate downstream component of the pathway. Based on our findings, we propose that this pathway is elicited by activation of the receptor NIK1, which results in phosphorylation and translocation of rpL10A to the nucleus. We also provided genetic and biochemical evidence that this regulated trafficking of rpL10A may effectively mount a defense strategy that negatively impacts geminivirus proliferation or movement. Nevertheless, the virulence function of NSP from the bipartite geminivirus CaLCuV (Cabbage leaf curl virus) is capable of overcoming the NIK1-mediated defense and thereby enhances the pathogenicity of CaLCuV in Arabidopsis. The NIK1-mediated signaling response may be involved in restricting the host range of other viruses.
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