AlgR-binding sites within the algD promoter make up a set of inverted repeats separated by a large intervening segment of DNA

Mohr, Christian; Leveau, Johan H. J.; Krieg, D; Hibler, N S; Deretić, Vojo

doi:10.1128/jb.174.20.6624-6633.1992

Cited by 78 publications

(101 citation statements)

References 35 publications

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“…In addition, at least two response regulators from bacterial signal transduction systems, algR and algB, affect algD expression. As in the case of algU, inactivation of algR abrogates algD transcription and mucoidy (59). AlgR binds to three sites within the algD promoter defined by the recognition sequence ACCGTTGTC (41,59,60).…”

Section: Introductionmentioning

confidence: 99%

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Conversion of Pseudomonas aeruginosa to mucoidy in cystic fibrosis: environmental stress and regulation of bacterial virulence by alternative sigma factors

et al. 1994

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Section: Introductionmentioning

confidence: 99%

“…As in the case of algU, inactivation of algR abrogates algD transcription and mucoidy (59). AlgR binds to three sites within the algD promoter defined by the recognition sequence ACCGTTGTC (41,59,60). Similar sites occur in the algC promoter (25).…”

Section: Introductionmentioning

confidence: 99%

Conversion of Pseudomonas aeruginosa to mucoidy in cystic fibrosis: environmental stress and regulation of bacterial virulence by alternative sigma factors

et al. 1994

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“…Because AlgR is part of a two-component system that is important for both acute and chronic infections (19,32), it was necessary to address the mechanism for AlgR activation of rsmA in order to create a framework to understand how AlgR regulation of rsmA might impact virulence gene expression. AlgR binds a consensus sequence CCGTTCGTC (21,48,49), and phosphorylation is thought to enable AlgR to bind potential binding sites that deviate from this consensus, such as the sites found in the fimU promoter (32,47). However, the rsmA promoter deviates from the AlgR-binding consensus, and AlgR phosphorylation was not required for rsmA expression.…”

Section: Discussionmentioning

confidence: 99%

“…In the case of acute infections, AlgR activates the fimU operon, enabling the production of T4P (19,21,47). In chronic infections, AlgR, AlgU, and other transcriptional regulators activate the production of alginate (22,(48)(49)(50). These and other virulence factors in P. aeruginosa are often considered mutually exclusive, depending on whether there is an acute or chronic infection (51)(52)(53).…”

Section: Discussionmentioning

confidence: 99%

The Pseudomonas aeruginosa Two-Component Regulator AlgR Directly Activates rsmA Expression in a Phosphorylation-Independent Manner

2017

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Pseudomonas aeruginosa is an important pathogen of the immunocompromised, causing both acute and chronic infections. In cystic fibrosis (CF) patients, P. aeruginosa causes chronic disease. The impressive sensory network of P. aeruginosa allows the bacterium to sense and respond to a variety of stimuli found in diverse environments. Transcriptional regulators, including alternative sigma factors and response regulators, integrate signals changing gene expression, allowing P. aeruginosa to cause infection. The two-component transcriptional regulator AlgR is important in P. aeruginosa pathogenesis in both acute and chronic infections. In chronic infections, AlgR and the alternative sigma factor AlgU activate the genes responsible for alginate production. Previous work demonstrated that AlgU controls rsmA expression. RsmA is a posttranscriptional regulator that is antagonized by two small RNAs, RsmY and RsmZ. In this work, we demonstrate that AlgR directly activates rsmA expression from the same promoter as AlgU. In addition, phosphorylation was not necessary for AlgR activation of rsmA using algR and algZ mutant strains. AlgU and AlgR appear to affect the antagonizing small RNAs rsmY and rsmZ indirectly. RsmA was active in a mucA22 mutant strain using leader fusions of two RsmA targets, tssA1 and hcnA. AlgU and AlgR were necessary for posttranscriptional regulation of tssA1 and hcnA. Altogether, our work demonstrates that the alginate regulators AlgU and AlgR are important in the control of the RsmA posttranscriptional regulatory system. These findings suggest that RsmA plays an unknown role in mucoid strains due to AlgU and AlgR activities.IMPORTANCE P. aeruginosa infections are difficult to treat and frequently cause significant mortality in CF patients. Understanding the mechanisms of persistence is important. Our work has demonstrated that the alginate regulatory system also significantly impacts the posttranscriptional regulator system RsmA/Y/Z. We demonstrate that AlgR directly activates rsmA expression, and this impacts the RsmA regulon. This leads to the possibility that the RsmA/Y/Z system plays a role in helping P. aeruginosa persist during chronic infection. In addition, this furthers our understanding of the reach of the alginate regulators AlgU and AlgR.KEYWORDS P. aeruginosa, RsmA, AlgR, mucoid, Pseudomonas aeruginosa, cystic fibrosis, mucA, two-component regulatory systems T he opportunistic pathogen Pseudomonas aeruginosa possesses multiple virulence factors for causing disease. This allows P. aeruginosa to cause both acute and chronic infections. Acute infecting strains are characterized by the presence of type IV pili (T4P), flagella, and a type III secretion system (T3SS) (1-3). In contrast, chronic infecting strains diversify (4, 5) and frequently do not express T3SS, T4P, or flagella (6, 7). Chronic infecting strains often form biofilms composed of exopolysaccharides, such as alginate, and signal a decline in lung function in CF patients (8-11). Alginate

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“…Both AlgU and AlgR are necessary for activation of the genes encoding the biosynthetic enzymes required for alginate production, resulting in the mucoid phenotype (Mohr, 1992;Martin, 1994). Loss-of-function mutations in mucA are also associated with reduced expression of many acute virulence factors, including: the T3SS, ETA, LasA protease, and Tfp ( Figure 1E) (Mohr, 1990;Wu, 2004;Jones, 2010).…”

Section: P Aeruginosa Environmental Lifestyle and Virulence 61mentioning

confidence: 99%

Global Regulatory Pathways and Cross-talk ControlPseudomonas aeruginosaEnvironmental Lifestyle and Virulence Phenotype

Coggan

Wolfgang

2012

Current Issues in Molecular Biology

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Pseudomonas aeruginosa is a metabolically versatile environmental bacterium and an opportunistic human pathogen that relies on numerous signaling pathways to sense, respond, and adapt to fluctuating environmental cues. Although the environmental signals sensed by these pathways are poorly understood, they are largely responsible for determining whether P. aeruginosa adopts a planktonic or sessile lifestyle. These environmental lifestyle extremes parallel the acute and chronic infection phenotypes observed in human disease. In this review, we focus on four major pathways (cAMP/Vfr and c-di-GMP signaling, quorum sensing, and the Gac/Rsm pathway) responsible for sensing and integrating external stimuli into coherent regulatory control at the transcriptional, translational, and post-translational level. A common theme among these pathways is the inverse control of factors involved in promoting motility and acute infection and those associated with biofilm formation and chronic infection. In many instances these regulatory pathways influence one another, forming a complex network allowing P. aeruginosa to assimilate numerous external signals into an integrated regulatory circuit that controls a lifestyle continuum.

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AlgR-binding sites within the algD promoter make up a set of inverted repeats separated by a large intervening segment of DNA

Cited by 78 publications

References 35 publications

Conversion of Pseudomonas aeruginosa to mucoidy in cystic fibrosis: environmental stress and regulation of bacterial virulence by alternative sigma factors

Conversion of Pseudomonas aeruginosa to mucoidy in cystic fibrosis: environmental stress and regulation of bacterial virulence by alternative sigma factors

The Pseudomonas aeruginosa Two-Component Regulator AlgR Directly Activates rsmA Expression in a Phosphorylation-Independent Manner

Global Regulatory Pathways and Cross-talk ControlPseudomonas aeruginosaEnvironmental Lifestyle and Virulence Phenotype

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