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A Long Non-Coding RNA of Citrus tristeza virus: Role in the Virus Interplay with the Host Immunity

机译:柑橘柑橘长病毒的非编码长RNA:在病毒与宿主免疫相互作用中的作用

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摘要

During infection, Citrus tristeza virus (CTV) produces a non-coding subgenomic RNA referred to as low-molecular-weight tristeza 1 (LMT1), which for a long time has been considered as a by-product of the complex CTV replication machinery. In this study, we investigated the role of LMT1 in the virus infection cycle using a CTV variant that does not produce LMT1 (CTV-LMT1d). We showed that lack of LMT1 did not halt virus ability to replicate or form proper virions. However, the mutant virus demonstrated significantly reduced invasiveness and systemic spread in Nicotiana benthamiana as well as an inability to establish infection in citrus. Introduction of CTV-LMT1d into the herbaceous host resulted in elevation of the levels of salicylic acid (SA) and SA-responsive pathogenesis-related genes beyond those upon inoculation with wild-type (WT) virus (CTV-WT). Further analysis showed that the LMT1 RNA produced by CTV-WT or via ectopic expression in the N. benthamiana leaves suppressed SA accumulation and up-regulated an alternative oxidase gene, which appeared to mitigate the accumulation of reactive oxygen species. To the best of our knowledge, this is the first report of a plant viral long non-coding RNA being involved in counter-acting host response by subverting the SA-mediated plant defense.
机译:在感染过程中,柑桔类Tristeza病毒(CTV)会产生称为低分子量Tristeza 1(LMT1)的非编码亚基因组RNA,长期以来一直被认为是复杂的CTV复制机制的副产物。在这项研究中,我们使用不产生LMT1的CTV变体(CTV-LMT1d)调查了LMT1在病毒感染周期中的作用。我们表明缺乏LMT1不会阻止病毒复制或形成合适的病毒粒子的能力。但是,该突变病毒在本氏烟草中显示出明显降低的侵袭性和系统性扩散,并且无法在柑橘中建立感染。将CTV-LMT1d引入草本植物宿主后,水杨酸(SA)和SA反应性发病相关基因的水平升高,超过了接种野生型(WT)病毒(CTV-WT)的水平。进一步的分析表明,由CTV-WT或通过异位表达在本氏烟草中产生的LMT1 RNA抑制了SA的积累,并上调了另一种氧化酶基因,从而减轻了活性氧的积累。据我们所知,这是第一篇有关植物病毒长非编码RNA参与通过破坏SA介导的植物防御来对抗宿主反应的报道。

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