Infection and coaccumulation of tobacco mosaic virus proteins alter microRNA levels, correlating with symptom and plant development
Infection and coaccumulation of tobacco mosaic virus proteins alter microRNA levels, correlating with symptom and plant development
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DOI：
10.1073/pnas.0705114104
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发表时间：
2007-07-17
影响因子：
11.1
通讯作者：
Asurmendi, S.
中科院分区：
文献类型：
--
作者：
Bazzini, A. A.;Hopp, H. E.;Asurmendi, S.
植物病毒的感染通常通过干扰细胞过程而引起疾病症状。在这里，我们证明了烟草（NA）的烟草病毒科，马铃薯Y病毒科和马铃薯X病毒科的代表性的植物病毒的感染改变了某些microRNA（miRNA）的积累。观察到症状严重程度与miRNAs 156、160、164、166、169和171水平变化之间的相关性，其独立于病毒转录后基因沉默抑制剂活性。杂交转基因植物，产生烟草花叶病毒（TMV）的运动蛋白（MIP）和外壳蛋白（CP）（T42 W）（CP的变体）表现出类似疾病的表型，包括植物发育异常。用两种转基因都沉默的植物系进行的嫁接研究证实，疾病样表型是由于CIP和MIP的共表达。在杂种MpxCp（T42W）植株和TMV感染植株中，miRNAs 156、164、165和167的积累水平高于非转基因和未感染组织。双分子荧光互补分析显示，MP与CPT 42 W在体内相互作用，并导致MP和CP之间形成的复合物引起导致疾病症状的miRNA增加的假设。这项工作提供的证据表明，病毒感染和病毒蛋白影响miRNA平衡，而不影响转录后基因沉默，并有助于病毒在发病过程中利用miRNA途径的假设。
Infections by plant virus generally cause disease symptoms by interfering with cellular processes. Here we demonstrated that infection of Nicotiana tabacum (NA) by plant viruses representative of the Tobamoviridae, Potyviridae, and Potexviridae families altered accumulation of certain microRNAs (miRNAs). A correlation was observed between symptom severity and alteration in levels of miRNAs 156, 160, 164,166, 169, and 171 that is independent of viral posttranscriptional gene silencing suppressor activity. Hybrid transgenic plants that produced tobacco mosaic virus (TMV) movement protein (MIP) plus coat protein (Cp)(T42W) (a variant of CP) exhibited disease-like phenotypes, including abnormal plant development. Grafting studies with a plant line in which both transgenes are silenced confirmed that the disease-like phenotypes are due to the coexpression of CIP and MIP. In hybrid MpxCp(T42W) plants and TMV-infected plants, miRNAs 156,164,165, and 167 accumulated to higher levels compared with nontransgenic and noninfected tissues. Bimolecular fluorescence complementation assays revealed that MP interacts with CPT42W in vivo and leads to the hypothesis that complexes formed between MP and CP caused increases in miRNAs that result in disease symptoms. This work presents evidence that virus infection and viral proteins influence miRNA balance without affecting posttranscriptional gene silencing and contributes to the hypothesis that viruses exploit miRNA pathways during pathogenesis.