4.4 Article

Comparative transcriptome profiling reveals the basis of differential sheath blight disease response in tolerant and susceptible rice genotypes

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PROTOPLASMA
卷 259, 期 1, 页码 61-73

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SPRINGER WIEN
DOI: 10.1007/s00709-021-01637-x

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Sheath blight; Rhizoctonia solani; Resistant rice germplasm; RNA-Seq; Rice disease resistance; Coordinated defense

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Rice sheath blight caused by Rhizoctonia solani AG1-IA is devastating worldwide, with no completely resistant germplasm identified. A new ShB-tolerant rice germplasm CR 1014 was discovered, showing upregulation of genes related to glycosyl hydrolase, secondary metabolite biosynthesis, cytoskeleton and membrane integrity, and photosynthesis to resist the pathogen. This study is valuable in understanding molecular response to ShB infection and devising strategies for disease management.
Rice sheath blight (ShB) disease, caused by the fungal pathogen Rhizoctonia solani AG1-IA, is one of the devastating diseases and causes severe yield losses all over the world. No completely resistant germplasm is known till now, and as a result, the progress in resistance breeding is unsatisfactory. Basic studies to identify candidate genes, QTLs, and to better understand the host-pathogen interaction are also scanty. In this study, we report the identification of a new ShB-tolerant rice germplasm, CR 1014. Further, we investigated the basis of tolerance by exploring the disease responsive differentially expressed transcriptome and comparing them with that of a susceptible variety, Swarna-Sub1. A total of 815 and 551 genes were found to be differentially regulated in CR 1014 and Swarna-Sub1, respectively, at two different time points. The result shows that the ability to upregulate genes for glycosyl hydrolase, secondary metabolite biosynthesis, cytoskeleton and membrane integrity, the glycolytic pathway, and maintaining photosynthesis make CR 1014 a superior performer in resisting the ShB pathogen. We discuss several putative candidate genes for ShB resistance. The present study, for the first time, revealed the basis of ShB tolerance in the germplasm CR1014 and should prove to be particularly valuable in understanding molecular response to ShB infection. The knowledge could be utilized to devise strategies to manage the disease better.

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