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Your search keyword '"Robins‐Browne, Roy"' showing total 90 results
Start Over Author "Robins‐Browne, Roy" Publisher american society for microbiology
90 results on '"Robins‐Browne, Roy"'

1. Persistence of Rare Salmonella Typhi Genotypes Susceptible to First-Line Antibiotics in the Remote Islands of Samoa

Author

Sikorski, Michael J., primary, Hazen, Tracy H., additional, Desai, Sachin N., additional, Nimarota-Brown, Susana, additional, Tupua, Siaosi, additional, Sialeipata, Michelle, additional, Rambocus, Savitra, additional, Ingle, Danielle J., additional, Duchene, Sebastian, additional, Ballard, Susan A., additional, Valcanis, Mary, additional, Zufan, Sara, additional, Ma, Jianguo, additional, Sahl, Jason W., additional, Maes, Mailis, additional, Dougan, Gordon, additional, Thomsen, Robert E., additional, Robins-Browne, Roy M., additional, Howden, Benjamin P., additional, Naseri, Take K., additional, Levine, Myron M., additional, and Rasko, David A., additional

Published
2022
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2. Transcriptional analysis of the grlRA virulence operon from Citrobacter rodentium

Author

Tauschek, Marija, Yang, Ji, Hocking, Dianna, Azzopardi, Kristy, Tan, Aimee, Hart, Emily, Praszkier, Judyta, and Robins-Browne, Roy M.

Subjects
Promoters (Genetics) -- Physiological aspects, Virulence (Microbiology) -- Genetic aspects, Operons -- Physiological aspects, Enterobacter -- Genetic aspects, Enterobacter -- Physiological aspects, Enterobacteriaceae -- Genetic aspects, Enterobacteriaceae -- Physiological aspects, Biological sciences
Abstract

The locus for enterocyte effacement (LEE) is the virulence hallmark of the attaching-and-effacing (A/E) intestinal pathogens, namely, enteropathogenic Escherichia coli, enterohemorrhagic E. coli, and Citrobacter rodentium. The LEE carries more than 40 genes that are arranged in several operons, e.g., LEE1 to LEE5. Expression of the various transcriptional units is subject to xenogeneic silencing by the histone-like protein H-NS. The LEE1-encoded regulator, Ler, plays a key role in relieving this repression at several major LEE promoters, including LEE2 to LEE5. To achieve appropriate intracellular concentrations of Ler in different environments, A/E pathogens have evolved a sophisticated regulatory network to control ler expression. For example, the LEE-encoded GrlA and GrlR proteins work as activator and antiactivator, respectively, of ler transcription. Thus, control of the transcriptional activities of the LEE1 (ler) promoter and the grlRA operon determines the rate of transcription of all of the LEE-encoded virulence factors. To date, only a single promoter has been identified for the grlRA operon. In this study, we showed that the non-LEE-encoded AraC-like regulatory protein RegA of C. rodentium directly stimulates transcription of the grlRA promoter by binding to an upstream region in the presence of bicarbonate ions. In addition, in vivo and in vitro transcription assays revealed a [[sigma].sup.70] promoter that is specifically responsible for transcription of grlA. Expression from this promoter was strongly repressed by H-NS and its paralog StpA but was activated by Ler. DNase I footprinting demonstrated that Let binds to a region upstream of the grlA promoter, whereas H-NS interacts specifically with a region extending from the grlA core promoter into its coding sequence. Together, these findings provide new insights into the environmental regulation and differential expressions of the grlR and grlA genes of C. rodentium. doi: 10.1128/JB.01540-09

Published
2010

3. Transcriptional regulation of the yghJ-pppA-yghG-gspCDEFGHIJKLM cluster, encoding the type II secretion pathway in enterotoxigenic Escherichia coli

Author

Yang, Ji, Baldi, Deborah L., Tauschek, Marija, Strugnell, Richard A., and Robins-Browne, Roy M.

Subjects
Escherichia coli -- Genetic aspects, Escherichia coli -- Research, Secretion -- Structure, Secretion -- Research, Genetic regulation -- Research, Genetic transcription -- Research, Biological sciences
Abstract

The gene cluster gspCDEFGHIJKLM codes for various structural components of the type II secretion pathway which is responsible for the secretion of heat-labile enterotoxin by enterotoxigenic Escherichia coli (ETEC). In this work, we used a variety of molecular approaches to elucidate the transcriptional organization of the ETEC type II secretion system and to unravel the mechanisms by which the expression of these genes is controlled. We showed that the gspCDEFGHIJKLM cluster and three other upstream genes, yghJ, pppA, and yghG, are cotranscribed and that a promoter located in the upstream region of yghJ plays a major role in the expression of this 14-gene transcriptional unit. Transcription of the yghJ promoter was repressed 168-fold upon a temperature downshift from 37[degrees]C to 22[degrees]C. This temperature-induced repression was mediated by the global regulatory proteins H-NS and StpA. Deletion mutagenesis showed that the promoter region encompassing positions -321 to +301 relative to the start site of transcription of yghJ was required for full repression. The yghJ promoter region is predicted to be highly curved and bound H-NS or StpA directly. The binding of H-NS or StpA blocked transcription initiation by inhibiting promoter open complex formation. Unraveling the mechanisms of regulation of type II secretion by ETEC enhances our understanding of the pathogenesis of ETEC and other pathogenic varieties of E. coli.

Published
2007

15. The Type II Secretion System and Its Ubiquitous Lipoprotein Substrate, SslE, Are Required for Biofilm Formation and Virulence of Enteropathogenic Escherichia coli

Author

Baldi, Deborah L., primary, Higginson, Ellen E., additional, Hocking, Dianna M., additional, Praszkier, Judyta, additional, Cavaliere, Rosalia, additional, James, Catherine E., additional, Bennett-Wood, Vicki, additional, Azzopardi, Kristy I., additional, Turnbull, Lynne, additional, Lithgow, Trevor, additional, Robins-Browne, Roy M., additional, Whitchurch, Cynthia B., additional, and Tauschek, Marija, additional

Published
2012
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27. TccP2 of O157:H7 and Non-O157 Enterohemorrhagic Escherichia coli (EHEC): Challenging the Dogma of EHEC-Induced Actin Polymerization

Author

Ogura, Yoshitoshi, primary, Ooka, Tadasuke, additional, Whale, Andrew, additional, Garmendia, Junkal, additional, Beutin, Lothar, additional, Tennant, Sharon, additional, Krause, Gladys, additional, Morabito, Stefano, additional, Chinen, Isabel, additional, Tobe, Toru, additional, Abe, Hiroyuki, additional, Tozzoli, Rosangela, additional, Caprioli, Alfredo, additional, Rivas, Marta, additional, Robins-Browne, Roy, additional, Hayashi, Tetsuya, additional, and Frankel, Gad, additional

Published
2007
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31. Distribution of tccP in Clinical Enterohemorrhagic and Enteropathogenic Escherichia coli Isolates

Author

Garmendia, Junkal, primary, Ren, Zhihong, additional, Tennant, Sharon, additional, Midolli Viera, Monica Aparecida, additional, Chong, Yuwen, additional, Whale, Andrew, additional, Azzopardi, Kristy, additional, Dahan, Sivan, additional, Sircili, Marcelo Palma, additional, Franzolin, Marcia Regina, additional, Trabulsi, Luiz R., additional, Phillips, Alan, additional, Gomes, Tânia A. T., additional, Xu, Jianguo, additional, Robins-Browne, Roy, additional, and Frankel, Gad, additional

Published
2005
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49. Positive Autoregulation of mrkHI by the Cyclic Di-GMP-Dependent MrkH Protein in the Biofilm Regulatory Circuit of Klebsiella pneumoniae.

Author

Tan, Jason W. H., Wilksch, Jonathan J., Hocking, Dianna M., Wang, Nancy, Srikhanta, Yogitha N., Tauschek, Marija, Lithgow, Trevor, Robins-Browne, Roy M., Ji Yang, and Strugnell, Richard A.

Subjects
*KLEBSIELLA pneumoniae, *NOSOCOMIAL infections, *POLYMERASES, *MAYER-Rokitansky-Kuster-Hauser syndrome, *DIAGNOSIS
Abstract

Klebsiella pneumoniae is an important cause of nosocomial infections, primarily through the formation of surface-associated biofilms to promote microbial colonization on host tissues. Expression of type 3 fimbriae by K. pneumoniae facilitates surface adherence, a process strongly activated by the cyclic di-GMP (c-di-GMP)-dependent transcriptional activator MrkH. In this study, we demonstrated the critical importance of MrkH in facilitating K. pneumoniae attachment on a variety of medically relevant materials and demonstrated the mechanism by which bacteria activate expression of type 3 fimbriae to colonize these materials. Sequence analysis revealed a putative MrkH recognition DNA sequence ("MrkH box"; TATCAA) located in the regulatory region of the mrkHI operon. Mutational analysis, electrophoretic mobility shift assay, and quantitative PCR experiments demonstrated that MrkH binds to the cognate DNA sequence to autoregulate mrkHI expression in a c-di-GMP-dependent manner. A half-turn deletion, but not a full-turn deletion, between the MrkH box and the_35 promoter element rendered MrkH ineffective in activating mrkHI expression, implying that a direct interaction between MrkH and RNA polymerase exists. In vivo analyses showed that residues L260, R265, N268, C269, E273, and I275 in the C-terminal domain of the RNA polymerase α subunit are involved in the positive control of mrkHI expression by MrkH and revealed the regions of MrkH required for DNA binding and transcriptional activation. Taken together, the data suggest a model whereby c-di-GMP-dependent MrkH recruits RNA polymerase to the mrkHI promoter to autoactivate mrkH expression. Increased MrkH production subsequently drives mrkABCDF expression when activated by c-di-GMP, leading to biosynthesis of type 3 fimbriae and biofilm formation. [ABSTRACT FROM AUTHOR]

Published
2015
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50. Control of acid resistance pathways of enterohemorrhagic Escherichia coli strain EDL933 by PsrB, a prophage-encoded AraC-like regulator.

Author

Yang J, Russell TW, Hocking DM, Bender JK, Srikhanta YN, Tauschek M, and Robins-Browne RM

Subjects
Animals, Artificial Gene Fusion, DNA, Bacterial metabolism, Electrophoretic Mobility Shift Assay, Escherichia coli O157 genetics, Escherichia coli O157 physiology, Escherichia coli O157 virology, Escherichia coli Proteins genetics, Gene Expression Profiling, Genes, Reporter, Mice, Inbred C57BL, Microbial Viability drug effects, Protein Binding, Transcription Factors genetics, beta-Galactosidase analysis, beta-Galactosidase genetics, Acids toxicity, Escherichia coli O157 drug effects, Escherichia coli Proteins metabolism, Gene Expression Regulation, Bacterial, Prophages genetics, Stress, Physiological, Transcription Factors metabolism
Abstract

Enterohemorrhagic Escherichia coli (EHEC) O157:H7 causes bloody diarrhea and hemolytic-uremic syndrome (HUS) and is the most prevalent E. coli serotype associated with food-borne illness worldwide. This pathogen is transmitted via the fecal-oral route and has a low infectious dose that has been estimated to be between 10 and 100 cells. We and others have previously identified three prophage-encoded AraC-like transcriptional regulators, PatE, PsrA, and PsrB in the EHEC O157:H7 EDL933 strain. Our analysis showed that PatE plays an important role in facilitating survival of EHEC under a number of acidic conditions, but the contribution of PsrA and PsrB to acid resistance (AR) was unknown. Here, we investigated the involvement of PsrA and PsrB in the survival of E. coli O157:H7 in acid. Our results showed that PsrB, but not PsrA, enhanced the survival of strain EDL933 under various acidic conditions. Transcriptional analysis using promoter-lacZ reporters and electrophoretic mobility shift assays demonstrated that PsrB activates transcription of the hdeA operon, which encodes a major acid stress chaperone, by interacting with its promoter region. Furthermore, using a mouse model, we showed that expression of PsrB significantly enhanced the ability of strain EDL933 to overcome the acidic barrier of the mouse stomach. Taken together, our results indicate that EDL933 acquired enhanced acid tolerance via horizontally acquired regulatory genes encoding transcriptional regulators that activate its AR machinery., (Copyright © 2015, American Society for Microbiology. All Rights Reserved.)

Published
2015
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