Disease relevance of flhC

• To investigate the contribution of flhC in the relationship between E. coli O157:H7 and cattle, we constructed a similar flhC regulatory mutant in the well-characterized strain ATCC 43894 [1].

High impact information on flhC

• Thus, the regulatory mutant survived passage through the bovine gastrointestinal tract better than the wild type but failed to efficiently colonize cattle, and the requirement of flhC for colonization was not dependent on a functional flagellum [1].
• In this study, we have determined that the loss of motility in these German sorbitol-fermenting (SF) O157 strains is due to a 12-bp in-frame deletion in flhC that is required for transcriptional activation of genes involved in flagellum biosynthesis [2].
• Growth phenotypes of flhD and flhC mutants were determined with Phenotype MicroArrays and correlated with gene expression [3].
• Wild-type cells and flhC mutant cells divided exponentially until they reached a cell density of 4 x 10(7) cells per ml. flhD mutant cells divided 5 times more than wild-type cells before they reduced their cell division rate and reached a cell density 37 times higher than that of wild-type or flhC mutant cultures [4].

Analytical, diagnostic and therapeutic context of flhC

• PCR analysis of several nonmotile E. coli O157 strains from various geographical sources confirmed that the 12-bp flhC deletion is found only in the cluster of German SF O157 strains, providing a potentially useful marker by which these atypical strains can be identified [2].

References