Global Regulatory Pathways and Cross-talk Control<i>Pseudomonas aeruginosa</i>Environmental Lifestyle and Virulence Phenotype

Coggan, Kimberly A.; Wolfgang, Matthew C.

doi:10.21775/cimb.014.047

Cited by 83 publications

(18 citation statements)

References 183 publications

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“…In P. aeruginosa , mutation in either suhB or retS results in similar phenotypes from motility to biofilm formation, and SuhB-mediated regulatory pathways have been demonstrated to partially overlap those under the control of RetS (Goodman et al, 2004; Coggan and Wolfgang, 2012; Li et al, 2013). The retS mutant displays elevated levels of c-di-GMP, and RetS has been demonstrated to switch the T3SS/T6SS via c-di-GMP signaling (Moscoso et al, 2011).…”

Section: Resultsmentioning

confidence: 99%

“…Recent data indicate that the motile/toxic or sessile/biofilm lifestyle of P. aeruginosa directly relates to the acute or chronic infection mode (Coggan and Wolfgang, 2012). P. aeruginosa swimming motility is powered by the rotation of a single, polar flagellum (Rashid and Kornberg, 2000).…”

Section: Introductionmentioning

confidence: 99%

“…Two-component signal transduction systems (TCS) have been implicated as key mediators of P. aeruginosa lifestyle (Coggan and Wolfgang, 2012; Jimenez et al, 2012). A conserved and perhaps the most interesting TCS is referred to as the GacS/GacA system (Brencic et al, 2009).…”

Section: Introductionmentioning

confidence: 99%

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SuhB Regulates the Motile-Sessile Switch in Pseudomonas aeruginosa through the Gac/Rsm Pathway and c-di-GMP Signaling

Gao

Debru

et al. 2017

Front. Microbiol.

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Many Pseudomonas aeruginosa virulence traits that contribute to human infections are accepted as being associated with its environmental lifestyle. Therefore, identifying the molecular mechanisms that govern the lifestyle choice is of high significance. We previously reported that a mutation in suhB results in a decrease in swimming motility and increased biofilm formation compared to the wild-type strain. Yet, little is known about how this occurs. In this study, we demonstrated that SuhB inversely regulates motility and biofilm formation through the GacA-RsmY/Z-RsmA cascade. Mutations in gacA or the two small RNAs rsmY/rsmZ, or overproduction of the RsmA protein essentially rescued the motility defect of the suhB mutant. Additionally, we identified a c-di-GMP mediated mechanism for SuhB regulation of motility and biofilm formation. We showed that the ΔsuhB mutant displayed elevated levels of c-di-GMP, and the ΔsuhB motility and biofilm phenotypes could be switched by artificially decreasing c-di-GMP levels. Further experiments led to the identification of the diguanylate cyclase GcbA responsible for regulating the c-di-GMP concentration in ΔsuhB and hence the switch between planktonic and surface-associated growth. Together, our results demonstrate a novel mechanism for SuhB regulation of the lifestyle transition via the Gac/Rsm and c-di-GMP signaling networks in P. aeruginosa.

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Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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SuhB Regulates the Motile-Sessile Switch in Pseudomonas aeruginosa through the Gac/Rsm Pathway and c-di-GMP Signaling

Gao

Debru

et al. 2017

Front. Microbiol.

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“…This system can also control other important features of the interaction with the host, such as biofilm formation, carbon metabolism, or stress responses (Romeo and Babitzke, 2018). Central to this system is the Gac/Rsm pathway, where the GacS/GacA two component system has a fundamental role (Coggan and Wolfgang, 2012; Figure 4). GacA induces the expression of the sRNAs rsmY and rsmZ, which can bind to the central regulatory protein RsmA (CsrA) to block its regulatory functions (Kay et al, 2006; Figure 4).…”

Section: Virulencementioning

confidence: 99%

“…Text boxes: indicate downstream effects of RsmA. References:Wei et al, 2001;Records and Gross, 2010;Sonnleitner et al, 2011;Coggan and Wolfgang, 2012;Nadal Jimenez et al, 2012;Marden et al, 2013;Yakhnin et al, 2013;Chambonnier et al, 2016;Janssen et al, 2018a;Romeo and Babitzke, 2018;Valentini et al, 2018.…”

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confidence: 99%

Small RNAs as Fundamental Players in the Transference of Information During Bacterial Infectious Diseases

Plaza

2020

Front. Mol. Biosci.

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Communication shapes life on Earth. Transference of information has played a paramount role on the evolution of all living or extinct organisms since the appearance of life. Success or failure in this process will determine the prevalence or disappearance of a certain set of genes, the basis of Darwinian paradigm. Among different molecules used for transmission or reception of information, RNA plays a key role. For instance, the early precursors of life were information molecules based in primitive RNA forms. A growing field of research has focused on the contribution of small non-coding RNA forms due to its role on infectious diseases. These are short RNA species that carry out regulatory tasks in cis or trans. Small RNAs have shown their relevance in fine tuning the expression and activity of important regulators of essential genes for bacteria. Regulation of targets occurs through a plethora of mechanisms, including mRNA stabilization/destabilization, driving target mRNAs to degradation, or direct binding to regulatory proteins. Different studies have been conducted during the interplay of pathogenic bacteria with several hosts, including humans, animals, or plants. The sRNAs help the invader to quickly adapt to the change in environmental conditions when it enters in the host, or passes to a free state. The adaptation is achieved by direct targeting of the pathogen genes, or subversion of the host immune system. Pathogens trigger also an immune response in the host, which has been shown as well to be regulated by a wide range of sRNAs. This review focuses on the most recent host-pathogen interaction studies during bacterial infectious diseases, providing the perspective of the pathogen.

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Cyclic‐di‐GMP regulation of virulence in bacterial pathogens

Hall

Lee

2017

WIREs RNA

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Signaling pathways allow bacteria to adapt to changing environments. For pathogenic bacteria, signaling pathways allow for timely expression of virulence factors and the repression of antivirulence factors within the mammalian host. As the bacteria exit the mammalian host, signaling pathways enable the expression of factors promoting survival in the environment and/or nonmammalian hosts. One such signaling pathway uses the dinucleotide cyclic-di-GMP (c-di-GMP), and many bacterial genomes encode numerous proteins that are responsible for synthesizing and degrading c-di-GMP. Once made, c-di-GMP binds to individual protein and RNA receptors to allosterically alter the macromolecule function to drive phenotypic changes. Each bacterial genome encodes unique sets of genes for c-di-GMP signaling and virulence factors so the regulation by c-di-GMP is organism specific. Recent works have pointed to evidence that c-di-GMP regulates virulence in different bacterial pathogens of mammalian hosts. In this review, we discuss the criteria for determining the contribution of signaling nucleotides to pathogenesis using a well-characterized signaling nucleotide, cyclic AMP (cAMP), in Pseudomonas aeruginosa. Using these criteria, we review the roles of c-di-GMP in mediating virulence and highlight common themes that exist among eight diverse pathogens that cause different diseases through different routes of infection and transmission. © 2017 Wiley Periodicals, Inc. How to cite this article:WIREs RNA 2018, 9:e1454. doi: 10.1002/wrna.1454 INTRODUCTIONB is-(3 0 -5 0 )-cyclic dimeric guanosine monophosphate (c-di-GMP) is a widely utilized signaling pathway that regulates bacterial adaptation to different environments. 1 C-di-GMP is synthesized from two GTP by diguanylate cyclases (DGCs) that contain a GGDEF domain and degraded into pGpG by phosphodiesterases (PDE-As) that contain EAL or HD-GYP domain. Signaling by c-di-GMP is completed when pGpG is degraded further to GMP by oligoribonuclease and related RNA degradation enzymes. [2][3][4] Thus, c-di-GMP represents one of the shortest signaling ribonucleotides. In addition, a number of genes can encode proteins with both GGDEF and EAL domains (GGDEF-EAL), indicating that levels of c-di-GMP in the cell are regulated by a complicated number of synthetic and degradative enzymes. Once made, c-di-GMP binds a diverse set of protein receptors and RNA riboswitches. 1 C-di-GMP binding to molecular receptors allosterically alters their function and downstream cellular phenotypes. 5 Genes encoding c-di-GMP signaling components are found in a large number of bacterial pathogens. This review seeks to cover the contribution of c-di-GMP signaling to bacterial pathogenesis for a number of different pathogens to identify common themes. For this review, virulence and pathogenesis is considered as the ability of the bacteria to replicate and cause disease symptoms in the mammalian host. Owing to space limitation, for each pathogen, we have referenced reviews that cover their virulence factors and their c...

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

Cited by 83 publications

References 183 publications

SuhB Regulates the Motile-Sessile Switch in Pseudomonas aeruginosa through the Gac/Rsm Pathway and c-di-GMP Signaling

SuhB Regulates the Motile-Sessile Switch in Pseudomonas aeruginosa through the Gac/Rsm Pathway and c-di-GMP Signaling

Small RNAs as Fundamental Players in the Transference of Information During Bacterial Infectious Diseases

Cyclic‐di‐GMP regulation of virulence in bacterial pathogens

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