<i>Pseudomonas aeruginosa cupA</i>‐encoded fimbriae expression is regulated by a GGDEF and EAL domain‐dependent modulation of the intracellular level of cyclic diguanylate

Meissner, Andree; Wild, Verena; Simm, Roger; Rohde, Manfred; Erck, Christian; Bredenbruch, Florian; Morr, Michael; Römling, Ute; Häußler, Susanne

doi:10.1111/j.1462-2920.2007.01366.x

Cited by 109 publications

(143 citation statements)

References 66 publications

(63 reference statements)

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“…How and when c-di-GMP signaling pathways affect acute infections is still poorly understood, in part because we do not have the means to observe or modulate bacteria inside their hosts during infection with sufficient spatiotemporal resolution. In contrast to acute infections, the vast majority of chronic infections involve biofilms, which are often associated with elevated c-di-GMP levels in bacterial pathogens (97,206).…”

Section: Scope Of C-di-gmp Signalingmentioning

confidence: 99%

Cyclic di-GMP: the First 25 Years of a Universal Bacterial Second Messenger

Römling

Galperin

Gomelsky

2013

Microbiol Mol Biol Rev

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1,501

1,698

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SUMMARY Twenty-five years have passed since the discovery of cyclic dimeric (3′→5′) GMP (cyclic di-GMP or c-di-GMP). From the relative obscurity of an allosteric activator of a bacterial cellulose synthase, c-di-GMP has emerged as one of the most common and important bacterial second messengers. Cyclic di-GMP has been shown to regulate biofilm formation, motility, virulence, the cell cycle, differentiation, and other processes. Most c-di-GMP-dependent signaling pathways control the ability of bacteria to interact with abiotic surfaces or with other bacterial and eukaryotic cells. Cyclic di-GMP plays key roles in lifestyle changes of many bacteria, including transition from the motile to the sessile state, which aids in the establishment of multicellular biofilm communities, and from the virulent state in acute infections to the less virulent but more resilient state characteristic of chronic infectious diseases. From a practical standpoint, modulating c-di-GMP signaling pathways in bacteria could represent a new way of controlling formation and dispersal of biofilms in medical and industrial settings. Cyclic di-GMP participates in interkingdom signaling. It is recognized by mammalian immune systems as a uniquely bacterial molecule and therefore is considered a promising vaccine adjuvant. The purpose of this review is not to overview the whole body of data in the burgeoning field of c-di-GMP-dependent signaling. Instead, we provide a historic perspective on the development of the field, emphasize common trends, and illustrate them with the best available examples. We also identify unresolved questions and highlight new directions in c-di-GMP research that will give us a deeper understanding of this truly universal bacterial second messenger.

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Section: Scope Of C-di-gmp Signalingmentioning

confidence: 99%

Cyclic di-GMP: the First 25 Years of a Universal Bacterial Second Messenger

Römling

Galperin

Gomelsky

2013

Microbiol Mol Biol Rev

Self Cite

1,501

1,698

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“…CupA expression was elevated in SCV20265 relative to its clonal wild type while the cupA gene cluster transposon mutants displayed no CupA expression. CupA expression was also diminished in the other transposon mutants that displayed reversion to the wild type phenotype (Meissner, 2007).…”

Section: P Aeruginosa Environmental Lifestyle and Virulence 59mentioning

confidence: 96%

“…Taken together these results demonstrate that alteration of global c-di-GMP levels is sufficient to induce CupA expression. Additionally, the GGDEF domain of MorA, but not the EAL domain, is important for its enzymatic activity as PA1120 overexpression could complement the SCV 20265 morA mutant for CupA expression (Meissner, 2007).…”

Section: P Aeruginosa Environmental Lifestyle and Virulence 59mentioning

confidence: 99%

“…Two transposon insertions mapped to the cupA gene cluster involved in biofilm formation (Vallet, 2001), and two others mapped to PA1119 and PA1120, encoding hypothetical proteins (Meissner, 2007). To determine the involvement of CupA expression in the SCV phenotype, Meissner et al compared CupA expression in SCV 20265 to the wild type strain and the cupA gene cluster transposon mutants via immunoblot.…”

Section: P Aeruginosa Environmental Lifestyle and Virulence 59mentioning

confidence: 99%

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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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“…Additionally, clues may be offered through recent and ongoing research concerning other genes and molecules linked to SCV production. For instance, the intracellular signalling molecule cyclic di-GMP (c-di-GMP) has recently been implicated in SCV production (Meissner et al, 2007;Starkey et al, 2009). Mutations in the wspF gene constitutively activate the diguanylate cyclase WspR, which elevates c-di-GMP levels and subsequently converts a WT P. aeruginosa strain into SCVs.…”

Section: Having Selected Gacsmentioning

confidence: 99%

Phenotypic diversification in vivo: Pseudomonas aeruginosa gacS− strains generate small colony variants in vivo that are distinct from in vitro variants

et al. 2010

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Pseudomonas aeruginosa has long been known to produce phenotypic variants during chronic mucosal surface infections. These variants are thought to be generated to ensure bacterial survival against the diverse challenges in the mucosal environment. Studies have begun to elucidate the mechanisms by which these variants emerge in vitro; however, too little information exists on phenotypic variation in vivo to draw any links between variants generated in vitro and in vivo. Consequently, in this study, the P. aeruginosa gacS gene, which has previously been linked to the generation of small colony variants (SCVs) in vitro, was studied in an in vivo mucosal surface infection model. More specifically, the rat prostate served as a model mucosal surface to test for the appearance of SCVs in vivo following infections with P. aeruginosa gacS− strains. As in in vitro studies, deletion of the gacS gene led to SCV production in vivo. The appearance of these in vivo SCVs was important for the sustainability of a chronic infection. In the subset of rats in which P. aeruginosa gacS− did not convert to SCVs, clearance of the bacteria took place and healing of the tissue ensued. When comparing the SCVs that arose at the mucosal surface (MS-SCVs) with in vitro SCVs (IV-SCVs) from the same gacS− parent, some differences between the phenotypic variants were observed. Whereas both MS-SCVs and IV-SCVs formed dense biofilms, MS-SCVs exhibited a less diverse resistance profile to antimicrobial agents than IV-SCVs. Additionally, MS-SCVs were better suited to initiate an infection in the rat model than IV-SCVs. Together, these observations suggest that phenotypic variation in vivo can be important for maintenance of infection, and that in vivo variants may differ from in vitro variants generated from the same genetic parent.

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Pseudomonas aeruginosa cupA‐encoded fimbriae expression is regulated by a GGDEF and EAL domain‐dependent modulation of the intracellular level of cyclic diguanylate

Cited by 109 publications

References 66 publications

Cyclic di-GMP: the First 25 Years of a Universal Bacterial Second Messenger

Cyclic di-GMP: the First 25 Years of a Universal Bacterial Second Messenger

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

Phenotypic diversification in vivo: Pseudomonas aeruginosa gacS− strains generate small colony variants in vivo that are distinct from in vitro variants

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