Regulation of nleA in Shiga Toxin-Producing Escherichia coli O84:H4 Strain 4795/97

Autor(en): Schwidder, Maike
Hensel, Michael 
Schmidt, Herbert
Stichwörter: CITROBACTER-RODENTIUM; CONTROLS EXPRESSION; ENTEROCYTE EFFACEMENT GENES; III EFFECTOR PROTEIN; LEE PATHOGENICITY ISLAND; LOCUS; Microbiology; O157-H7; SECRETION; VIBRIO-HARVEYI; VIRULENCE FACTOR NLEA
Erscheinungsdatum: 2011
Herausgeber: AMER SOC MICROBIOLOGY
Journal: JOURNAL OF BACTERIOLOGY
Volumen: 193
Ausgabe: 4
Startseite: 832
Seitenende: 841
Zusammenfassung: 
Many Shiga toxin-producing Escherichia coli (STEC) strains express a type III secretion system (TTSS) encoded by the locus of enterocyte effacement (LEE). Using the TTSS, STEC is able to inject effector proteins directly into eukaryotic host cells, where they cause characteristic attaching and effacing (A/E) lesions. In addition to the LEE-encoded effectors, a number of non-LEE-encoded effectors, located on phage-associated elements, have been described. One of them, the non-LEE-encoded effector A (NleA), is widely distributed among pathogenic E. coli. In this study, we investigated the influence of environmental conditions on the expression of the phage-encoded effector nleA gene (designated nleA(4795)) present in STEC O84:H4 strain 4795/97. We demonstrated that a particular NaCl concentration and starvation stress increase the activity of the nleA(4795) promoter. Moreover, several regulators that control nleA(4795) expression were identified. The involvement of the LEE regulators Ler, GrlA, and GrlR show that nleA(4795) is integrated in the LEE regulation circuit. Furthermore, the binding of Ler to sequences upstream of nleA(4795) underlined these findings.
ISSN: 00219193
DOI: 10.1128/JB.00582-10

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