ArticleMolecular plant pathology2023
SstF, a novel sulforaphane-sensing transcription factor of Xanthomonas campestris, is required for sulforaphane tolerance and virulence.
Article in Molecular plant pathology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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2 citing papers in PubMed, 4 citations in OpenAlex.
- How plants manage pathogen infection.EMBO reports · 2024Review
- SstF, a novel sulforaphane-sensing transcription factor of Xanthomonas campestris, is required for sulforaphane tolerance and virulence.Molecular plant pathology · 2023Article
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Authors and funding
10 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Avoiding the host defence system is necessary for the survival of pathogens. However, the mechanisms by which pathogenic bacteria sense and resist host defence signals are still unknown. Sulforaphane (SFN) is a secondary metabolite of crucifers. It not only plays an important role in maintaining the local defence response but also directly inhibits the growth of some pathogens. In this study, we identified a key SFN tolerance-related gene, saxF, in Xanthomonas campestris pv. campestris (Xcc), the causal agent of black rot in crucifers. More interestingly, we found that the transcription of saxF was regulated by the novel transcription factor SFN-sensing transcription factor (SstF). As a LysR family transcription factor, SstF can sense SFN and regulate the expression of saxF cluster genes to increase SFN resistance by directly binding to the promoter of saxF. In addition, we found that SstF and saxF also play an important role in positively regulating the virulence of Xcc. Collectively, our results illustrate a previously unknown mechanism by which Xcc senses the host defence signal SFN and activates the expression of SFN tolerance-related genes to increase virulence. Therefore, this study provides a remarkable result; that is, during pathogen-plant co-evolution, new functions of existing scaffolds are activated, thus improving the proficiency of the pathogenic mechanism.
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