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VirS, an OmpR/PhoB subfamily response regulator, is required for activation of vapA gene expression in Rhodococcus equi
BACKGROUND: Rhodococcus equi is an important pulmonary pathogen in foals and in immunocompromised individuals. Virulent R. equi strains carry an 80-90 kb virulence plasmid that expresses the virulence-associated protein A (VapA). VapA expression is regulated by temperature and pH. The LysR-type tran...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2014
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4190465/ https://www.ncbi.nlm.nih.gov/pubmed/25281192 http://dx.doi.org/10.1186/s12866-014-0243-1 |
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author | Kakuda, Tsutomu Hirota, Takuya Takeuchi, Tatsuya Hagiuda, Hirofumi Miyazaki, Shiko Takai, Shinji |
author_facet | Kakuda, Tsutomu Hirota, Takuya Takeuchi, Tatsuya Hagiuda, Hirofumi Miyazaki, Shiko Takai, Shinji |
author_sort | Kakuda, Tsutomu |
collection | PubMed |
description | BACKGROUND: Rhodococcus equi is an important pulmonary pathogen in foals and in immunocompromised individuals. Virulent R. equi strains carry an 80-90 kb virulence plasmid that expresses the virulence-associated protein A (VapA). VapA expression is regulated by temperature and pH. The LysR-type transcriptional regulator, VirR, is involved in the regulation of the vapA gene. To examine the mechanism underlying transcriptional regulation of vapA, we characterized an R. equi mutant in which another putative transcriptional regulator encoded on the virulence plasmid, VirS, was deleted. RESULTS: Deletion of virS reduced vapA promoter activity to non-inducible levels. Complementary expression of VirS in the virS deletion mutant restored transcription at the P(vapA) promoter, even under non-inducing conditions (30°C and pH 8.0). In addition, VirS expression increased P(vapA) promoter activity in the absence of functional VirR. Further, transcription of the icgA operon containing virS was regulated by pH and temperature in the same manner as vapA. CONCLUSIONS: This study suggests that VirS is required for VapA expression and that regulation of P(vapA)-promoter activity may be achieved by controlling VirS expression levels. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/s12866-014-0243-1) contains supplementary material, which is available to authorized users. |
format | Online Article Text |
id | pubmed-4190465 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2014 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-41904652014-10-10 VirS, an OmpR/PhoB subfamily response regulator, is required for activation of vapA gene expression in Rhodococcus equi Kakuda, Tsutomu Hirota, Takuya Takeuchi, Tatsuya Hagiuda, Hirofumi Miyazaki, Shiko Takai, Shinji BMC Microbiol Research Article BACKGROUND: Rhodococcus equi is an important pulmonary pathogen in foals and in immunocompromised individuals. Virulent R. equi strains carry an 80-90 kb virulence plasmid that expresses the virulence-associated protein A (VapA). VapA expression is regulated by temperature and pH. The LysR-type transcriptional regulator, VirR, is involved in the regulation of the vapA gene. To examine the mechanism underlying transcriptional regulation of vapA, we characterized an R. equi mutant in which another putative transcriptional regulator encoded on the virulence plasmid, VirS, was deleted. RESULTS: Deletion of virS reduced vapA promoter activity to non-inducible levels. Complementary expression of VirS in the virS deletion mutant restored transcription at the P(vapA) promoter, even under non-inducing conditions (30°C and pH 8.0). In addition, VirS expression increased P(vapA) promoter activity in the absence of functional VirR. Further, transcription of the icgA operon containing virS was regulated by pH and temperature in the same manner as vapA. CONCLUSIONS: This study suggests that VirS is required for VapA expression and that regulation of P(vapA)-promoter activity may be achieved by controlling VirS expression levels. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/s12866-014-0243-1) contains supplementary material, which is available to authorized users. BioMed Central 2014-10-03 /pmc/articles/PMC4190465/ /pubmed/25281192 http://dx.doi.org/10.1186/s12866-014-0243-1 Text en © Kakuda et al.; licensee BioMed Central Ltd. 2014 This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated. |
spellingShingle | Research Article Kakuda, Tsutomu Hirota, Takuya Takeuchi, Tatsuya Hagiuda, Hirofumi Miyazaki, Shiko Takai, Shinji VirS, an OmpR/PhoB subfamily response regulator, is required for activation of vapA gene expression in Rhodococcus equi |
title | VirS, an OmpR/PhoB subfamily response regulator, is required for activation of vapA gene expression in Rhodococcus equi |
title_full | VirS, an OmpR/PhoB subfamily response regulator, is required for activation of vapA gene expression in Rhodococcus equi |
title_fullStr | VirS, an OmpR/PhoB subfamily response regulator, is required for activation of vapA gene expression in Rhodococcus equi |
title_full_unstemmed | VirS, an OmpR/PhoB subfamily response regulator, is required for activation of vapA gene expression in Rhodococcus equi |
title_short | VirS, an OmpR/PhoB subfamily response regulator, is required for activation of vapA gene expression in Rhodococcus equi |
title_sort | virs, an ompr/phob subfamily response regulator, is required for activation of vapa gene expression in rhodococcus equi |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4190465/ https://www.ncbi.nlm.nih.gov/pubmed/25281192 http://dx.doi.org/10.1186/s12866-014-0243-1 |
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