A novel quorum sensing regulator LuxT contributes to the virulence of Vibrio cholerae

ABSTRACTVibrio cholerae is a waterborne bacterium that primarily infects the human intestine and causes cholera fatality. Quorum sensing (QS) negatively regulates the expression of V. cholerae virulence gene. However, the primary associated mechanisms remain undetermined. This investigation identifi...

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Main Authors: Yuehua Li, Junxiang Yan, Jinghao Li, Xinke Xue, Ying Wang, Boyang Cao
Format: Article
Language:English
Published: Taylor & Francis Group 2023-12-01
Series:Virulence
Subjects:
Online Access:https://www.tandfonline.com/doi/10.1080/21505594.2023.2274640
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author Yuehua Li
Junxiang Yan
Jinghao Li
Xinke Xue
Ying Wang
Boyang Cao
author_facet Yuehua Li
Junxiang Yan
Jinghao Li
Xinke Xue
Ying Wang
Boyang Cao
author_sort Yuehua Li
collection DOAJ
description ABSTRACTVibrio cholerae is a waterborne bacterium that primarily infects the human intestine and causes cholera fatality. Quorum sensing (QS) negatively regulates the expression of V. cholerae virulence gene. However, the primary associated mechanisms remain undetermined. This investigation identified a new QS regulator from the TetR family, LuxT, which increases V. cholerae virulence by directly inhibiting hapR expression. HapR is a master QS regulator that suppresses virulence cascade expression. The expression of luxT increased 4.8-fold in the small intestine of infant mice than in Luria-Bertani broth. ΔluxT mutant strain revealed a substantial defect in the colonizing ability of the small intestines. At low cell densities, the expression level of hapR was upregulated by luxT deletion, suggesting that LuxT can suppress hapR transcription. The electrophoretic mobility shift analysis revealed that LuxT directly binds to the hapR promoter region. Furthermore, luxT expression was upregulated by the two-component system ArcB/ArcA, which responses to changes in oxygen levels in response to the host’s small intestine’s anaerobic signals. In conclusion, this research reveals a novel cell density-mediated virulence regulation pathway and contributes to understanding the complex association between V. cholerae virulence and QS signals. This evidence furnishes new insights for future studies on cholerae’s pathogenic mechanisms.
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spelling doaj.art-f5e48a7527c846c995a8a3aa466fa5622024-01-03T17:26:57ZengTaylor & Francis GroupVirulence2150-55942150-56082023-12-0114110.1080/21505594.2023.2274640A novel quorum sensing regulator LuxT contributes to the virulence of Vibrio choleraeYuehua Li0Junxiang Yan1Jinghao Li2Xinke Xue3Ying Wang4Boyang Cao5TEDA Institute of Biological Sciences and Biotechnology, Nankai University, Tianjin, ChinaTEDA Institute of Biological Sciences and Biotechnology, Nankai University, Tianjin, ChinaTEDA Institute of Biological Sciences and Biotechnology, Nankai University, Tianjin, ChinaTEDA Institute of Biological Sciences and Biotechnology, Nankai University, Tianjin, ChinaTEDA Institute of Biological Sciences and Biotechnology, Nankai University, Tianjin, ChinaTEDA Institute of Biological Sciences and Biotechnology, Nankai University, Tianjin, ChinaABSTRACTVibrio cholerae is a waterborne bacterium that primarily infects the human intestine and causes cholera fatality. Quorum sensing (QS) negatively regulates the expression of V. cholerae virulence gene. However, the primary associated mechanisms remain undetermined. This investigation identified a new QS regulator from the TetR family, LuxT, which increases V. cholerae virulence by directly inhibiting hapR expression. HapR is a master QS regulator that suppresses virulence cascade expression. The expression of luxT increased 4.8-fold in the small intestine of infant mice than in Luria-Bertani broth. ΔluxT mutant strain revealed a substantial defect in the colonizing ability of the small intestines. At low cell densities, the expression level of hapR was upregulated by luxT deletion, suggesting that LuxT can suppress hapR transcription. The electrophoretic mobility shift analysis revealed that LuxT directly binds to the hapR promoter region. Furthermore, luxT expression was upregulated by the two-component system ArcB/ArcA, which responses to changes in oxygen levels in response to the host’s small intestine’s anaerobic signals. In conclusion, this research reveals a novel cell density-mediated virulence regulation pathway and contributes to understanding the complex association between V. cholerae virulence and QS signals. This evidence furnishes new insights for future studies on cholerae’s pathogenic mechanisms.https://www.tandfonline.com/doi/10.1080/21505594.2023.2274640Vibrio choleraequorum sensingluxThapRvirulenceArcA
spellingShingle Yuehua Li
Junxiang Yan
Jinghao Li
Xinke Xue
Ying Wang
Boyang Cao
A novel quorum sensing regulator LuxT contributes to the virulence of Vibrio cholerae
Virulence
Vibrio cholerae
quorum sensing
luxT
hapR
virulence
ArcA
title A novel quorum sensing regulator LuxT contributes to the virulence of Vibrio cholerae
title_full A novel quorum sensing regulator LuxT contributes to the virulence of Vibrio cholerae
title_fullStr A novel quorum sensing regulator LuxT contributes to the virulence of Vibrio cholerae
title_full_unstemmed A novel quorum sensing regulator LuxT contributes to the virulence of Vibrio cholerae
title_short A novel quorum sensing regulator LuxT contributes to the virulence of Vibrio cholerae
title_sort novel quorum sensing regulator luxt contributes to the virulence of vibrio cholerae
topic Vibrio cholerae
quorum sensing
luxT
hapR
virulence
ArcA
url https://www.tandfonline.com/doi/10.1080/21505594.2023.2274640
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