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Dual regulation of mucoidy in Pseudomonas aeruginosa and sigma factor antagonism
Author(s) -
Boucher J. C.,
Schurr M. J.,
Deretic V.
Publication year - 2000
Publication title -
molecular microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.857
H-Index - 247
eISSN - 1365-2958
pISSN - 0950-382X
DOI - 10.1046/j.1365-2958.2000.01846.x
Subject(s) - biology , sigma factor , transcription factor , antagonism , repressor , psychological repression , transcription (linguistics) , pseudomonas aeruginosa , promoter , microbiology and biotechnology , small hairpin rna , gene knockdown , cancer research , gene , gene expression , genetics , receptor , bacteria , linguistics , philosophy
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 (σ E ). 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 σ factor, RpoN (σ 54 ). The algD promoters dependent on σ 54 and σ E showed a complete overlap resulting in identical mRNA 5′ ends. The two pathways were not independent, as σ 54 also repressed σ E ‐dependent transcription of algD both in vitro and in vivo . The negative regulatory effect of σ 54 on σ E ‐dependent algD expression was based on σ 54 binding to the algD promoter and its interference with σ E ‐dependent transcription. This phenomenon, referred to here as σ factor antagonism, reflects the unique properties of σ 54 , which lacks an intrinsic ability to form open transcription initiation complexes. We propose that this peculiar feature of σ 54 has evolved in part to allow its recruitment as a repressor of certain promoter subsets. The repression of algD by σ 54 also depends on environmental conditions, supporting the notion that σ 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.