Abstract
Rhizoctonia solani is a necrotrophic fungal pathogen that causes disease in diverse plant species. In recent years, the genomic and transcriptomic studies have identified several candidate pathogenicity determinants of R. solani; however, most of them remain to be validated. In this study, we report a viral vector-based host-induced gene silencing (HIGS) as well as a dsRNA (double-stranded RNA)-based approach to effectively downregulate genes of R. solani AG1-IA (BRS1 strain) during pathogenesis in tomato. We tested a few of the in-planta upregulated R. solani genes and observed that silencing of one of them, i.e., RS_CRZ1 (a C2H2 type zinc finger transcription factor) significantly compromises the pathogenesis of R. solani in tomato. The RS_CRZ1-silenced plants not only exhibited significant reduction in disease symptoms, but the depth of pathogen colonization was also compromised. Furthermore, we identified the R. solani genes that were coregulated with RS_CRZ1 during the pathogenicity process. The HIGS-mediated silencing of a few of them [CL1756Contig1; subtilisin-like protease and CL1817Contig2; 2OG-Fe(II) oxygenase] compromised the pathogenesis of R. solani in tomato. The ectopic expression of RS_CRZ1 complemented the crz1 mutant of yeast and restored tolerance against various metal ion stress. Overall, our study reveals the importance of RS_CRZ1 in managing the hostile environment encountered during host colonization. Also, it emphasizes the relevance of the HIGS and dsRNA-based gene silencing approach toward functional characterization of pathogenicity determinants of R. solani.[Formula: see text] Copyright © 2021 The Author(s). This is an open access article distributed under the CC BY 4.0 International license.
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