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Research On The Mechanism Of Powdery Mildew Resistance Induced By Glycerol Application In Wheat

Posted on:2018-06-12Degree:DoctorType:Dissertation
Country:ChinaCandidate:Y H LiFull Text:PDF
GTID:1483305150973229Subject:Crop Genetics and Breeding
Abstract/Summary:PDF Full Text Request
Wheat powdery mildew,caused by the obligate biotrophic ascomycete fungus Blumeria graminis f.sp.tritici(Bgt),is one of the devastating diseases in wheat worldwide.The management of wheat powdery mildew mainly relies on host resistance and the use of fungicides.However,the employment of fungicides use is not always economically feasible and environmental friendly.Moreover,as the appearance of new races,many resistance genes identified in the past are no longer effective.Therefore,to study the disease resistance mechanisms and to search for new strategies in improving wheat powdery mildew management efficiently are two of the most important research directions.Early studies demonstrated that glycerol-3-phosphate(G3P)and oleic acid(18:1)are two important signal molecules during the plant-fungi interaction process.The main objective of this study is to understand the roles of the glycerol and fatty acids metabolism pathways in wheat-powdery mildew interaction.By regulating glycerol and fatty acids metabolism pathways,we would be able to establish new strategies to improve wheat resistance to powdery mildew.The main research results obtained in this study are as follows:1.Application of 3%glycerol induced the G3P level,decreased the level of oleic acid(18:1),and induced the resistance to powdery mildew.Glycerol application in the wheat fields significantly reduced the severity of powdery mildew disease and lessened disease-caused kernel weight losses.2.We used the RNA-seq technology to identify the differentially expressed genes(DEGs)responsed to glycerol or powdery mildew infection.GO enrichment analysis showed that those genes which responsed to glycerol were enriched in the gene function including response to fungus,response to jasmonic acid,jasmonic acid biosyntheticprocess,beta-glucosidase activity,glucan endo-1,3,-beta-D-glucosidase activity,lipidoxylipin biosynthetic,hydroperoxide dehydratase activity,etc.KEGG enrichment analysis of DEGs responsed to glycerol showed jasmonic acid precursor molecules linoleic acid and alpha-linonlenic acid metabolism were the most significantly enriched pathways.Some resistance related genes were also induced by glycerol,such as,HSP90,HSP70,PR1,PR10,RPM1,etc.;they may contribute to the wheat powdery mildew resistance.RNA-seq analysis revealed that transcriptome involved in glycerol and fatty acid metabolism responsed to powdery mildew inoculation.Those genes induced by powdery mildew,such as TaSSI2 and TaGLI1,might contribute to the accumulation of G3P and oleic acid 18:1.3.10-30m M DIECA application reduced the MeJA level and induced the resistance to powdery mildew in wheat,while the 0.2-1 mM MeJA application could not induce the resistance significantly.It proved that the changes of jasmonic acid signal pathway induced by glycerol application might take part in disease defense programs in wheat.4.TaSSI2,encoding stearoyl acyl carrier protein desaturase,can catalyze the formation of oleic acid by stearic acid.The expression of TaSSI2 was induced by powdery mildew infection.In the susceptible wheat genotype‘Xuezao'leaves,unsaturated fatty acid levels(18:1,18:2 and 18:3)increased in pathogen-infected leaves compared to the mock-inoculation leaves.We used RNAi silence the gene expression of TaSSI2 gene in Xuezao,and found the reduced the oleic acid content in wheat leaves and induced resistance to powdery mildew.5.TaGLI1,encoding glycerol kinase and catalyzing the formation of glycerol by G3P,were induced by powdery mildew infection.Over expression of TaGLI1-2D in Arabidopsis could improve the resistance to Arabidopsis powdery mildew,which may suggest its potential role in wheat powdery mildew resistance.
Keywords/Search Tags:Wheat, Powdery Mildew, Oleic Acid, G3P, TaSSI2, TaGLI1, Glycerol Induced Resistance
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