ExsD Inhibits Expression of the Pseudomonas aeruginosa Type III Secretion System by Disrupting ExsA Self-Association and DNA Binding Activity

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Published inJournal of Bacteriology Vol. 192; no. 6; pp. 1479 - 1486
Main Authors Brutinel, Evan D., Vakulskas, Christopher A., Yahr, Timothy L.
Format Journal Article
LanguageEnglish
Published Washington, DC American Society for Microbiology 01.03.2010
American Society for Microbiology (ASM)
Subjects
Bacteria
Bacterial Proteins - genetics
Bacterial Proteins - metabolism
Bacteriology
Binding sites
Biological and medical sciences
Deoxyribonucleic acid
DNA
DNA, Bacterial
Eukaryotes
Fundamental and applied biological sciences. Psychology
Gene Expression Regulation, Bacterial - physiology
Growth conditions
Microbiology
Miscellaneous
Molecular Biology of Pathogens
Mutation
Protein Binding
Pseudomonas aeruginosa
Pseudomonas aeruginosa - metabolism
Recombinant Fusion Proteins - genetics
Recombinant Fusion Proteins - metabolism
Repressor Proteins - genetics
Repressor Proteins - metabolism
Signal Transduction
Trans-Activators - genetics
Trans-Activators - metabolism
Transcription, Genetic
Pseudomonadales
Bacteria
Pseudomonadaceae
Pseudomonas aeruginosa
Type III secretion system
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Pseudomonas aeruginosa utilizes a type III secretion system (T3SS) to damage eukaryotic host cells and evade phagocytosis. Transcription of the T3SS regulon is controlled by ExsA, a member of the AraC/XylS family of transcriptional regulators. ExsA-dependent transcription is coupled to type III secretory activity through a cascade of three interacting proteins (ExsC, ExsD, and ExsE). Genetic data suggest that ExsD functions as an antiactivator by preventing ExsA-dependent transcription, ExsC functions as an anti-antiactivator by binding to and inhibiting ExsD, and ExsE binds to and inhibits ExsC. T3SS gene expression is activated in response to low-calcium growth conditions or contact with host cells, both of which trigger secretion of ExsE. In the present study we reconstitute the T3SS regulatory cascade in vitro using purified components and find that the ExsD.ExsA complex lacks DNA binding activity. As predicted by the genetic data, ExsC addition dissociates the ExsD.ExsA complex through formation of an ExsD.ExsC complex, thereby releasing ExsA to bind T3SS promoters and activate transcription. Addition of ExsE to the purified system results in formation of the ExsE.ExsC complex and prevents ExsC from dissociating the ExsD.ExsA complex. Although purified ExsA is monomeric in solution, bacterial two-hybrid analyses demonstrate that ExsA can self-associate and that ExsD inhibits self-association of ExsA. Based on these data we propose a model in which ExsD regulates ExsA-dependent transcription by inhibiting the DNA-binding and self-association properties of ExsA.
Pseudomonas aeruginosa utilizes a type III secretion system (T3SS) to damage eukaryotic host cells and evade phagocytosis. Transcription of the T3SS regulon is controlled by ExsA, a member of the AraC/XylS family of transcriptional regulators. ExsA-dependent transcription is coupled to type III secretory activity through a cascade of three interacting proteins (ExsC, ExsD, and ExsE). Genetic data suggest that ExsD functions as an antiactivator by preventing ExsA-dependent transcription, ExsC functions as an anti-antiactivator by binding to and inhibiting ExsD, and ExsE binds to and inhibits ExsC. T3SS gene expression is activated in response to low-calcium growth conditions or contact with host cells, both of which trigger secretion of ExsE. In the present study we reconstitute the T3SS regulatory cascade in vitro using purified components and find that the ExsD*ExsA complex lacks DNA binding activity. As predicted by the genetic data, ExsC addition dissociates the ExsD-ExsA complex through formation of an ExsD-ExsC complex, thereby releasing ExsA to bind T3SS promoters and activate transcription. Addition of ExsE to the purified system results in formation of the ExsE-ExsC complex and prevents ExsC from dissociating the ExsD-ExsA complex. Although purified ExsA is monomeric in solution, bacterial two-hybrid analyses demonstrate that ExsA can self-associate and that ExsD inhibits self-association of ExsA. Based on these data we propose a model in which ExsD regulates ExsA-dependent transcription by inhibiting the DNA-binding and self-association properties of ExsA. [PUBLICATION ABSTRACT]
Pseudomonas aeruginosa utilizes a type III secretion system (T3SS) to damage eukaryotic host cells and evade phagocytosis. Transcription of the T3SS regulon is controlled by ExsA, a member of the AraC/XylS family of transcriptional regulators. ExsA-dependent transcription is coupled to type III secretory activity through a cascade of three interacting proteins (ExsC, ExsD, and ExsE). Genetic data suggest that ExsD functions as an antiactivator by preventing ExsA-dependent transcription, ExsC functions as an anti-antiactivator by binding to and inhibiting ExsD, and ExsE binds to and inhibits ExsC. T3SS gene expression is activated in response to low-calcium growth conditions or contact with host cells, both of which trigger secretion of ExsE. In the present study we reconstitute the T3SS regulatory cascade in vitro using purified components and find that the ExsD·ExsA complex lacks DNA binding activity. As predicted by the genetic data, ExsC addition dissociates the ExsD·ExsA complex through formation of an ExsD·ExsC complex, thereby releasing ExsA to bind T3SS promoters and activate transcription. Addition of ExsE to the purified system results in formation of the ExsE·ExsC complex and prevents ExsC from dissociating the ExsD·ExsA complex. Although purified ExsA is monomeric in solution, bacterial two-hybrid analyses demonstrate that ExsA can self-associate and that ExsD inhibits self-association of ExsA. Based on these data we propose a model in which ExsD regulates ExsA-dependent transcription by inhibiting the DNA-binding and self-association properties of ExsA.
Pseudomonas aeruginosa utilizes a type III secretion system (T3SS) to damage eukaryotic host cells and evade phagocytosis. Transcription of the T3SS regulon is controlled by ExsA, a member of the AraC/XylS family of transcriptional regulators. ExsA-dependent transcription is coupled to type III secretory activity through a cascade of three interacting proteins (ExsC, ExsD, and ExsE). Genetic data suggest that ExsD functions as an antiactivator by preventing ExsA-dependent transcription, ExsC functions as an anti-antiactivator by binding to and inhibiting ExsD, and ExsE binds to and inhibits ExsC. T3SS gene expression is activated in response to low-calcium growth conditions or contact with host cells, both of which trigger secretion of ExsE. In the present study we reconstitute the T3SS regulatory cascade in vitro using purified components and find that the ExsD.ExsA complex lacks DNA binding activity. As predicted by the genetic data, ExsC addition dissociates the ExsD.ExsA complex through formation of an ExsD.ExsC complex, thereby releasing ExsA to bind T3SS promoters and activate transcription. Addition of ExsE to the purified system results in formation of the ExsE.ExsC complex and prevents ExsC from dissociating the ExsD.ExsA complex. Although purified ExsA is monomeric in solution, bacterial two-hybrid analyses demonstrate that ExsA can self-associate and that ExsD inhibits self-association of ExsA. Based on these data we propose a model in which ExsD regulates ExsA-dependent transcription by inhibiting the DNA-binding and self-association properties of ExsA.Pseudomonas aeruginosa utilizes a type III secretion system (T3SS) to damage eukaryotic host cells and evade phagocytosis. Transcription of the T3SS regulon is controlled by ExsA, a member of the AraC/XylS family of transcriptional regulators. ExsA-dependent transcription is coupled to type III secretory activity through a cascade of three interacting proteins (ExsC, ExsD, and ExsE). Genetic data suggest that ExsD functions as an antiactivator by preventing ExsA-dependent transcription, ExsC functions as an anti-antiactivator by binding to and inhibiting ExsD, and ExsE binds to and inhibits ExsC. T3SS gene expression is activated in response to low-calcium growth conditions or contact with host cells, both of which trigger secretion of ExsE. In the present study we reconstitute the T3SS regulatory cascade in vitro using purified components and find that the ExsD.ExsA complex lacks DNA binding activity. As predicted by the genetic data, ExsC addition dissociates the ExsD.ExsA complex through formation of an ExsD.ExsC complex, thereby releasing ExsA to bind T3SS promoters and activate transcription. Addition of ExsE to the purified system results in formation of the ExsE.ExsC complex and prevents ExsC from dissociating the ExsD.ExsA complex. Although purified ExsA is monomeric in solution, bacterial two-hybrid analyses demonstrate that ExsA can self-associate and that ExsD inhibits self-association of ExsA. Based on these data we propose a model in which ExsD regulates ExsA-dependent transcription by inhibiting the DNA-binding and self-association properties of ExsA.
Author Christopher A. Vakulskas
Evan D. Brutinel
Timothy L. Yahr
AuthorAffiliation Department of Microbiology, University of Iowa, Iowa City, Iowa
AuthorAffiliation_xml – name: Department of Microbiology, University of Iowa, Iowa City, Iowa
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  surname: Brutinel
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  surname: Vakulskas
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  organization: Department of Microbiology, University of Iowa, Iowa City, Iowa
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  givenname: Timothy L.
  surname: Yahr
  fullname: Yahr, Timothy L.
  organization: Department of Microbiology, University of Iowa, Iowa City, Iowa
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Keywords Pseudomonadales
Bacteria
Pseudomonadaceae
Pseudomonas aeruginosa
Type III secretion system
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Pseudomonas aeruginosa utilizes a type III secretion system (T3SS) to damage eukaryotic host cells and evade phagocytosis. Transcription of the T3SS regulon is...
Pseudomonas aeruginosa utilizes a type III secretion system (T3SS) to damage eukaryotic host cells and evade phagocytosis. Transcription of the T3SS regulon is...
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StartPage 1479
SubjectTerms Bacteria
Bacterial Proteins - genetics
Bacterial Proteins - metabolism
Bacteriology
Binding sites
Biological and medical sciences
Deoxyribonucleic acid
DNA
DNA, Bacterial
Eukaryotes
Fundamental and applied biological sciences. Psychology
Gene Expression Regulation, Bacterial - physiology
Growth conditions
Microbiology
Miscellaneous
Molecular Biology of Pathogens
Mutation
Protein Binding
Pseudomonas aeruginosa
Pseudomonas aeruginosa - metabolism
Recombinant Fusion Proteins - genetics
Recombinant Fusion Proteins - metabolism
Repressor Proteins - genetics
Repressor Proteins - metabolism
Signal Transduction
Trans-Activators - genetics
Trans-Activators - metabolism
Transcription, Genetic
Title ExsD Inhibits Expression of the Pseudomonas aeruginosa Type III Secretion System by Disrupting ExsA Self-Association and DNA Binding Activity
URI http://jb.asm.org/content/192/6/1479.abstract
https://www.ncbi.nlm.nih.gov/pubmed/20008065
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https://www.proquest.com/docview/21296493
https://www.proquest.com/docview/733620701
https://pubmed.ncbi.nlm.nih.gov/PMC2832532
Volume 192
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