The SfaX II protein from newborn meningitis E. coli is involved in regulation of motility and type 1 fimbriae expression

• Published in: Microbial pathogenesis 2009, Vol.46 (5), p.243-252
• Main Authors: Sjöström, Annika E., Balsalobre, Carlos, Emödy, Levente, Westerlund-Wikström, Benita, Hacker, Jörg, Uhlin, Bernt Eric
• Format: Article
• Language: English
• Subjects: Biologi; Biology; Cell and molecular biology; Cell- och molekylärbiologi; Molecular biology; Molekylärbiologi; Motility; NATURAL SCIENCES; NATURVETENSKAP; NMEC; Regulation; S fimbriae; Type 1 fimbriae
• ISSN: 0882-4010; 1096-1208; 1096-1208
• DOI: 10.1016/j.micpath.2009.01.007

The genomes of pathogenic Escherichia coli may contain several different fimbrial operons. How bacteria regulate and coordinate the choice of fimbrial expression under different circumstances remains largely unanswered. In this report we have investigated the role of the sfaX II gene associated to the Sfa II fimbrial determinant in the E. coli isolate IHE3034. sfaX II belongs to a subfamily of genes, the 17 kDa genes, located near different fimbrial operons in uropathogenic and newborn meningitis E. coli (NMEC) strains. Using the NMEC isolate IHE3034 and non-pathogenic E. coli strains we found that the sfaX II gene had an inhibitory effect on type 1 fimbriae expression. Down-regulation of type 1 fimbriae was exerted at transcriptional level both by inhibiting expression from the fimA promoter and by reducing the frequency of OFF-to-ON switching. The effect of sfaX II on expression of the recombinase FimB that catalyzes OFF-to-ON switching might explain the described reduction in percentage of ON cells. Moreover, expression of the sfaX II gene strongly influenced motility and flagella production of the NMEC isolate IHE3034. We propose that the sfaX II gene, and presumably other members in the 17 kDa gene family, may play a role in the control of virulence related gene expression in pathogenic E. coli.