Regulation and Binding Properties of S Fimbriae Cloned from E. coli Strains Causing Urinary Tract Infection and Meningitis

Abstract

SummaryS fimbriae are able to recognize receptor molecules containing sialic acid and are produced by pathogenic E. coli strains causing urinary tract infection and menigitis. In order to characterize the corresponding genetic determinant, termed S fimbrial adhesin ( sfa) gene duster, we have cloned the S-specific genes from a urinary pathogen and from a meningitis isolate. Nine genes are involved in the production of S fimbriae, two of these, sfaB and sfaC code for regulatory proteins being necessary for the expression of S fimbriae. Two promoters, PB and Pc, are located in front of these genes. Transcription of the sfa determinant is influenced by activation of the promotersvia SfaB and SfaC, the action of the H-NS protein and an RNaseE-specific mRNA processing. In addition, a third promoter, P A• located in front of the major subunit gene sfaA, can be activated under special circumstances. Four genes of the sfa determinant code for the subunit-specific proteins, SfaA (16 kda), SfaG (17 kda), SfaS (14 kda) and SfaH (29 kda). lt was demonstrated that the protein SfaA is the major subunit protein while SfaS is identical to the sialic-acid-specific adhesin of S fimbriae.The introduction of specific mutations into sfaS revealed that a region of six amino acids of the adhesin which includes two lysine and one arginine residues is involved in the receptor specific interaction of S fimbriae. Additionally, it has been shown that SfaS is necessary for the induction of fimbriation while SfaH plays a role in the stringency of binding of S fimbriae to erythrocytes. Zusammenfassung S-Fimbrien können Sialinsäure-haltige Rezeptoren erkennen. Sie werden von pathogenen E. co/i-Isolaten gebildet, die Harnwegsinfektionen oder Meningitiden auslösen können. Um die für S-Fimbrien kodierenden Gene zu bestimmen und zu charakterisieren, haben wir die

Type-Specific Contributions to Chromosome Size Differences in Escherichia coli

“…Herein we demonstrate the association of these virulence factors with the RS218-specific segments at zcc to zch (ϳ24 min), zeh to purF (ϳ47 min), cys to zgf (ϳ64 min), zid to zii (ϳ87 min), and zji to thrA (ϳ98 min), respectively. The uropathogenic strain J96 carries genes putatively for penetration of epithelial basement membrane (sfa) (37,42), for ascendance of the host's ureters (pap) (30), for disruption of eukaryotic cells by ␣-hemolysin (hly) and by cytotoxic necrotizing factor 1 (cnf) (11), and for adhesion to host tissues (prs) (31). The coordinates for these virulence genes within the E. coli chromosome are as follows: sfa at 24 min (41); hlyB/D and pap at 64 min (47); and hlyB/D, prs, and cnf at 94 min (47).…”

Chemistry, biochemistry and biology of sialic acids

“…These studies were extended by investigation of the crystal structures of this influenza virus hemagglutinin with different high-affinity analogues The interest in sialic-acid-specific adhesion of bacteria is increasing, since it often is a critical step in infectious diseases. The introduction of specific mutations into the subunit gene sfaS revealed that a region of six amino acids of the adhesin which includes two lysine and one arginine residues is involved in the interaction of S fimbriae with sialic acid [990]. The binding of the latter bacteria via their S fimbriae to epithelial, e.g.…”

A central metabolic circuit controlled by QseC in pathogenic Escherichia coli

“…Type 1 pili belong to a class of extracellular fibres assembled by the chaperone‐usher pathway (CUP) (Waksman and Hultgren, 2009). Multiple CUP pili within E. coli genomes are thought to be required for tuning adhesive properties specific for different environmental niches (Uhlin et al ., 1985; Morschhauser et al ., 1993; Mulvey et al ., 1998; Kline et al ., 2010). Other factors important for UPEC virulence include the salmochelin and yersiniabactin iron scavenging siderophores, which are expressed at higher levels in urinary strains than in the gut strains from the same patients suffering from UTI (Henderson et al ., 2009), surface structures (such as flagella and curli) (Wright et al ., 2005; Cegelski et al ., 2009), stress response pathways (such as sulA , surA ) (Justice et al ., 2005; Justice et al ., 2006) and core metabolic genes (Alteri et al ., 2009).…”