Genome sequencing and comparative genomic analysis of highly and weakly virulent strains of Sclerotium rolfsii, the causal agent of peanut stem rot

semanticscholar(2020)

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Abstract
Background Stem rot caused by Sclerotium rolfsii is a very important soil-borne disease to peanut worldwide. S. rolfsii is a necrotrophic plant pathogenic fungus with an extensive host range and worldwide distribution. It can infect peanut stems, roots, pegs and pods, leading to varied yield losses. S. rolfsii strains GP3 and ZY collected from peanut in different provinces of China exhibited significant difference in virulence on peanut by artificial inoculation test. In this study, de-novo genome sequencing of these two distinct strains was performed in the hopes of revealing the genomic basis of virulence differentiation. Results Scleotium rolfsii strains GP3 and ZY, with weak and high virulence on peanut, respectively, exhibited similar growth rate and oxalic acid production in laboratory. The genomes of S. rolfsii strains GP3 and ZY were sequenced by Pacbio long read technology and exhibited 70.61 Mb and 70.51 Mb, with contigs of 27 and 23, and encoded 17,097 and 16,743 putative protein genes, respectively. Comparative genomic analysis revealed that the pathogenicity-related gene repertoires, which might be associated with the virulence, diverged between GP3 and ZY. Detailed analysis further revealed 58 and 45 unique pathogen-host interaction (PHI) genes in GP3 and ZY, respectively. The ZY strain had more carbohydrate-active enzymes (CAZymes) in its secretome than GP3, especially in the glycoside hydrolase family (GH), the carbohydrate esterase family (CBM), and the polysaccharide lyase family (PL). GP3 and ZY also had different effector candidates. These results indicated that differences in PHI, secreted CAZymes, and effectors may play important roles in virulence differentiation between these two strains. Conclusions The data provided a further understanding of the S. rolfsii genome. Detailed comparative genomic analysis provided clues into the genomic basis of its necrotrophic lifestyle and virulence diversification.
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