Cytokinin (CTK)-mediated pathways play essential roles in plant stress responses. How CTK receptors affect plant resistance to viral pathogens remains unclear. Tobacco mosaic virus [recombinant TMV encoding green fluorescent protein (TMV-GFP)] was used to investigate the role of Nicotiana tabacum CRE1 (CTK receptor 1) in modulating virus susceptibility in N. tabacum. CRE1 deficiency enhanced the susceptibility of N. tabacum to TMV-GFP. The cre1 RNAi mutants showed extensive green florescence and higher transcript levels of the TMV coat protein gene than the wild type (WT) plants. CRE1 deficiency affected the antioxidant response to TMV-GFP, and the RNAi mutants had depressed antioxidant enzyme activities compared to the WT plants under virus infection. In addition, endogenous salicylic acid (SA) accumulation and the expression levels of SA pathway-related defence genes induced by TMV-GFP were significantly repressed in the RNAi mutants compared with the WT plants. Furthermore, the presence of exogenous CTK could only partially reduce the susceptibility of tobacco to TMV caused by CRE1 deficiency. Taken together, these results suggest that CRE1 plays a positive role in the tobacco defence response to the virus and is required for the induction and development of complete defence responses.

细胞分裂素（CTK）介导的途径在植物胁迫反应中起重要作用。目前尚不清楚CTK受体如何影响植物对病毒病原体的抗性。烟草花叶病毒[编码绿色荧光蛋白的TMV重组蛋白（TMV-GFP）]用于研究烟草CRE1（CTK受体1）在烟草中调节病毒敏感性的作用。CRE1缺乏症增强了烟草对TMV-GFP的敏感性。该CRE1 RNAi的突变表明大量绿色荧光和TMV外壳蛋白基因比野生型（WT）植物的高转录水平。CRE1缺乏影响了对TMV-GFP的抗氧化反应，与病毒感染的野生型植物相比，RNAi突变体的抗氧化酶活性降低。此外，与野生型植物相比，RNAi突变体显着抑制了内源性水杨酸（SA）的积累和TMV-GFP诱导的SA途径相关防御基因的表达水平。此外，外源性CTK的存在只能部分减少由CRE1缺乏引起的烟草对TMV的敏感性。综上所述，这些结果表明CRE1在烟草对病毒的防御反应中发挥了积极作用，并且是诱导和发展完整防御反应所必需的。