SuhB Is a Regulator of Multiple Virulence Genes and Essential for Pathogenesis of <named-content content-type="genus-species">Pseudomonas aeruginosa</named-content>

ABSTRACT During initial colonization and chronic infection, pathogenic bacteria encounter distinct host environments. Adjusting gene expression accordingly is essential for the pathogenesis. Pseudomonas aeruginosa has evolved complicated regulatory networks to regulate different sets of virulence fa...

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Autores principales: Kewei Li, Chang Xu, Yongxin Jin, Ziyu Sun, Chang Liu, Jing Shi, Gukui Chen, Ronghao Chen, Shouguang Jin, Weihui Wu
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Publicado: American Society for Microbiology 2013
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spelling oai:doaj.org-article:a7c2d93515bb4bc0a0af15f10e66689a2021-11-15T15:42:32ZSuhB Is a Regulator of Multiple Virulence Genes and Essential for Pathogenesis of <named-content content-type="genus-species">Pseudomonas aeruginosa</named-content>10.1128/mBio.00419-132150-7511https://doaj.org/article/a7c2d93515bb4bc0a0af15f10e66689a2013-12-01T00:00:00Zhttps://journals.asm.org/doi/10.1128/mBio.00419-13https://doaj.org/toc/2150-7511ABSTRACT During initial colonization and chronic infection, pathogenic bacteria encounter distinct host environments. Adjusting gene expression accordingly is essential for the pathogenesis. Pseudomonas aeruginosa has evolved complicated regulatory networks to regulate different sets of virulence factors to facilitate colonization and persistence. The type III secretion system (T3SS) and motility are associated with acute infections, while biofilm formation and the type VI secretion system (T6SS) are associated with chronic persistence. To identify novel regulatory genes required for pathogenesis, we screened a P. aeruginosa transposon (Tn) insertion library and found suhB to be an essential gene for the T3SS gene expression. The expression of suhB was upregulated in a mouse acute lung infection model, and loss of suhB resulted in avirulence. Suppression of T3SS gene expression in the suhB mutant is linked to a defective translation of the T3SS master regulator, ExsA. Further studies demonstrated that suhB mutation led to the upregulation of GacA and its downstream small RNAs, RsmY and RsmZ, triggering T6SS expression and biofilm formation while inhibiting the T3SS. Our results demonstrate that an in vivo-inducible gene, suhB, reciprocally regulates genes associated with acute and chronic infections and plays an essential role in the pathogenesis of P. aeruginosa. IMPORTANCE A variety of bacterial pathogens, such as Pseudomonas aeruginosa, cause acute and chronic infections in humans. During infections, pathogens produce different sets of virulence genes for colonization, tissue damage, and dissemination and for countering host immune responses. Complex regulatory networks control the delicate tuning of gene expression in response to host environments to enable the survival and growth of invading pathogens. Here we identified suhB as a critical gene for the regulation of virulence factors in P. aeruginosa. The expression of suhB was upregulated during acute infection in an animal model, and mutation of suhB rendered P. aeruginosa avirulent. Moreover, we demonstrate that SuhB is required for the activation of virulence factors associated with acute infections while suppressing virulence factors associated with chronic infections. Our report provides new insights into the multilayered regulatory network of virulence genes in P. aeruginosa.Kewei LiChang XuYongxin JinZiyu SunChang LiuJing ShiGukui ChenRonghao ChenShouguang JinWeihui WuAmerican Society for MicrobiologyarticleMicrobiologyQR1-502ENmBio, Vol 4, Iss 6 (2013)
institution DOAJ
collection DOAJ
language EN
topic Microbiology
QR1-502
spellingShingle Microbiology
QR1-502
Kewei Li
Chang Xu
Yongxin Jin
Ziyu Sun
Chang Liu
Jing Shi
Gukui Chen
Ronghao Chen
Shouguang Jin
Weihui Wu
SuhB Is a Regulator of Multiple Virulence Genes and Essential for Pathogenesis of <named-content content-type="genus-species">Pseudomonas aeruginosa</named-content>
description ABSTRACT During initial colonization and chronic infection, pathogenic bacteria encounter distinct host environments. Adjusting gene expression accordingly is essential for the pathogenesis. Pseudomonas aeruginosa has evolved complicated regulatory networks to regulate different sets of virulence factors to facilitate colonization and persistence. The type III secretion system (T3SS) and motility are associated with acute infections, while biofilm formation and the type VI secretion system (T6SS) are associated with chronic persistence. To identify novel regulatory genes required for pathogenesis, we screened a P. aeruginosa transposon (Tn) insertion library and found suhB to be an essential gene for the T3SS gene expression. The expression of suhB was upregulated in a mouse acute lung infection model, and loss of suhB resulted in avirulence. Suppression of T3SS gene expression in the suhB mutant is linked to a defective translation of the T3SS master regulator, ExsA. Further studies demonstrated that suhB mutation led to the upregulation of GacA and its downstream small RNAs, RsmY and RsmZ, triggering T6SS expression and biofilm formation while inhibiting the T3SS. Our results demonstrate that an in vivo-inducible gene, suhB, reciprocally regulates genes associated with acute and chronic infections and plays an essential role in the pathogenesis of P. aeruginosa. IMPORTANCE A variety of bacterial pathogens, such as Pseudomonas aeruginosa, cause acute and chronic infections in humans. During infections, pathogens produce different sets of virulence genes for colonization, tissue damage, and dissemination and for countering host immune responses. Complex regulatory networks control the delicate tuning of gene expression in response to host environments to enable the survival and growth of invading pathogens. Here we identified suhB as a critical gene for the regulation of virulence factors in P. aeruginosa. The expression of suhB was upregulated during acute infection in an animal model, and mutation of suhB rendered P. aeruginosa avirulent. Moreover, we demonstrate that SuhB is required for the activation of virulence factors associated with acute infections while suppressing virulence factors associated with chronic infections. Our report provides new insights into the multilayered regulatory network of virulence genes in P. aeruginosa.
format article
author Kewei Li
Chang Xu
Yongxin Jin
Ziyu Sun
Chang Liu
Jing Shi
Gukui Chen
Ronghao Chen
Shouguang Jin
Weihui Wu
author_facet Kewei Li
Chang Xu
Yongxin Jin
Ziyu Sun
Chang Liu
Jing Shi
Gukui Chen
Ronghao Chen
Shouguang Jin
Weihui Wu
author_sort Kewei Li
title SuhB Is a Regulator of Multiple Virulence Genes and Essential for Pathogenesis of <named-content content-type="genus-species">Pseudomonas aeruginosa</named-content>
title_short SuhB Is a Regulator of Multiple Virulence Genes and Essential for Pathogenesis of <named-content content-type="genus-species">Pseudomonas aeruginosa</named-content>
title_full SuhB Is a Regulator of Multiple Virulence Genes and Essential for Pathogenesis of <named-content content-type="genus-species">Pseudomonas aeruginosa</named-content>
title_fullStr SuhB Is a Regulator of Multiple Virulence Genes and Essential for Pathogenesis of <named-content content-type="genus-species">Pseudomonas aeruginosa</named-content>
title_full_unstemmed SuhB Is a Regulator of Multiple Virulence Genes and Essential for Pathogenesis of <named-content content-type="genus-species">Pseudomonas aeruginosa</named-content>
title_sort suhb is a regulator of multiple virulence genes and essential for pathogenesis of <named-content content-type="genus-species">pseudomonas aeruginosa</named-content>
publisher American Society for Microbiology
publishDate 2013
url https://doaj.org/article/a7c2d93515bb4bc0a0af15f10e66689a
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