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The pmrF polymyxin-resistance operon of Yersinia pseudotuberculosis is upregulated by the PhoP-PhoQ two-component system but not by PmrA-PmrB, and is not required for virulence.
Microbiology (Reading). 2004 Dec; 150(Pt 12):3947-57.M

Abstract

The Yersinia pseudotuberculosis chromosome contains a seven-gene polycistronic unit (the pmrF operon) whose products share extensive homologies with their pmrF counterparts in Salmonella enterica serovar Typhimurium (S. typhimurium), another Gram-negative bacterial enteropathogen. This gene cluster is essential for addition of 4-aminoarabinose to the lipid moiety of LPS, as demonstrated by MALDI-TOF mass spectrometry of lipid A from both wild-type and pmrF-mutated strains. As in S. typhimurium, 4-aminoarabinose substitution of lipid A contributes to in vitro resistance of Y. pseudotuberculosis to the antimicrobial peptide polymyxin B. Whereas pmrF expression in S. typhimurium is mediated by both the PhoP-PhoQ and PmrA-PmrB two-component regulatory systems, it appears to be PmrA-PmrB-independent in Y. pseudotuberculosis, with the response regulator PhoP interacting directly with the pmrF operon promoter region. This result reveals that the ubiquitous PmrA-PmrB regulatory system controls different regulons in distinct bacterial species. In addition, pmrF inactivation in Y. pseudotuberculosis has no effect on bacterial virulence in the mouse, again in contrast to the situation in S. typhimurium. The marked differences in pmrF operon regulation in these two phylogenetically close bacterial species may be related to their dissimilar lifestyles.

Authors+Show Affiliations

E0364 Inserm--Université Lille II (Faculté de Médecine Henri Warembourg)--Institut Pasteur de Lille, Lille, France. michael.marceau@ibl.frNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

15583148

Citation

Marceau, M, et al. "The pmrF Polymyxin-resistance Operon of Yersinia Pseudotuberculosis Is Upregulated By the PhoP-PhoQ Two-component System but Not By PmrA-PmrB, and Is Not Required for Virulence." Microbiology (Reading, England), vol. 150, no. Pt 12, 2004, pp. 3947-57.
Marceau M, Sebbane F, Ewann F, et al. The pmrF polymyxin-resistance operon of Yersinia pseudotuberculosis is upregulated by the PhoP-PhoQ two-component system but not by PmrA-PmrB, and is not required for virulence. Microbiology (Reading). 2004;150(Pt 12):3947-57.
Marceau, M., Sebbane, F., Ewann, F., Collyn, F., Lindner, B., Campos, M. A., Bengoechea, J. A., & Simonet, M. (2004). The pmrF polymyxin-resistance operon of Yersinia pseudotuberculosis is upregulated by the PhoP-PhoQ two-component system but not by PmrA-PmrB, and is not required for virulence. Microbiology (Reading, England), 150(Pt 12), 3947-57.
Marceau M, et al. The pmrF Polymyxin-resistance Operon of Yersinia Pseudotuberculosis Is Upregulated By the PhoP-PhoQ Two-component System but Not By PmrA-PmrB, and Is Not Required for Virulence. Microbiology (Reading). 2004;150(Pt 12):3947-57. PubMed PMID: 15583148.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - The pmrF polymyxin-resistance operon of Yersinia pseudotuberculosis is upregulated by the PhoP-PhoQ two-component system but not by PmrA-PmrB, and is not required for virulence. AU - Marceau,M, AU - Sebbane,F, AU - Ewann,F, AU - Collyn,F, AU - Lindner,B, AU - Campos,M A, AU - Bengoechea,J-A, AU - Simonet,M, PY - 2004/12/8/pubmed PY - 2005/3/8/medline PY - 2004/12/8/entrez SP - 3947 EP - 57 JF - Microbiology (Reading, England) JO - Microbiology (Reading) VL - 150 IS - Pt 12 N2 - The Yersinia pseudotuberculosis chromosome contains a seven-gene polycistronic unit (the pmrF operon) whose products share extensive homologies with their pmrF counterparts in Salmonella enterica serovar Typhimurium (S. typhimurium), another Gram-negative bacterial enteropathogen. This gene cluster is essential for addition of 4-aminoarabinose to the lipid moiety of LPS, as demonstrated by MALDI-TOF mass spectrometry of lipid A from both wild-type and pmrF-mutated strains. As in S. typhimurium, 4-aminoarabinose substitution of lipid A contributes to in vitro resistance of Y. pseudotuberculosis to the antimicrobial peptide polymyxin B. Whereas pmrF expression in S. typhimurium is mediated by both the PhoP-PhoQ and PmrA-PmrB two-component regulatory systems, it appears to be PmrA-PmrB-independent in Y. pseudotuberculosis, with the response regulator PhoP interacting directly with the pmrF operon promoter region. This result reveals that the ubiquitous PmrA-PmrB regulatory system controls different regulons in distinct bacterial species. In addition, pmrF inactivation in Y. pseudotuberculosis has no effect on bacterial virulence in the mouse, again in contrast to the situation in S. typhimurium. The marked differences in pmrF operon regulation in these two phylogenetically close bacterial species may be related to their dissimilar lifestyles. SN - 1350-0872 UR - https://www.unboundmedicine.com/medline/citation/15583148/The_pmrF_polymyxin_resistance_operon_of_Yersinia_pseudotuberculosis_is_upregulated_by_the_PhoP_PhoQ_two_component_system_but_not_by_PmrA_PmrB_and_is_not_required_for_virulence_ L2 - http://mic.microbiologyresearch.org/pubmed/content/journal/micro/10.1099/mic.0.27426-0 DB - PRIME DP - Unbound Medicine ER -