Interplay between MgtC and PagC in Salmonella enterica serovar Typhimurium |
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Authors: | Alix Eric Miki Tsuyoshi Felix Christine Rang Cécile Figueroa-Bossi Nara Demettre Edith Blanc-Potard Anne-Béatrice |
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Affiliation: | 1. Inserm, ESPRI 26, Avenue J.F. Kennedy, 30908 Nîmes Cedex 02, France;2. Université Montpellier 1, UFR de Médecine, Avenue J.F. Kennedy, 30908 Nîmes Cedex 02, France;3. Department of Microbiology, School of Pharmaceutical Sciences, Kitasato University, 5-9-1 Shirokane, Minato-ku, Tokyo 108-8641, Japan;4. Centre de Génétique Moléculaire, CNRS, 91198 Gif-sur-Yvette Cedex, France;5. Institut de Génomique Fonctionnelle, CNRS UMR 5203, INSERM, U661, 141 rue de la Cardonnille, Cedex 34094, Montpellier, France;6. Université Montpellier 1,2, 141 rue de la Cardonille, Cedex 34094, Montpellier, France |
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Abstract: | In Salmonella enterica serovar Typhimurium, MgtC and PagC are positively regulated by the PhoP-PhoQ two-component system, which is activated under magnesium deprivation. Both MgtC and PagC are of unknown function but have been involved in intramacrophage survival. We have found that the amount of PagC is lowered in a DeltamgtC mutant strain grown in magnesium depleted medium. However, the effect of MgtC on PagC does not account for the growth defect of a DeltamgtC mutant in macrophages since, in contrast to previous reports, our results indicate that PagC does not contribute to intramacrophage survival. In addition, a pagC null mutant is only poorly attenuated in Nramp1-negative or Nramp1-positive mice. On the other hand, a mgtC null mutant is significantly more attenuated with Nramp1-positive than Nramp1-negative mice, suggesting that a functional Nramp1 (Slc11a1) further limits the multiplication of this mutant within the host. |
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Keywords: | Macrophage MgtC Nramp1 PagC Salmonella typhimurium |
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