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Transcriptome analysis reveals the host selection fitness mechanisms of the Rhizoctonia solani AG1IA pathogen
Rhizoctonia solani AG1IA is a major generalist pathogen that causes sheath blight. Its genome, which was the first to be sequenced from the Rhizoctonia genus, may serve as a model for studying pathogenic mechanisms. To explore the pathogen-host fitness mechanism of sheath-blight fungus, a comprehens...
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Published in: | Scientific reports 2017-08, Vol.7 (1), p.10120-10120, Article 10120 |
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Main Authors: | , , , , , , , , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | Rhizoctonia solani
AG1IA is a major generalist pathogen that causes sheath blight. Its genome, which was the first to be sequenced from the
Rhizoctonia
genus, may serve as a model for studying pathogenic mechanisms. To explore the pathogen-host fitness mechanism of sheath-blight fungus, a comprehensive comparative transcriptome ecotype analysis of
R. solani
AG1IA isolated from rice, soybean and corn during infection was performed. Special characteristics in gene expression, gene ontology terms and expression of pathogenesis-associated genes, including genes encoding secreted proteins, candidate effectors, hydrolases, and proteins involved in secondary metabolite production and the MAPK pathway, were revealed. Furthermore, as an important means of pathogenic modulation, diverse alternative splicing of key pathogenic genes in
Rhizoctonia solani
AG1IA during infections of the abovementioned hosts was uncovered for the first time. These important findings of key factors in the pathogenicity of
R. solani
AG1IA ecotypes during infection of various hosts explain host preference and provide novel insights into the pathogenic mechanisms and host-pathogen selection. Furthermore, they provide information on the fitness of
Rhizoctonia
, a severe pathogen with a wide host range. |
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ISSN: | 2045-2322 2045-2322 |
DOI: | 10.1038/s41598-017-10804-1 |