Chrysanthemum white rust (CWR), a disease caused by the fungus Henn., seriously impairs the production and ornamental value of chrysanthemums. We previously isolated the disease-resistance gene from the chrysanthemum and generated transgenic plants. Here, we determined that -overexpressing lines of the susceptible cultivar 'Jinba' show higher defensive enzyme activity and lower HO levels than a wild type after inoculation with , indicating that positively regulates plant responses to . To further explore the mechanism underlying this effect, we performed RNA sequencing using the leaves of wild-type and -RNA interference lines of the resistant cultivar 'C029' after treatment with . We identified seven differentially expressed genes in the salicylic acid (SA) pathway, including (), encoding an important regulator of this pathway. We isolated the promoter by hiTAIL-PCR and predicted that it contains pathogen-induced W-box elements. The promoter region of was activated by in a β-glucuronidase activity assay. Yeast one-hybrid assays showed that CmWRKY15-1 binds to the promoter region to regulate its expression. Finally, we confirmed the interaction between CmWRKY15-1 and CmNPR1 in a bimolecular fluorescence complementation assay. We propose that CmWRKY15-1 interacts with CmNPR1 to activate the expression of downstream pathogenesis-related genes that enhance resistance to through the SA pathway. These findings shed light on the mechanism underlying resistance to CWR.

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9094113PMC
http://dx.doi.org/10.3389/fpls.2022.865607DOI Listing

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