BioMed Research International / 2014 / Article / Tab 1

Research Article

Interactions of Neuropathogenic Escherichia coli K1 (RS218) and Its Derivatives Lacking Genomic Islands with Phagocytic Acanthamoeba castellanii and Nonphagocytic Brain Endothelial Cells

Table 1

Summary of E. coli K1 RS218 derived islands (RDI’s) and its genomic islands mutants tested in the present study.

E. coli K1

IdentityFunction and potential virulence factor
K1 (RS218)Isolate from a meningitis patient.
Plasmid cured RS218 Plasmid-free strain
RS218 complemented with HB101 DNAStrain, in which genomic deletion (black hole) observed in RS218 was filled with respective DNA from HB101
RDI 1Invasins (IcmF and IcmH).
RDI 2Prophage genes.
RDI 4Adhesins (S fimbriae, antigen 43). Protein secretion system (T5SS for antigen 43). Iron uptake system (Iro system and hmu system).
RDI 9Iron uptake system (Ybt system).
RDI 10Toxins (peptide toxin).
RDI 12Other virulence factors (sia operon). Prophage genes.
RDI 14Prophage genes.
RDI 15Metabolism (sugar metabolism).
RDI 16Protein secretion system (T2SS). Other virulence factors (K1 capsule biosynthesis).
RDI 17Metabolism (phosphor-sugar metabolism).
RDI 18Prophage genes.
RDI 21Adhesins (P fimbriae, F17-like fimbriae, non-fimbrial adhesins, Hek and hemagglutinin). Protein secretion system (T1SS for hemolysin). Invasins (CNF1). Metabolism (D-serine catabolism).
RDI 22Invasins (IbeA). Toxins (α-hemolysin). Metabolism (dihydroxyacetone, glycerol, and glyoxylate metabolism).

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