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The global regulators ArcA and CytR collaboratively modulate Vibrio cholerae motility
BACKGROUND: Vibrio cholerae, a Gram-negative bacterium, is highly motile owing to the presence of a single polar flagellum. The global anaerobiosis response regulator, ArcA regulates the expression of virulence factors and enhance biofilm formation in V. cholerae. However, the function of ArcA for t...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8753867/ https://www.ncbi.nlm.nih.gov/pubmed/35021992 http://dx.doi.org/10.1186/s12866-022-02435-y |
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author | Li, Yuehua Yan, Junxiang Guo, Xueqian Wang, Xiaochen Liu, Fenxia Cao, Boyang |
author_facet | Li, Yuehua Yan, Junxiang Guo, Xueqian Wang, Xiaochen Liu, Fenxia Cao, Boyang |
author_sort | Li, Yuehua |
collection | PubMed |
description | BACKGROUND: Vibrio cholerae, a Gram-negative bacterium, is highly motile owing to the presence of a single polar flagellum. The global anaerobiosis response regulator, ArcA regulates the expression of virulence factors and enhance biofilm formation in V. cholerae. However, the function of ArcA for the motility of V. cholerae is yet to be elucidated. CytR, which represses nucleoside uptake and catabolism, is known to play a chief role in V. cholerae pathogenesis and flagellar synthesis but the mechanism that CytR influences motility is unclear. RESULTS: In this study, we found that the ΔarcA mutant strain exhibited higher motility than the WT strain due to ArcA directly repressed flrA expression. We further discovered that CytR directly enhanced fliK expression, which explained why the ΔcytR mutant strain was retarded in motility. On the other hand, cytR was a direct ArcA target and cytR expression was directly repressed by ArcA. As expected, cytR expression was down-regulated. CONCLUSIONS: Overall, ArcA plays a critical role in V. cholerae motility by regulating flrA expression directly and fliK indirectly in the manner of cytR. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s12866-022-02435-y. |
format | Online Article Text |
id | pubmed-8753867 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-87538672022-01-18 The global regulators ArcA and CytR collaboratively modulate Vibrio cholerae motility Li, Yuehua Yan, Junxiang Guo, Xueqian Wang, Xiaochen Liu, Fenxia Cao, Boyang BMC Microbiol Research BACKGROUND: Vibrio cholerae, a Gram-negative bacterium, is highly motile owing to the presence of a single polar flagellum. The global anaerobiosis response regulator, ArcA regulates the expression of virulence factors and enhance biofilm formation in V. cholerae. However, the function of ArcA for the motility of V. cholerae is yet to be elucidated. CytR, which represses nucleoside uptake and catabolism, is known to play a chief role in V. cholerae pathogenesis and flagellar synthesis but the mechanism that CytR influences motility is unclear. RESULTS: In this study, we found that the ΔarcA mutant strain exhibited higher motility than the WT strain due to ArcA directly repressed flrA expression. We further discovered that CytR directly enhanced fliK expression, which explained why the ΔcytR mutant strain was retarded in motility. On the other hand, cytR was a direct ArcA target and cytR expression was directly repressed by ArcA. As expected, cytR expression was down-regulated. CONCLUSIONS: Overall, ArcA plays a critical role in V. cholerae motility by regulating flrA expression directly and fliK indirectly in the manner of cytR. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s12866-022-02435-y. BioMed Central 2022-01-12 /pmc/articles/PMC8753867/ /pubmed/35021992 http://dx.doi.org/10.1186/s12866-022-02435-y Text en © The Author(s) 2022 https://creativecommons.org/licenses/by/4.0/Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) . The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/ (https://creativecommons.org/publicdomain/zero/1.0/) ) applies to the data made available in this article, unless otherwise stated in a credit line to the data. |
spellingShingle | Research Li, Yuehua Yan, Junxiang Guo, Xueqian Wang, Xiaochen Liu, Fenxia Cao, Boyang The global regulators ArcA and CytR collaboratively modulate Vibrio cholerae motility |
title | The global regulators ArcA and CytR collaboratively modulate Vibrio cholerae motility |
title_full | The global regulators ArcA and CytR collaboratively modulate Vibrio cholerae motility |
title_fullStr | The global regulators ArcA and CytR collaboratively modulate Vibrio cholerae motility |
title_full_unstemmed | The global regulators ArcA and CytR collaboratively modulate Vibrio cholerae motility |
title_short | The global regulators ArcA and CytR collaboratively modulate Vibrio cholerae motility |
title_sort | global regulators arca and cytr collaboratively modulate vibrio cholerae motility |
topic | Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8753867/ https://www.ncbi.nlm.nih.gov/pubmed/35021992 http://dx.doi.org/10.1186/s12866-022-02435-y |
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