Although the pathogen Fusarium proliferatum is responsible for soybean root rot, the mechanisms underlying its pathogenicity remain unclear. We detected limited soybean resistance to six F. proliferatum strains isolated from China. To elucidate the mechanisms underlying F. proliferatum pathogenicity, we conducted RNA sequencing analysis of the F. proliferatum isolate Fp6-1 during the mycelial and infection stages. Transcriptome sequencing analysis identified 10 significantly upregulated candidate effector molecules; these were selected for subsequent transcriptional pattern analysis. Bioinformatics analysis predicted 80 candidate effectors that were cysteine-rich, contained signal peptides, lacked transmembrane domains, and were secreted extracellularly. The conserved domains, pathogenicity, and functions of these candidate effectors were assessed. Pathogen host interaction database comparisons demonstrated that 44 of the candidate effectors were associated with virulence. Among these, 12 were upregulated during the infection stage and contained the pectate lyase, Hce2, FKBP-C, abhydrolase, DUF196, SGNH hydrolase, CE4 superfamily, ZnMc pappalysin-like, GH16 Streptomyces laminarinase-like, MhpC, and glyco-hydro-11 domains. The majority of the predicted candidate effectors were upregulated during F. proliferatum infection. Given that domestic soybean cultivars resistant to F. proliferatum are scarce in China, this study provides invaluable resources for subsequent functional analyses and guidance for future soybean breeding efforts.
Yang et al. (Wed,) studied this question.
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