Sulforaphane, a secondary metabolite in crucifers, inhibits the oxidative stress adaptation and virulence of Xanthomonas by directly targeting OxyR

Plant secondary metabolites perform numerous functions in the interactions between plants and pathogens. However, little is known about the precise mechanisms underlying their contribution to the direct inhibition of pathogen growth and virulence in planta. Here, we show that the secondary metabolit...

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Bibliographic Details
Published in:Molecular plant pathology 2022-10, Vol.23 (10), p.1508-1523
Main Authors: Wang, Bo, Li, Kaihuai, Wu, Guichun, Xu, Zhizhou, Hou, Rongxian, Guo, Baodian, Zhao, Yancun, Liu, Fengquan
Format: Article
Language:English
Subjects:
Adaptation
Antioxidants
Bacteria
Catalase
Detoxification
Electrophoretic mobility
Enzymes
Flowers & plants
Gene expression
Genes
Genetic aspects
Genetic transcription
Genomes
Health aspects
Host plants
Metabolites
Molecular modelling
Original
Oxidative stress
Oxidoreductase
OxyR
Pathogens
Pesticides
Plant bacterial diseases
Plant metabolites
Proteins
Secondary metabolites
Sulforaphane
Thermophoresis
Transcription factors
Virulence
Virulence (Microbiology)
Xanthomonas
Xanthomonas species
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Summary:Plant secondary metabolites perform numerous functions in the interactions between plants and pathogens. However, little is known about the precise mechanisms underlying their contribution to the direct inhibition of pathogen growth and virulence in planta. Here, we show that the secondary metabolite sulforaphane (SFN) in crucifers inhibits the growth, virulence, and ability of Xanthomonas species to adapt to oxidative stress, which is essential for the successful infection of host plants by phytopathogens. The transcription of oxidative stress detoxification‐related genes (catalase [katA and katG] and alkylhydroperoxide‐NADPH oxidoreductase subunit C [ahpC]) was substantially inhibited by SFN in Xanthomonas campestris pv. campestris (Xcc), and this phenomenon was most obvious in sax gene mutants sensitive to SFN. By performing microscale thermophoresis (MST) and electrophoretic mobility shift assay (EMSA), we observed that SFN directly bound to the virulence‐related redox‐sensing transcription factor OxyR and weakened the ability of OxyR to bind to the promoters of oxidative stress detoxification‐related genes. Collectively, these results illustrate that SFN directly targets OxyR to inhibit the bacterial adaptation to oxidative stress, thereby decreasing bacterial virulence. Interestingly, this phenomenon occurs in multiple Xanthomonas species. This study provides novel insights into the molecular mechanisms by which SFN limits Xanthomonas adaptation to oxidative stress and virulence, and the findings will facilitate future studies on the use of SFN as a biopesticide to control Xanthomonas. Crucifers deploying the secondary metabolite sulforaphane limit Xanthomonas virulence and adaptation to oxidative stress by disturbing the DNA‐binding ability of the redox‐sensing transcription factor OxyR.
ISSN:1464-6722
1364-3703
DOI:10.1111/mpp.13245