[No authors listed]
The expression of type 1 fimbriae is dependent on the intracellular levels of ppGpp through stimulation of fimB transcription. Here we show that in contrast to the previously described decreased fimbriation observed in a ppGpp-deficient strain, DksA deficiency results in a hyperfimbriated state. In vivo assays show that the effect of DksA deficiency on the type 1 fimbriae occurs at the phase variation level because of elevated transcription from the fimB P2 promoter. In contrast, our in vitro transcription studies demonstrate that ppGpp and DksA can stimulate transcription from the fimB P2 promoter both independently and codependently. We provide evidences that the apparently contradictory results from the in vivo and in vitro transcriptional studies are at least in part a consequence of the increased association of the anti-pausing factors (GreA and GreB) to the RNA polymerase in the absence of DksA in vivo.
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