The Pai-associated leuX specific tRNA5(Leu) affects type 1fimbriation in pathogenic Escherichia coli by control of FimB recombinase expression

The uropathogenic Escherichia coli strain 536 (06:K15:H31) carries two large chromosomalpathogenicity islands (Pais). Both Pais are flanked by tRNA genes. Spontaneous deletion of Pai IIresults in truncation of the leuX tRNA5Leu gene. This tRNA is required for the expression of type 1fimbriae (Fim) and other virulence factors. Transcription of fimA, encoding the major type 1 fimbrialsubunit is controlled by an invertable DNA switch. The inversion is catalysed by two recombinases,FimB and FimE. FimB is able to turn the switch on, FimE only off. The fimB gene of strain 536contains five TTG codons recognized by tRNA5Leu, fimE contains only two. It was proposed thatturning on the fim switch requires efficient translation of FimB, in turn requiring tRNA5Leu. Strainsin which the TTG codons in fimB were replaced with CTG codons at the wild-type locus were ableto produce type 1 fimbriae in the absence of leuX. fimB transcription was influenced by thepresence of leuX, but only slightly affected by the presence or absence of leuX codons in fimB.FimB translation was significantly higher from codon-replaced fimB genes than that of wild-typefimB genes in various strain backgrounds. The fim switch was shown to be switched off inleuX-derivatives of E. coli 536, but could be found in the on position when the codon-altered fimBgene was exchanged into the chromosome of these strains. From these data, it is apparent thattRNA5Leu is required for efficient translation of FimB, in turn, leading to type 1 fimbrial expression.