or E. pyrifoliae and E. billingiae but not in the genome of E. tasmaniensis, Virulence assays of E. amylovora srl mutants showed reduced symptoms on apple seed lings but only weak effects on pear slices due to their low TCID content of sorbitol. The content of sorbitol is high in leaves and in transport tissue, and its amount varies dur ing plant development, Sucrose is another important transport sugar AZ20 in plants. Mutants of E. amylovora in the scr operon are non viru lent, The disaccharide is actively transported into the cells and subsequently cleaved. Besides the repressor gene scrR, four genes encoding steps in sucrose metabo lism are present in E. amylovora, E. pyrifoliae and E. tas maniensis. The genes scrKYABR are located in an operon for these three species, but E.
tasmaniensis carries a sec ond copy IU1 of scrAB, Alignments with MAUVE of the srl regions of E. pyrifoliae and E. billingiae as well as the scr region of E. pyrifoliae and E. tasmaniensis show a remarkable similarity for these gene clusters including the second scrAB copy in the genome of E. tasmaniensis, This region does not completely comprise the scrAB gene cluster, but is extended to 400 bp down stream of scrB and to a partial similarity at 1000 bp upstream of scrA. An interesting feature of E. billingiae is its possible abil ity to metabolize xylitol. This sugar alcohol is widely dis tributed in nature and can interfere with bacterial activities, E. billingiae may degrade xylitol to avoid interference with its growth and to use it as a carbon source despite its low nutritional value.
A similar gene is missing in the genomes of E. pyrifoliae strain Ep1 96 and the E. tasmaniensis strain Et1 99. On the other hand, E. tasmaniensis Carcinoid strain Et2 99 can grow with xylitol as car bon source, Miscellaneous determinants with potential impact to virulence of pathogenic erwinias A striking difference between IU1 the pathogenic species E. pyrifoliae TCID and the non pathogenic E. tasmaniensis is the existence of a nearly complete Type I fimbrial gene clus ter in the latter one, Enterobacterial Type I fimbriae are implied to be involved in cell attach ment and adhesion to surfaces leading to biofilm forma tion, Beside being a virulence determinant the fimbriae may therefore be a tool of epiphytic bacteria for colonization and protection against environmental effects. Without production of a capsular polysaccharide by E.
tasmaniensis, the fimbriae may replace the capsules to allow bacterial aggregation, This is supported by the lack of a Type I fimbrial gene cluster in E. billingiae, which produces EPS and may thus not depend on fim briae. On the other hand, the existence of Type I fimbriae may induce plant defence responses comparable to the effect of FimH on mammalian cells, While IU1 the distribution of Type I fimbriae genes seems to differ, all Erwinia species except E. billingiae possess a comparable incomplete instrumentation of K88 fim briae genes. These fimbriae were found in enterotoxi genic E. coli strains and identified as virulence factors, to determine attachment to specific receptors of intestinal cells, The cluster, build up with faeBCDEFGHIJ, could be reconstructed except for the regulator FaeB and the component FaeJ, without known expression and function, However, a CDS coding for a possible regu latory protein was found in E.
pyrifoliae instead of FaeB, leading to the assumption that functional F4 fimbriae participate in adhesion of these species. There are no hints if TCID they are related to pathogenicity. Another gene cluster first described in enterotoxigenic E. coli strains IU1 and also found in the erwinias forms the class 5 fimbriae with the surface antigen CS14 in the csu ABCDE operon, They are involved for E. coli in attachment to specific intestinal epithelial cells. Whether F4 and class 5 fimbriae have a cumulative effect by adher ing to receptors of the same cells or aim at different cells and have specific functions is difficult to determine on the molecular level. Sinc
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