Involvement of σ S accumulation in repression of the flhDC operon in acidic phospholipid-deficient mutants of Escherichia coli

Escherichia coli pgsA mutations, which cause acidic phospholipid deficiency, repress transcription of the flagellar master operon flhDC , and thus impair flagellar formation and motility. The molecular mechanism of the strong repression of flhDC transcription in the mutant cells, however, has not yet been clarified. In order to shed light on this mechanism we isolated genes which, when supplied in multicopy, suppress the repression of flhD , and found that three genes, gadW , metE and yeaB, were capable of suppression. Taking into account a previous report that gadW represses σ S production, the level of σ S in the pgsA3 mutant was examined. We found that pgsA3 cells had a high level of σ S and that introduction of a gadW plasmid into pgsA3 cells did reduce the σ S level. The pgsA3 cells exhibited a sharp increase in σ S levels that can only be partially attributed to the slight increase in rpoS transcription; the largest part of the effect is due to a post-transcriptional accumulation of σ S . GadW in multicopy exerts its effect by post-transcriptionally downregulating σ S . YeaB and MetE in multicopy also exert their effect via σ S . Disruption of rpoS caused an increase of the flhD mRNA level, and induction from P trc - rpoS repressed the flhD mRNA level. The strong repression of flhD transcription in pgsA3 mutant cells is thus suggested to be caused by the accumulated σ S .