Mutations in the flhD gene of Escherichia coli K-12 do not cause the reported effect on cell division

Abstract

The hetero-oligomeric FlhD/FlhC complex is a global regulator of transcription in Escherichia coli. FlhD alone, independent of FlhC, has also been reported to control when E. coli cells stop dividing and enter the stationary phase. This work is frequently cited as evidence that FlhD regulates cell division; however, our data indicate that this is not the case. The results presented here show that the previously observed phenotype is not due to the flhD locus, but is instead due to differences in the thyA alleles present in the flhD(+) and flhD(-) strains used in the original studies. We find that when the strains being compared have the same thyA allele (wild type or mutant), flhD mutations have no effect on growth.

Fig. 1. Exchange of flhD alleles does not alter growth phenotypes

Cultures were grown and CFU ml^-1 determined as described in the Methods. Growth of YK410 (flhD⁺) is shown by closed circles and of YK4131 (flhD4131) by closed squares. Growth of YK410 flhD4131 is shown by open circles and of YK4131 flhD⁺ by open squares. (Note that all four strains also carry uvrC279∷Tn10 and are lysogenic for λPmcb-lacZ.) The data shown are the mean and standard deviation of 3 independent cultures of each strain (except for the 270 and 300 min time points, which were assayed only twice). The standard deviations for YK410 (flhD⁺) and YK410 flhD4131 are shown as short, horizontal black or grey lines, respectively. The standard deviations for YK4131 (flhD4131) and YK4131 flhD⁺ are shown as long, horizontal black or grey lines, respectively.