High impact information on flhA

• Unexpectedly, the flhA mutant adhered significantly better to corneal epithelial cells than wild-type bacteria or the fliC mutant did [1].
• Invasion was restored by complementing the flhA mutant with flhA in trans but not by the plasmid vector control [1].
• FleQ and RpoN positively regulate expression of flhA, fliE, fliL, and fleSR genes, among others [2].
• DNase I footprinting was performed to determine the FleQ binding sites on flhA, fliE, fliL, and fleSR promoters [2].
• Primer extension analysis revealed the transcription start sites (TSSs) to be localized above the FleQ binding sites in flhA, fliE, and fliL promoters [2].

Biological context of flhA

• Deletion of the flhA promoter upstream of the RNA polymerase binding site did not result in a significant loss of promoter activity [2].
• Infection of cells with an internalization-defective flhA mutant of P. aeruginosa was associated with less ERK 1/2 tyrosine phosphorylation than infection with wild-type invasive P. aeruginosa [3].

Analytical, diagnostic and therapeutic context of flhA

• However, loss of motility was not sufficient to explain the reduced invasion by flhA mutants, since centrifugation of bacteria onto cells did not restore invasion to wild-type levels [1].

References