MPK6-bHLH-SWEET11信号途径调控水稻对纹枯病抗性分子机制研究

纹枯病是我国水稻三大病害之一，其危害日益严重，筛选并利用抗性基因来选育并种植抗病品种是防治该病害最经济、有效途径。我们前期研究结果证实，敲除糖转运蛋白基因SWEET11可有效提高水稻对纹枯病的抗性，但SWEET11的转录调控模式在水稻抗纹枯病中的作用机制尚不清楚。预实验结果表明，转录因子bHLH结合SWEET11启动子区域并激活其转录，敲除bHLH抑制SWEET11表达水平并提高水稻对纹枯病的抗性；纹枯病菌侵染水稻诱导MPK6和bHLH的磷酸化水平，而MPK6通过结合并磷酸化bHLH来增强其对SWEET11的转录激活活性。本研究将基于前期研究结果，利用分子生物学、生物化学和遗传学等手段，明确MPK6磷酸化修饰bHLH及其对SWEET11转录激活的作用机制，进而解析MPK6-bHLH-SWEET11途径调控水稻抗纹枯病的分子机理。本研究成果将丰富水稻抗纹枯病机制并为抗病育种提供重要分子靶点。

Sheath blight, one of the three major rice diseases, is becoming more and more serious in China. The most economical and effective way to control this disease is to select and cultivate resistant varieties by screening and utilizing resistance genes. Our previous results confirmed that knockout SWEET11, a sugar transporter gene, could effectively improve rice resistance to sheath blight disease, but the role of transcriptional regulatory module of SWEET11 in regulation of rice resistance to sheath blight disease remains elusive. The preliminary results indicated that the transcription factor bHLH bound the promoter region to activate the transcription of SWEET11. Knockout of bHLH inhibited the expression level of SWEET11 and enhanced rice resistance to sheath blight disease. In addition, phosphorylation levels of rice MPK6 and bHLH were induced by inoculation of Rhizoctonia solani AG1-IA. MPK6 interacts and phosphorylates bHLH to enhance its transcriptional activation activity against SWEET11. Based on the preliminary results, this study will use molecular biological, biochemical and genetic approaches to clarify the mechanism of MPK6 mediated bHLH phosphorylation as well as transcriptional activation of SWEET11 by bHLH, and finally analyze the molecular mechanism of MPK6-bHLH-SWEET11 pathway in regulation of rice resistance to sheath blight. The results of this study will extend the mechanism of rice resistance to sheath blight disease and provide important molecular targets for disease resistance breeding.