The conversion to mucoid, exopolysaccharide alginate-overproducing phenotype in Pseudomonas aeruginosa during chronic respiratory infections in cystic fibrosis patients occurs via mutations that activate the alternative sigma factor AlgU (sigmaE). In this study, we demonstrate that conversion to mucoidy can be caused via a second, algU-independent pathway, in which alginate production and transcription of the critical algD promoter depend on another alternative sigma factor, RpoN (sigma54). The algD promoters dependent on sigma54 and sigmaE showed a complete overlap resulting in identical mRNA 5' ends. The two pathways were not independent, as sigma54 also repressed sigmaE-dependent transcription of algD both in vitro and in vivo. The negative regulatory effect of sigma54 on sigmaE-dependent algD expression was based on sigma54 binding to the algD promoter and its interference with sigmaE-dependent transcription. This phenomenon, referred to here as sigma factor antagonism, reflects the unique properties of sigma54, which lacks an intrinsic ability to form open transcription initiation complexes. We propose that this peculiar feature of sigma54 has evolved in part to allow its recruitment as a repressor of certain promoter subsets. The repression of algD by sigma54 also depends on environmental conditions, supporting the notion that sigma factor antagonism plays a physiological role in controlling alginate production in P. aeruginosa during adaptation to different ecological sites (e.g. biofilm development, stress and other growth conditions) and unique environments in the chronically infected host.
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