Sheng Yangyang, Yang Lijun, Li Chunfu, Wang Yuping, Guo Hongxiang
1College of Life Sciences, Henan Agricultural University, Zhengzhou, 450002 Henan China.
Zhumadian Branch of Henan Province Tobacco Company, Zhumadian, 463000 Henan China.
3 Biotech. 2019 Jun;9(6):220. doi: 10.1007/s13205-019-1740-6. Epub 2019 May 20.
To provide a detailed insight into the early biological process of tobacco mosaic disease, transcriptomic changes in tobacco leaves were surveyed at 1, 3 and 5 days after mono-infected by (TMV) and co-infected by (CMV) and TMV. At the three different stages, there were 2372, 3168 and 2045 differentially expressed genes (DEGs) in mono-infected leaves, and 2388, 3281 and 3417 DEGs were identified in co-infected leaves. There were 836, 1538 and 1185 common DEGs between the mono-infection and co-infection at the three time points, respectively. These common DEGs were enriched in the pathways, such as photosynthesis, biosynthesis of secondary metabolites, plant-pathogen interaction, porphyrin and chlorophyll metabolism, phenylalanine metabolism and phenylpropanoid biosynthesis. Photosynthesis pathway was observably down-regulated, and defense response pathways were markedly up-regulated. These pathways have been found to be related to tobacco mosaic disease. Of these common DEGs, the changes in expression of argonaute proteins, thioredoxins and peroxidases showed that the activation of RNA silencing and the destruction of redox balance can be induced by tobacco mosaic virus infection, resulting in the reset of biology process and damage in tobacco plants. Additionally, the occurrence of symptoms in co-infected tobacco plants was more early and serious than mono-infection, indicating that there is synergy between TMV and CMV in co-infected tobacco plants. The timely usage of antiviral agents and plant resistance inducers can decrease the incidence of tobacco mosaic disease through changing the expression of some DEGs, indicating that these genes can be used to screen novel plant resistance inducers and antiviral agents. Overall, our results were helpful in clarifying the mechanism of tobacco mosaic disease and provided novel strategies for the prevention of tobacco mosaic disease.
为深入了解烟草花叶病的早期生物学过程，在烟草单接种烟草花叶病毒（TMV）以及同时接种黄瓜花叶病毒（CMV）和TMV后的第1、3和5天，对烟草叶片的转录组变化进行了研究。在这三个不同阶段，单接种叶片中分别有2372、3168和2045个差异表达基因（DEG），同时接种叶片中分别鉴定出2388、3281和3417个DEG。在这三个时间点，单接种和同时接种之间分别有836、1538和1185个共同的DEG。这些共同的DEG在光合作用、次生代谢物生物合成、植物 - 病原体相互作用、卟啉和叶绿素代谢、苯丙氨酸代谢以及苯丙烷生物合成等途径中富集。光合作用途径明显下调，防御反应途径显著上调。已发现这些途径与烟草花叶病有关。在这些共同的DEG中，AGO蛋白、硫氧还蛋白和过氧化物酶表达的变化表明，烟草花叶病毒感染可诱导RNA沉默的激活和氧化还原平衡的破坏，从而导致烟草植株生物学过程的重置和损伤。此外，同时接种的烟草植株症状出现更早且更严重，表明TMV和CMV在同时接种的烟草植株中存在协同作用。及时使用抗病毒剂和植物抗性诱导剂可通过改变一些DEG的表达来降低烟草花叶病的发病率，这表明这些基因可用于筛选新型植物抗性诱导剂和抗病毒剂。总体而言，我们的结果有助于阐明烟草花叶病的发病机制，并为预防烟草花叶病提供了新策略。
