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Biosynthesis and IroC‐dependent export of the siderophore salmochelin are essential for virulence of Salmonella enterica serovar Typhimurium
Author(s) -
Crouch MarieLaure V.,
Castor Margaret,
Karlinsey Joyce E.,
Kalhorn Thomas,
Fang Ferric C.
Publication year - 2008
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.1365-2958.2007.06089.x
Subject(s) - enterobactin , siderophore , virulence , biology , salmonella enterica , microbiology and biotechnology , salmonella , major facilitator superfamily , secretion , mutant , type three secretion system , aerobactin , enterobacteriaceae , bacteria , escherichia coli , biochemistry , gene , genetics
Summary In response to iron deprivation, Salmonella enterica serovar Typhimurium secretes two catecholate‐type siderophores, enterobactin and its glucosylated derivative salmochelin. Although the systems responsible for enterobactin synthesis and acquisition are well characterized, the mechanisms of salmochelin secretion and acquisition, as well as its role in Salmonella virulence, are incompletely understood. Herein we show by liquid chromatography‐mass spectrometry analysis of culture supernatants from wild type and isogenic mutant bacterial strains that the Major Facilitator Superfamily pump EntS is the major exporter of enterobactin and the ABC transporter IroC exports both salmochelin and enterobactin. Growth promotion experiments demonstrate that IroC is not required for utilization of Fe‐enterobactin or Fe‐salmochelin, as had been previously suggested, but the ABC transporter protein FepD is required for utilization of both siderophores. Salmonella mutants deficient in salmochelin synthesis or secretion exhibit reduced virulence during systemic infection of mice.