Contribution of the PhoP-PhoQ and PmrA-PmrB Two-Component Regulatory Systems to Mg2+-Induced Gene Regulation in Pseudomonas aeruginosa
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| Published in | Journal of Bacteriology Vol. 188; no. 11; pp. 3995 - 4006 |
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| Main Authors | , , , , , , , |
| Format | Journal Article |
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American Society for Microbiology
01.06.2006
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| AbstractList | When grown in divalent cation-limited medium, Pseudomonas aeruginosa becomes resistant to cationic antimicrobial peptides and polymyxin B. This resistance is regulated by the PhoP-PhoQ and PmrA-PmrB two-component regulatory systems. To further characterize Mg(2+) regulation in P. aeruginosa, microarray transcriptional profiling was conducted to compare wild-type P. aeruginosa grown under Mg(2+)-limited and Mg(2+)-replete conditions to isogenic phoP and pmrA mutants grown under Mg(2+)-limited conditions. Under Mg(2+)-limited conditions (0.02 mM Mg(2+)), approximately 3% of the P. aeruginosa genes were differentially expressed compared to the expression in bacteria grown under Mg(2+)-replete conditions (2 mM Mg(2+)). Only a modest subset of the Mg(2+)-regulated genes were regulated through either PhoP or PmrA. To determine which genes were directly regulated, a bioinformatic search for conserved binding motifs was combined with confirmatory reverse transcriptase PCR and gel shift promoter binding assays, and the results indicated that very few genes were directly regulated by these response regulators. It was found that in addition to the previously known oprH-phoP-phoQ operon and the pmrHFIJKLM-ugd operon, the PA0921 and PA1343 genes, encoding small basic proteins, were regulated by Mg(2+) in a PhoP-dependent manner. The number of known PmrA-regulated genes was expanded to include the PA1559-PA1560, PA4782-PA4781, and feoAB operons, in addition to the previously known PA4773-PA4775-pmrAB and pmrHFIJKLM-ugd operons. When grown in divalent cation-limited medium, Pseudomonas aeruginosa becomes resistant to cationic antimicrobial peptides and polymyxin B. This resistance is regulated by the PhoP-PhoQ and PmrA-PmrB two-component regulatory systems. To further characterize Mg 2+ regulation in P. aeruginosa , microarray transcriptional profiling was conducted to compare wild-type P. aeruginosa grown under Mg 2+ -limited and Mg 2+ -replete conditions to isogenic phoP and pmrA mutants grown under Mg 2+ -limited conditions. Under Mg 2+ -limited conditions (0.02 mM Mg 2+ ), approximately 3% of the P. aeruginosa genes were differentially expressed compared to the expression in bacteria grown under Mg 2+ -replete conditions (2 mM Mg 2+ ). Only a modest subset of the Mg 2+ -regulated genes were regulated through either PhoP or PmrA. To determine which genes were directly regulated, a bioinformatic search for conserved binding motifs was combined with confirmatory reverse transcriptase PCR and gel shift promoter binding assays, and the results indicated that very few genes were directly regulated by these response regulators. It was found that in addition to the previously known oprH-phoP-phoQ operon and the pmrHFIJKLM-ugd operon, the PA0921 and PA1343 genes, encoding small basic proteins, were regulated by Mg 2+ in a PhoP-dependent manner. The number of known PmrA-regulated genes was expanded to include the PA1559-PA1560, PA4782-PA4781, and feoAB operons, in addition to the previously known PA4773-PA4775- pmrAB and pmrHFIJKLM-ugd operons. Article Usage Stats Services JB Citing Articles Google Scholar PubMed Related Content Social Bookmarking CiteULike Delicious Digg Facebook Google+ Mendeley Reddit StumbleUpon Twitter current issue JB About JB Subscribers Authors Reviewers Advertisers Inquiries from the Press Permissions & Commercial Reprints ASM Journals Public Access Policy JB RSS Feeds 1752 N Street N.W. • Washington DC 20036 202.737.3600 • 202.942.9355 fax • journals@asmusa.org Print ISSN: 0021-9193 Online ISSN: 1098-5530 Copyright © 2014 by the American Society for Microbiology. For an alternate route to JB .asm.org, visit: JB When grown in divalent cation-limited medium, Pseudomonas aeruginosa becomes resistant to cationic antimicrobial peptides and polymyxin B. This resistance is regulated by the PhoP-PhoQ and PmrA-PmrB two-component regulatory systems. To further characterize Mg2+ regulation in P. aeruginosa, microarray transcriptional profiling was conducted to compare wild-type P. aeruginosa grown under Mg2+-limited and Mg2+-replete conditions to isogenic phoP and pmrA mutants grown under Mg2+-limited conditions. Under Mg2+-limited conditions (0.02 mM Mg2+), approximately 3% of the P. aeruginosa genes were differentially expressed compared to the expression in bacteria grown under Mg2+-replete conditions (2 mM Mg2+). Only a modest subset of the Mg2+-regulated genes were regulated through either PhoP or PmrA. To determine which genes were directly regulated, a bioinformatic search for conserved binding motifs was combined with confirmatory reverse transcriptase PCR and gel shift promoter binding assays, and the results indicated that very few genes were directly regulated by these response regulators. It was found that in addition to the previously known oprH-phoP-phoQ operon and the pmrHFIJKLM-ugd operon, the PA0921 and PA1343 genes, encoding small basic proteins, were regulated by Mg2+ in a PhoP-dependent manner. The number of known PmrA-regulated genes was expanded to include the PA1559-PA1560, PA4782-PA4781, and feoAB operons, in addition to the previously known PA4773-PA4775-pmrAB and pmrHFIJKLM-ugd operons. [PUBLICATION ABSTRACT] |
| Author | Agnieszka Kwasnicka Geoff Winsor Manjeet Bains Michelle D. Brazas Fiona S. L. Brinkman Joseph B. McPhee R. E. W. Hancock Shawn Lewenza |
| AuthorAffiliation | Department of Microbiology and Immunology and Centre for Microbial Diseases and Immunity Research, University of British Columbia, 232-2259 Lower Mall, Vancouver, BC, Canada V6T 1Z4, 1 Department of Molecular Biology and Biochemistry, Simon Fraser University, 8888 University Dr., Burnaby, BC, Canada V5A 1S6 2 2 |
| AuthorAffiliation_xml | – name: Department of Microbiology and Immunology and Centre for Microbial Diseases and Immunity Research, University of British Columbia, 232-2259 Lower Mall, Vancouver, BC, Canada V6T 1Z4, 1 Department of Molecular Biology and Biochemistry, Simon Fraser University, 8888 University Dr., Burnaby, BC, Canada V5A 1S6 2 2 |
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| Keywords | Pseudomonadales Gene Microbiology Bacteria Pseudomonadaceae Pseudomonas aeruginosa Bacteriology |
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| Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 Corresponding author. Mailing address: Department of Microbiology and Immunology and Centre for Microbial Diseases and Immunity Research, University of British Columbia, 232-2259 Lower Mall, Vancouver, BC, Canada V6T 1Z4. Phone: (604) 822-2682. Fax: (604) 827-5566. E-mail: bob@cmdr.ubc.ca. |
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Mendeley... When grown in divalent cation-limited medium, Pseudomonas aeruginosa becomes resistant to cationic antimicrobial peptides and polymyxin B. This resistance is... When grown in divalent cation-limited medium, Pseudomonas aeruginosa becomes resistant to cationic antimicrobial peptides and polymyxin B. This resistance is... |
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| StartPage | 3995 |
| SubjectTerms | Bacteria Bacterial Proteins - genetics Bacteriology Base Sequence Biological and medical sciences Comparative analysis DNA Primers Drug resistance Fundamental and applied biological sciences. Psychology Gene expression Gene Expression Regulation, Bacterial - drug effects Gene Regulation Genes Genotype Kinetics Magnesium Magnesium - pharmacology Microbiology Miscellaneous Oligonucleotide Array Sequence Analysis Pseudomonas aeruginosa - drug effects Pseudomonas aeruginosa - genetics Pseudomonas aeruginosa - growth & development Transcription Factors - genetics |
| Title | Contribution of the PhoP-PhoQ and PmrA-PmrB Two-Component Regulatory Systems to Mg2+-Induced Gene Regulation in Pseudomonas aeruginosa |
| URI | http://jb.asm.org/content/188/11/3995.abstract https://www.ncbi.nlm.nih.gov/pubmed/16707691 https://www.proquest.com/docview/227090346 https://search.proquest.com/docview/67987049 https://pubmed.ncbi.nlm.nih.gov/PMC1482896 |
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