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Identification of the lipopolysaccharide modifications controlled by the Salmonella PmrA/PmrB system mediating resistance to Fe(III) and Al(III)
Author(s) -
Nishino Kunihiko,
Hsu FongFu,
Turk John,
Cromie Michael J.,
Wösten Marc M. S. M.,
Groisman Eduardo A.
Publication year - 2006
Publication title -
molecular microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.857
H-Index - 247
eISSN - 1365-2958
pISSN - 0950-382X
DOI - 10.1111/j.1365-2958.2006.05273.x
Subject(s) - salmonella enterica , lipid a , biology , bacterial outer membrane , lipopolysaccharide , microbiology and biotechnology , polymyxin , mutant , salmonella , polymyxin b , bacteria , rpos , gene , biochemistry , genetics , antibiotics , escherichia coli , gene expression , immunology , promoter
Summary Iron is an essential metal but can be toxic in excess. While several homeostatic mechanisms prevent oxygen‐dependent killing promoted by Fe(II), little is known about how cells cope with Fe(III), which kills by oxygen‐independent means. Several Gram‐negative bacterial species harbour a regulatory system – termed PmrA/PmrB – that is activated by and required for resistance to Fe(III). We now report the identification of the PmrA‐regulated determinants mediating resistance to Fe(III) and Al(III) in Salmonella enterica serovar Typhimurium. We establish that these determinants remodel two regions of the lipopolysaccharide, decreasing the negative charge of this major constituent of the outer membrane. Remodelling entails the covalent modification of the two phosphates in the lipid A region with phosphoethanolamine and 4‐aminoarabinose, which has been previously implicated in resistance to polymyxin B, as well as dephosphorylation of the Hep(II) phosphate in the core region by the PmrG protein. A mutant lacking the PmrA‐regulated Fe(III) resistance genes bound more Fe(III) than the wild‐type strain and was defective for survival in soil, suggesting that these PmrA‐regulated lipopolysaccharide modifications aid Salmonella 's survival and spread in non‐host environments.