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The flagellar systems of  Escherichia coli  and  Salmonella enterica  exhibit a significant level of genetic and functional synteny. Both systems are controlled by the flagellar specific master regulator FlhD 4 C 2 . Since the early days of genetic analyses of flagellar systems it has been known that  E. coli flhDC  can complement a ∆ flhDC  mutant in  S. enterica . The genomic revolution has identified how genetic changes to transcription factors and/or DNA binding sites can impact the phenotypic outcome across related species. We were therefore interested in asking: using modern tools to interrogate flagellar gene expression and assembly, what would the impact be of replacing the  flhDC  coding sequences in  S. enterica  for the  E. coli  genes at the  flhDC S. entercia  chromosomal locus? We show that even though all strains created are motile, flagellar gene expression is measurably lower when  flhDC  EC  are present. These changes can be attributed to the impact of FlhD 4 C 2  DNA recognition and the protein-protein interactions required to generate a stable FlhD 4 C 2  complex. Furthermore, our data suggests that in  E. coli  the internal flagellar FliT regulatory feedback loop has a marked difference with respect to output of the flagellar systems. We argue due diligence is required in making assumptions based on heterologous expression of regulators and that even systems showing significant synteny may not behave in exactly the same manner.

scientific reports

Driving the expression of the Salmonella enterica sv Typhimurium flagellum using flhDC from Escherichia coli results in key regulatory and cellular differences