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.
病原體-宿主相互作用是一個復(fù)雜的過程，病原菌主要侵染寄主植物以獲取營養(yǎng)物質(zhì)，尤其是糖。水稻紋枯病的病原菌是水稻紋枯病的主要病原。然而，目前還不清楚這種病原體是如何從水稻植株中獲取糖的。本研究發(fā)現(xiàn)，水稻糖轉(zhuǎn)運蛋白OsSWEET11參與了水稻紋枯病的發(fā)病機制。實時定量聚合酶鏈反應(yīng)(qRT-PCR)和β-d-葡萄糖醛酸苷酶(β-d-glucuronidase)的表達分析表明，立枯絲核菌侵染顯著提高了葉片中OsSWEET11的表達。轉(zhuǎn)基因植株分析表明，與野生型相比，Ossweet11突變體對紋枯病敏感性下降，而過表達Ossweet11的植株更易受紋枯病影響，但突變體和過表達株系的產(chǎn)量均降低。SWEETs在寡聚過程中變得活躍。分裂泛素酵母雙雜交、雙分子熒光互補和免疫共沉淀實驗表明，突變的OsSWEET11與正常的OsSWEET11相互作用。此外，保守殘基AtSWEET1的表達抑制了正常AtSWEET1的活性。為了分析在葉肉細胞中抑制OsSWEET11的功能是否與防御該疾病有關(guān)，突變的OsSWEET11在Rubisco啟動子控制下表達，這是綠色組織特有的。轉(zhuǎn)基因植株對紋枯病的抗性有明顯提高，但對其他病害無明顯影響。綜上所述，這些結(jié)果表明立枯絲核菌可能通過激活OsSWEET11的表達來從水稻葉片中獲取糖。水稻也通過調(diào)控OsSWEET11的表達，在不影響產(chǎn)量的情況下保護植物免受感染。