ArticleJournal of bacteriology2011
The CgrA and CgrC proteins form a complex that positively regulates cupA fimbrial gene expression in Pseudomonas aeruginosa.
Article in Journal of bacteriology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Article
- Harnessing hypoxia: bacterial adaptation and chronic infection in cystic fibrosis.FEMS microbiology reviews · 2025Review
- Global transcriptional response of Pseudomonas aeruginosa to UVA radiation.Photochemical & photobiological sciences : Official journal of the European Photochemistry Association and the European Society for Photobiology · 2024Article
- Hydroquinine Enhances the Efficacy of Contact Lens Solutions for InhibitingAntibiotics (Basel, Switzerland) · 2024Article
- Links between Anr and Quorum Sensing in Pseudomonas aeruginosa Biofilms.Journal of bacteriology · 2015Article
- Pseudomonas aeruginosa Genome Evolution in Patients and under the Hospital Environment.Pathogens (Basel, Switzerland) · 2014Article
- Anr and its activation by PlcH activity in Pseudomonas aeruginosa host colonization and virulence.Journal of bacteriology · 2013Article
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Authors and funding
2 authors.
Funding
Abstract
The CgrA and CgrC proteins of Pseudomonas aeruginosa are coregulators that are required for the phase-variable expression of the cupA fimbrial genes. Neither CgrA nor CgrC resembles a classical transcription regulator, and precisely how these proteins exert their regulatory effects on cupA gene expression is poorly understood. Here, we show that CgrA and CgrC interact with one another directly. We identify a mutant of CgrC that is specifically defective for interaction with CgrA and demonstrate that this mutant cannot restore the phase-variable expression of the cupA fimbrial genes to cells of a cgrC mutant strain. Using this mutant, we also show that CgrC associates with the cupA promoter regardless of whether or not it interacts with CgrA. Our findings establish that interaction between CgrA and CgrC is required for the phase-variable expression of the cupA fimbrial genes and suggest that CgrC exerts its regulatory effects directly at the cupA promoter, possibly by recruiting CgrA. Because the regions of CgrA and CgrC that we have identified as interacting with one another are highly conserved among orthologs, our findings raise the possibility that CgrA- and CgrC-related regulators present in other bacteria function coordinately through a direct protein-protein interaction.
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