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SstF, a novel sulforaphane‐sensing transcription factor of Xanthomonas campestris, is required for sulforaphane tolerance and virulence

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...

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Autores principales: Wang, Bo, Xu, Zhizhou, Zhao, Yangyang, Wu, Guichun, Li, Kaihuai, Hou, Rongxian, Guo, Baodian, Tang, Bao, Zhao, Yancun, Liu, Fengquan
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10098062/
https://www.ncbi.nlm.nih.gov/pubmed/36829260
http://dx.doi.org/10.1111/mpp.13314
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author Wang, Bo
Xu, Zhizhou
Zhao, Yangyang
Wu, Guichun
Li, Kaihuai
Hou, Rongxian
Guo, Baodian
Tang, Bao
Zhao, Yancun
Liu, Fengquan
author_facet Wang, Bo
Xu, Zhizhou
Zhao, Yangyang
Wu, Guichun
Li, Kaihuai
Hou, Rongxian
Guo, Baodian
Tang, Bao
Zhao, Yancun
Liu, Fengquan
author_sort Wang, Bo
collection PubMed
description 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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spelling pubmed-100980622023-04-14 SstF, a novel sulforaphane‐sensing transcription factor of Xanthomonas campestris, is required for sulforaphane tolerance and virulence Wang, Bo Xu, Zhizhou Zhao, Yangyang Wu, Guichun Li, Kaihuai Hou, Rongxian Guo, Baodian Tang, Bao Zhao, Yancun Liu, Fengquan Mol Plant Pathol Original Articles 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. John Wiley and Sons Inc. 2023-02-24 /pmc/articles/PMC10098062/ /pubmed/36829260 http://dx.doi.org/10.1111/mpp.13314 Text en © 2023 The Authors. Molecular Plant Pathology published by British Society for Plant Pathology and John Wiley & Sons Ltd. https://creativecommons.org/licenses/by-nc-nd/4.0/This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc-nd/4.0/ (https://creativecommons.org/licenses/by-nc-nd/4.0/) License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made.
spellingShingle Original Articles
Wang, Bo
Xu, Zhizhou
Zhao, Yangyang
Wu, Guichun
Li, Kaihuai
Hou, Rongxian
Guo, Baodian
Tang, Bao
Zhao, Yancun
Liu, Fengquan
SstF, a novel sulforaphane‐sensing transcription factor of Xanthomonas campestris, is required for sulforaphane tolerance and virulence
title SstF, a novel sulforaphane‐sensing transcription factor of Xanthomonas campestris, is required for sulforaphane tolerance and virulence
title_full SstF, a novel sulforaphane‐sensing transcription factor of Xanthomonas campestris, is required for sulforaphane tolerance and virulence
title_fullStr SstF, a novel sulforaphane‐sensing transcription factor of Xanthomonas campestris, is required for sulforaphane tolerance and virulence
title_full_unstemmed SstF, a novel sulforaphane‐sensing transcription factor of Xanthomonas campestris, is required for sulforaphane tolerance and virulence
title_short SstF, a novel sulforaphane‐sensing transcription factor of Xanthomonas campestris, is required for sulforaphane tolerance and virulence
title_sort sstf, a novel sulforaphane‐sensing transcription factor of xanthomonas campestris, is required for sulforaphane tolerance and virulence
topic Original Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10098062/
https://www.ncbi.nlm.nih.gov/pubmed/36829260
http://dx.doi.org/10.1111/mpp.13314
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