A transcription factor contributes to pathogenesis and virulence in Streptococcus pneumoniae
To date, the role of transcription factors (TFs) in the progression of disease for many pathogens is yet to be studied in detail. This is probably due to transient, and generally low expression levels of TFs, which are the central components controlling the expression of many genes during the course...
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| Veröffentlicht in: | PloS one 2013-08, Vol.8 (8), p.e70862 |
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| creator | Mahdi, Layla K Ebrahimie, Esmaeil Adelson, David L Paton, James C Ogunniyi, Abiodun D |
| description | To date, the role of transcription factors (TFs) in the progression of disease for many pathogens is yet to be studied in detail. This is probably due to transient, and generally low expression levels of TFs, which are the central components controlling the expression of many genes during the course of infection. However, a small change in the expression or specificity of a TF can radically alter gene expression. In this study, we combined a number of quality-based selection strategies including structural prediction of modulated genes, gene ontology and network analysis, to predict the regulatory mechanisms underlying pathogenesis of Streptococcus pneumoniae (the pneumococcus). We have identified two TFs (SP_0676 and SP_0927 [SmrC]) that might control tissue-specific gene expression during pneumococcal translocation from the nasopharynx to lungs, to blood and then to brain of mice. Targeted mutagenesis and mouse models of infection confirmed the role of SP_0927 in pathogenesis and virulence, and suggests that SP_0676 might be essential to pneumococcal viability. These findings provide fundamental new insights into virulence gene expression and regulation during pathogenesis. |
| doi_str_mv | 10.1371/journal.pone.0070862 |
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This is probably due to transient, and generally low expression levels of TFs, which are the central components controlling the expression of many genes during the course of infection. However, a small change in the expression or specificity of a TF can radically alter gene expression. In this study, we combined a number of quality-based selection strategies including structural prediction of modulated genes, gene ontology and network analysis, to predict the regulatory mechanisms underlying pathogenesis of Streptococcus pneumoniae (the pneumococcus). We have identified two TFs (SP_0676 and SP_0927 [SmrC]) that might control tissue-specific gene expression during pneumococcal translocation from the nasopharynx to lungs, to blood and then to brain of mice. Targeted mutagenesis and mouse models of infection confirmed the role of SP_0927 in pathogenesis and virulence, and suggests that SP_0676 might be essential to pneumococcal viability. These findings provide fundamental new insights into virulence gene expression and regulation during pathogenesis.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0070862</identifier><identifier>PMID: 23967124</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Animal models ; Animals ; Bacteria ; Bacterial Proteins - genetics ; Bioinformatics ; Biology ; Brain ; Brain research ; Computational Biology - methods ; Development and progression ; DNA binding proteins ; Experiments ; Female ; Gene expression ; Gene Expression Profiling ; Gene Expression Regulation, Bacterial ; Gene Regulatory Networks ; Genes ; Health aspects ; Host-Pathogen Interactions ; Infections ; Infectious diseases ; Lungs ; Medicine ; Mice ; Mutagenesis ; Mutation ; Nasopharynx ; Network analysis ; Organ Specificity ; Pathogenesis ; Pathogens ; Pneumococcal Infections - microbiology ; Pneumonia ; Proteins ; Regulatory mechanisms (biology) ; Science ; Site-directed mutagenesis ; Streptococcus infections ; Streptococcus pneumoniae ; Streptococcus pneumoniae - genetics ; Streptococcus pneumoniae - pathogenicity ; Targeted mutagenesis ; Transcription factors ; Transcription Factors - genetics ; Translocation ; Viability ; Virulence ; Virulence (Microbiology) ; Virulence - genetics</subject><ispartof>PloS one, 2013-08, Vol.8 (8), p.e70862</ispartof><rights>COPYRIGHT 2013 Public Library of Science</rights><rights>2013 Mahdi et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: https://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. 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These findings provide fundamental new insights into virulence gene expression and regulation during pathogenesis.</description><subject>Animal models</subject><subject>Animals</subject><subject>Bacteria</subject><subject>Bacterial Proteins - genetics</subject><subject>Bioinformatics</subject><subject>Biology</subject><subject>Brain</subject><subject>Brain research</subject><subject>Computational Biology - methods</subject><subject>Development and progression</subject><subject>DNA binding proteins</subject><subject>Experiments</subject><subject>Female</subject><subject>Gene expression</subject><subject>Gene Expression Profiling</subject><subject>Gene Expression Regulation, Bacterial</subject><subject>Gene Regulatory Networks</subject><subject>Genes</subject><subject>Health aspects</subject><subject>Host-Pathogen Interactions</subject><subject>Infections</subject><subject>Infectious diseases</subject><subject>Lungs</subject><subject>Medicine</subject><subject>Mice</subject><subject>Mutagenesis</subject><subject>Mutation</subject><subject>Nasopharynx</subject><subject>Network analysis</subject><subject>Organ Specificity</subject><subject>Pathogenesis</subject><subject>Pathogens</subject><subject>Pneumococcal Infections - 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This is probably due to transient, and generally low expression levels of TFs, which are the central components controlling the expression of many genes during the course of infection. However, a small change in the expression or specificity of a TF can radically alter gene expression. In this study, we combined a number of quality-based selection strategies including structural prediction of modulated genes, gene ontology and network analysis, to predict the regulatory mechanisms underlying pathogenesis of Streptococcus pneumoniae (the pneumococcus). We have identified two TFs (SP_0676 and SP_0927 [SmrC]) that might control tissue-specific gene expression during pneumococcal translocation from the nasopharynx to lungs, to blood and then to brain of mice. Targeted mutagenesis and mouse models of infection confirmed the role of SP_0927 in pathogenesis and virulence, and suggests that SP_0676 might be essential to pneumococcal viability. 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| source | MEDLINE; DOAJ Directory of Open Access Journals; Public Library of Science (PLoS) Journals Open Access; EZB-FREE-00999 freely available EZB journals; PubMed Central; Free Full-Text Journals in Chemistry |
| subjects | Animal models Animals Bacteria Bacterial Proteins - genetics Bioinformatics Biology Brain Brain research Computational Biology - methods Development and progression DNA binding proteins Experiments Female Gene expression Gene Expression Profiling Gene Expression Regulation, Bacterial Gene Regulatory Networks Genes Health aspects Host-Pathogen Interactions Infections Infectious diseases Lungs Medicine Mice Mutagenesis Mutation Nasopharynx Network analysis Organ Specificity Pathogenesis Pathogens Pneumococcal Infections - microbiology Pneumonia Proteins Regulatory mechanisms (biology) Science Site-directed mutagenesis Streptococcus infections Streptococcus pneumoniae Streptococcus pneumoniae - genetics Streptococcus pneumoniae - pathogenicity Targeted mutagenesis Transcription factors Transcription Factors - genetics Translocation Viability Virulence Virulence (Microbiology) Virulence - genetics |
| title | A transcription factor contributes to pathogenesis and virulence in Streptococcus pneumoniae |
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