Regulation of Type VI Secretion System during Burkholderia pseudomallei Infection

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Published inInfection and Immunity Vol. 79; no. 8; pp. 3064 - 3073
Main Authors Chen, Yahua, Wong, Jocelyn, Sun, Guang Wen, Liu, Yichun, Tan, Gek-Yen Gladys, Gan, Yunn-Hwen
Format Journal Article
LanguageEnglish
Published Washington, DC American Society for Microbiology 01.08.2011
Subjects
Animals
Bacteriology
Biological and medical sciences
Burkholderia Infections - microbiology
Burkholderia Infections - pathology
Burkholderia pseudomallei - genetics
Burkholderia pseudomallei - metabolism
Burkholderia pseudomallei - pathogenicity
Cellular Microbiology: Pathogen-Host Cell Molecular Interactions
Disease Models, Animal
Fundamental and applied biological sciences. Psychology
Gene Expression Regulation, Bacterial
Macromolecular Substances - metabolism
Membrane Transport Proteins - metabolism
Mice
Mice, Inbred BALB C
Microbiology
Miscellaneous
Rodent Diseases - microbiology
Rodent Diseases - pathology
Signal Transduction
Trans-Activators - metabolism
Virulence
Virulence Factors - metabolism
Bacteria
Burkholderia pseudomallei
Immunity
Type IV secretion system
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Abstract Classifications Services IAI Citing Articles Google Scholar PubMed Related Content Social Bookmarking CiteULike Delicious Digg Facebook Google+ Mendeley Reddit StumbleUpon Twitter current issue Spotlights in the Current Issue IAI About IAI Subscribers Authors Reviewers Advertisers Inquiries from the Press Permissions & Commercial Reprints ASM Journals Public Access Policy Connect to IAI IAI RSS Feeds 1752 N Street N.W. • Washington DC 20036 202.737.3600 • 202.942.9355 fax • journals@asmusa.org Print ISSN: 0019-9567 Online ISSN: 1098-5522 Copyright © 2014 by the American Society for Microbiology.   For an alternate route to IAI .asm.org, visit: IAI       
AbstractList Type III and type VI secretion systems (T3SSs and T6SSs, respectively) are critical virulence determinants in several Gram-negative pathogens. In Burkholderia pseudomallei , the T3SS-3 and T6SS-1 clusters have been implicated in bacterial virulence in mammalian hosts. We recently discovered a regulatory cascade that coordinately controls the expression of T3SS-3 and T6SS-1. BsaN is a central regulator located within T3SS-3 for the expression of T3SS-3 effectors and regulators for T6SS-1 such as VirA-VirG (VirAG) and BprC. Whereas T6SS-1 gene expression was completely dependent on BprC when bacteria were grown in medium, the expression inside host cells was dependent on the two-component sensor-regulator VirAG, with the exception of the tssAB operon, which was dependent primarily on BprC. VirAG and BprC initiate different transcriptional start sites within T6SS-1, and VirAG is able to activate the hcp1 promoter directly. We also provided novel evidence that virAG , bprC , and tssAB are critical for T6SS-1 function in macrophages. Furthermore, virAG and bprC regulator mutants were avirulent in mice, demonstrating the absolute dependence of T6SS-1 expression on these regulators in vivo .
Classifications Services IAI Citing Articles Google Scholar PubMed Related Content Social Bookmarking CiteULike Delicious Digg Facebook Google+ Mendeley Reddit StumbleUpon Twitter current issue Spotlights in the Current Issue IAI About IAI Subscribers Authors Reviewers Advertisers Inquiries from the Press Permissions & Commercial Reprints ASM Journals Public Access Policy Connect to IAI IAI RSS Feeds 1752 N Street N.W. • Washington DC 20036 202.737.3600 • 202.942.9355 fax • journals@asmusa.org Print ISSN: 0019-9567 Online ISSN: 1098-5522 Copyright © 2014 by the American Society for Microbiology.   For an alternate route to IAI .asm.org, visit: IAI       
Type III and type VI secretion systems (T3SSs and T6SSs, respectively) are critical virulence determinants in several Gram-negative pathogens. In Burkholderia pseudomallei, the T3SS-3 and T6SS-1 clusters have been implicated in bacterial virulence in mammalian hosts. We recently discovered a regulatory cascade that coordinately controls the expression of T3SS-3 and T6SS-1. BsaN is a central regulator located within T3SS-3 for the expression of T3SS-3 effectors and regulators for T6SS-1 such as VirA-VirG (VirAG) and BprC. Whereas T6SS-1 gene expression was completely dependent on BprC when bacteria were grown in medium, the expression inside host cells was dependent on the two-component sensor-regulator VirAG, with the exception of the tssAB operon, which was dependent primarily on BprC. VirAG and BprC initiate different transcriptional start sites within T6SS-1, and VirAG is able to activate the hcp1 promoter directly. We also provided novel evidence that virAG, bprC, and tssAB are critical for T6SS-1 function in macrophages. Furthermore, virAG and bprC regulator mutants were avirulent in mice, demonstrating the absolute dependence of T6SS-1 expression on these regulators in vivo.
Author Yahua Chen
Guang Wen Sun
Gek-Yen Gladys Tan
Jocelyn Wong
Yichun Liu
Yunn-Hwen Gan
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Type IV secretion system
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Type III and type VI secretion systems (T3SSs and T6SSs, respectively) are critical virulence determinants in several Gram-negative pathogens. In Burkholderia...
Type III and type VI secretion systems (T3SSs and T6SSs, respectively) are critical virulence determinants in several Gram-negative pathogens. In Burkholderia...
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SubjectTerms Animals
Bacteriology
Biological and medical sciences
Burkholderia Infections - microbiology
Burkholderia Infections - pathology
Burkholderia pseudomallei - genetics
Burkholderia pseudomallei - metabolism
Burkholderia pseudomallei - pathogenicity
Cellular Microbiology: Pathogen-Host Cell Molecular Interactions
Disease Models, Animal
Fundamental and applied biological sciences. Psychology
Gene Expression Regulation, Bacterial
Macromolecular Substances - metabolism
Membrane Transport Proteins - metabolism
Mice
Mice, Inbred BALB C
Microbiology
Miscellaneous
Rodent Diseases - microbiology
Rodent Diseases - pathology
Signal Transduction
Trans-Activators - metabolism
Virulence
Virulence Factors - metabolism
Title Regulation of Type VI Secretion System during Burkholderia pseudomallei Infection
URI http://iai.asm.org/content/79/8/3064.abstract
https://www.ncbi.nlm.nih.gov/pubmed/21670170
https://search.proquest.com/docview/878031199
https://pubmed.ncbi.nlm.nih.gov/PMC3147588
Volume 79
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