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.

Rhizoctonia solani causes sheath blight disease in rice; however, the defense mechanism of rice plants against R. solani remains elusive. To analyze the roles of brassinosteroid (BR) and ethylene signaling on rice defense to R. solani, wild-type (WT) rice and several mutants and overexpressing (OX) lines were inoculated with R. solani. Mutants d61-1 and d2 were less susceptible to sheath blight disease, bri1-D was more susceptible, and ravl1 and d61-1/EIL1 Ri5 were similarly susceptible compared with WT. The double mutant ravl1/d61-1 was phenotypically similar to the ravl1 mutant. Transcriptome analysis, chromatin immunoprecipitation assay, electrophoretic mobility shift assay, and transient assays indicted that RAVL1 might directly activate Ethylene insensitive 3-like 1 (EIL1), a master regulator of ethylene signaling. Mutants ers1 and d61-1/RAVL1 OX were resistant to sheath blight disease, whereas EIL1 RNAi mutants and RAVL1 OX were more susceptible than WT. BRI1 and D2 expression in EIL1 Ri5/RAVL1 OX and EIL1 expression in d61-1/RAVL1 OX indicated that RAVL1 activates BRI1/D2 and EIL1, respectively, independent of BR and ethylene signaling. Our analyses provide information on how BR and ethylene signaling regulate sheath blight disease and on the regulatory function of RAVL1 in rice sheath blight disease.

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Background: Loose Plant Architecture 1 (LPA1), an indeterminate domain (IDD) protein, exhibits almost no expression in the leaves, but the overexpression of LPA1 significantly increases the resistance of rice to sheath blight disease (ShB) via the activation of PIN-FORMED 1a (PIN1a). Results: In this study, we determined that Rhizoctonia solani infection significantly induced LPA1 expression in the leaves, and lpa1 was more susceptible to R. solani compared with the wild-type and revertant plants. In addition, infection with R. solani altered the expression of IDD3, IDD5, IDD10, and IDD13, and yeast two-hybrid, split-GFP, and coimmunoprecipitation assays showed that LPA1 interacts with IDD3 and IDD13. IDD13 RNAi plants were more susceptible, while IDD13 overexpressors were less susceptible to ShB compared with the wild-type. In parallel, idd3 exhibited no significant differences, while IDD3 overexpressors were more susceptible compared to the wild-type response to ShB. Additional chromatin-immunoprecipitation and electrophoretic mobility shift assay experiments indicated that IDD13 and IDD3 bound to the PIN1a promoter, and the transient assay indicated that IDD13 and IDD3 positively and negatively regulate PIN1a expression, respectively. Moreover, IDD13, IDD3, and LPA1 form a transcription factor complex that regulates PIN1a. A genetic study showed that the LPA1 repressor lines were similar to lpa1/IDD13 RNAi and were more susceptible than the lpa1 and IDD13 RNAi plants in response to ShB. The overexpression of IDD13 increased resistance to ShB in the lpa1 background.Conclusions: Taken together, our analyses established that IDD3, IDD13, and LPA1 form a transcription factor complex to regulate the defense of rice against ShB possibly via the regulation of PIN1a.

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