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1 E0364 Inserm Université Lille II (Faculté de Médecine Henri Warembourg) Institut Pasteur de Lille, Lille, France
2 U629 Inserm Institut Pasteur de Lille, Lille, France
3 Division of Biophysics, Research Center Borstel, Borstel, Germany
4 Unidad de Investigacion, Hospital Son Dureta and Institut Universitari d'Investigació en Ciències de la Salut (IUNICS), Palma Mallorca, Spain
Correspondence
M. Marceau
michael.marceau{at}ibl.fr
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 PhoPPhoQ and PmrAPmrB two-component regulatory systems, it appears to be PmrAPmrB-independent in Y. pseudotuberculosis, with the response regulator PhoP interacting directly with the pmrF operon promoter region. This result reveals that the ubiquitous PmrAPmrB 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.
These authors contributed equally to this work.
The GenBank/EMBL/DDBJ accession numbers for the Y. pseudotuberculosis pmrF, phoPphoQ and pmrApmrB operons are AF336802, AF333125 and AY259243 respectively.
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