College of Plant Protection, Shenyang Agricultural University, Shenyang 110866, China.
College of Biological Science and Engineering, Fuzhou University, Fuzhou 350108, China.
Mol Plant Pathol. 2018 Sep;19(9):2149-2161. doi: 10.1111/mpp.12689. Epub 2018 Jul 19.
Pathogen-host interaction is a complicated process; pathogens mainly infect host plants to acquire nutrients, especially sugars. Rhizoctonia solani, the causative agent of sheath blight disease, is a major pathogen of rice. However, it is not known how this pathogen obtains sugar from rice plants. In this study, we found that the rice sugar transporter OsSWEET11 is involved in the pathogenesis of sheath blight disease. Quantitative real-time polymerase chain reaction (qRT-PCR) and β-d-glucuronidase expression analyses showed that R. solani infection significantly enhanced OsSWEET11 expression in leaves amongst the clade III SWEET members. The analyses of transgenic plants revealed that Ossweet11 mutants were less susceptible, whereas plants overexpressing OsSWEET11 were more susceptible, to sheath blight compared with wild-type controls, but the yield of OsSWEET11 mutants and overexpressors was reduced. SWEETs become active on oligomerization. Split-ubiquitin yeast two-hybrid, bimolecular fluorescence complementation and co-immunoprecipitation assays showed that mutated OsSWEET11 interacted with normal OsSWEET11. In addition, expression of conserved residue mutated AtSWEET1 inhibited normal AtSWEET1 activity. To analyse whether inhibition of OsSWEET11 function in mesophyll cells is related to defence against this disease, mutated OsSWEET11 was expressed under the control of the Rubisco promoter, which is specific for green tissues. The resistance of transgenic plants to sheath blight disease, but not other disease, was improved, whereas yield production was not obviously affected. Overall, these results suggest that R. solani might acquire sugar from rice leaves by the activation of OsSWEET11 expression. The plants can be protected from infection by manipulation of the expression of OsSWEET11 without affecting the crop yield.
病原体-宿主相互作用是一个复杂的过程;病原体主要感染宿主植物以获取营养物质,特别是糖。丝核菌,引起叶鞘枯病的病原体,是水稻的主要病原体。然而,目前尚不清楚这种病原体如何从水稻植株中获取糖。在这项研究中,我们发现水稻糖转运蛋白 OsSWEET11 参与了叶鞘枯病的发病机制。定量实时聚合酶链反应(qRT-PCR)和β-d-葡糖苷酸表达分析表明,丝核菌感染显著增强了叶鞘枯病中 clade III SWEET 成员 OsSWEET11 的表达。转基因植物分析表明,与野生型对照相比,Ossweet11 突变体对叶鞘枯病的敏感性降低,而过表达 OsSWEET11 的植物则更易感染叶鞘枯病,但 Ossweet11 突变体和过表达体的产量降低。SWEET 蛋白在寡聚化时变得活跃。分裂泛素酵母双杂交、双分子荧光互补和共免疫沉淀实验表明,突变的 OsSWEET11 与正常的 OsSWEET11 相互作用。此外,保守残基突变的 AtSWEET1 的表达抑制了正常 AtSWEET1 的活性。为了分析抑制叶肉细胞中的 OsSWEET11 功能是否与该疾病的防御有关,用 Rubisco 启动子(该启动子特异性地在绿色组织中表达)控制表达突变的 OsSWEET11。转基因植物对叶鞘枯病的抗性得到了提高,但对其他疾病的抗性没有明显影响,而产量没有明显受到影响。总的来说,这些结果表明,丝核菌可能通过激活 OsSWEET11 的表达从水稻叶片中获取糖。通过操纵 OsSWEET11 的表达可以保护植物免受感染,而不会影响作物产量。