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Background  The  Yersinia enterocolitica  flagellar master regulator FlhD/FlhC affects the expression levels of non-flagellar genes, including 21 genes that are involved in central metabolism. The sigma factor of the flagellar system, FliA, has a negative effect on the expression levels of seven plasmid-encoded virulence genes in addition to its positive effect on the expression levels of eight of the flagellar operons. This study investigates the phenotypes of  flhD  and  fliA  mutants that result from the complex gene regulation.    Results  Phenotypes relating to central metabolism were investigated with Phenotype MicroArrays. Compared to the wild-type strain, isogenic  flhD  and  fliA  mutants exhibited increased growth on purines and reduced growth on N-acetyl-D-glucosamine and D-mannose, when used as a sole carbon source. Both mutants grew more poorly on pyrimidines and L-histidine as sole nitrogen source. Several intermediates of the tricarboxylic acid and the urea cycle, as well as several dipeptides, provided differential growth conditions for the two mutants. Gene expression was determined for selected genes and correlated with the observed phenotypes. Phenotypes relating to virulence were determined with the chicken embryo lethality assay. The assay that was previously established for  Escherichia coli  strains was modified for  Y. enterocolitica . The  flhD  mutant caused reduced chicken embryo lethality when compared to wild-type bacteria. In contrast, the  fliA  mutant caused wild-type lethality. This indicates that the virulence phenotype of the  flhD  mutant might be due to genes that are regulated by FlhD/FlhC but not FliA, such as those that encode the flagellar type III secretion system.    Conclusion  Phenotypes of  flhD  and  fliA  mutants are related to central metabolism and virulence and correlate with gene regulation.

Pleiotropic phenotypes of a Yersinia enterocolitica flhD mutant include reduced lethality in a chicken embryo model