scholarly journals The Global Response Regulator ExpA Controls Virulence Gene Expression through RsmA-Mediated and RsmA-Independent Pathways inPectobacterium wasabiaeSCC3193

2014 ◽  
Vol 80 (6) ◽  
pp. 1972-1984 ◽  
Author(s):  
M. Broberg ◽  
G. W. Lee ◽  
J. Nykyri ◽  
Y. H. Lee ◽  
M. Pirhonen ◽  
...  
Keyword(s):  
Plant Cell Wall ◽  
Rna Binding ◽  
Response Regulator ◽  
Virulence Gene ◽  
Soft Rot ◽  
In Planta ◽  
Cell Wall Degrading Enzymes ◽  
Global Response ◽  
Virulence Gene Expression ◽  
Transport Chain

ABSTRACTExpA (GacA) is a global response regulator that controls the expression of major virulence genes, such as those encoding plant cell wall-degrading enzymes (PCWDEs) in the model soft rot phytopathogenPectobacterium wasabiaeSCC3193. Several studies with pectobacteria as well as related phytopathogenic gammaproteobacteria, such asDickeyaandPseudomonas, suggest that the control of virulence by ExpA and its homologues is executed partly by modulating the activity of RsmA, an RNA-binding posttranscriptional regulator. To elucidate the extent of the overlap between the ExpA and RsmA regulons inP. wasabiae, we characterized both regulons by microarray analysis. To do this, we compared the transcriptomes of the wild-type strain, anexpAmutant, anrsmAmutant, and anexpA rsmAdouble mutant. The microarray data for selected virulence-related genes were confirmed through quantitative reverse transcription (qRT-PCR). Subsequently, assays were performed to link the observed transcriptome differences to changes in bacterial phenotypes such as growth, motility, PCWDE production, and virulencein planta. An extensive overlap between the ExpA and RsmA regulons was observed, suggesting that a substantial portion of ExpA regulation appears to be mediated through RsmA. However, a number of genes involved in the electron transport chain and oligogalacturonide metabolism, among other processes, were identified as being regulated by ExpA independently of RsmA. These results suggest that ExpA may only partially impact fitness and virulence via RsmA.

scholarly journals Photo sensing and quorum sensing are integrated to control bacterial group behaviors

2019 ◽  
Author(s):  
Sampriti Mukherjee ◽  
Matthew Jemielita ◽  
Vasiliki Stergioula ◽  
Mikhail Tikhonov ◽  
Bonnie L. Bassler
Keyword(s):  
Quorum Sensing ◽  
Biofilm Formation ◽  
Response Regulator ◽  
Sensory Information ◽  
Virulence Gene ◽  
Component System ◽  
Virulence Gene Expression ◽  
Bacterial Phyla ◽  
Expression Of Genes ◽  
Genes Encoding

ABSTRACTPseudomonas aeruginosa transitions between the free-swimming state and the sessile biofilm mode during its pathogenic lifestyle. We show that quorum sensing represses P. aeruginosa biofilm formation and virulence by activating expression of genes encoding the KinB-AlgB two-component system. Phospho-AlgB represses biofilm and virulence genes, while KinB dephosphorylates, and thereby, inactivates AlgB. We discover that the photoreceptor BphP is the kinase that, in response to light, phosphorylates and activates AlgB. Indeed, exposing P. aeruginosa to light represses biofilm formation and virulence gene expression. To our knowledge, P. aeruginosa was not previously known to detect light. The KinB-AlgB-BphP module is present in all Pseudomonads, and we demonstrate that AlgB is the cognate response regulator for BphP in diverse bacterial phyla. We propose that KinB-AlgB-BphP constitutes a “three-component” system and AlgB is the node at which varied sensory information is integrated. This study sets the stage for light-mediated control of P. aeruginosa infectivity.

scholarly journals Use of a Phosphorylation Site Mutant To Identify Distinct Modes of Gene Repression by the Control of Virulence Regulator (CovR) in Streptococcus pyogenes

2017 ◽  
Vol 199 (18) ◽  
Author(s):  
Nicola Horstmann ◽  
Pranoti Sahasrabhojane ◽  
Hui Yao ◽  
Xiaoping Su ◽  
Samuel A. Shelburne
Keyword(s):  
Gene Expression ◽  
Streptococcus Pyogenes ◽  
Response Regulator ◽  
Phosphorylation Site ◽  
Virulence Gene ◽  
Content Type ◽  
Virulence Gene Expression ◽  
Superficial Skin ◽  
Virulence Regulator ◽  
The Impact

ABSTRACT Control of the virulence regulator/sensor kinase (CovRS) two-component system (TCS) serves as a model for investigating the impact of signaling pathways on the pathogenesis of Gram-positive bacteria. However, the molecular mechanisms by which CovR, an OmpR/PhoB family response regulator, controls virulence gene expression are poorly defined, partly due to the labile nature of its aspartate phosphorylation site. To better understand the regulatory effect of phosphorylated CovR, we generated the phosphorylation site mutant strain 10870-CovR-D53E, which we predicted to have a constitutive CovR phosphorylation phenotype. Interestingly, this strain showed CovR activity only for a subset of the CovR regulon, which allowed for classification of CovR-influenced genes into D53E-regulated and D53E-nonregulated groups. Inspection of the promoter sequences of genes belonging to each group revealed distinct promoter architectures with respect to the location and number of putative CovR-binding sites. Electrophoretic mobility shift analysis demonstrated that recombinant CovR-D53E protein retains its ability to bind promoter DNA from both CovR-D53E-regulated and -nonregulated groups, implying that factors other than mere DNA binding are crucial for gene regulation. In fact, we found that CovR-D53E is incapable of dimerization, a process thought to be critical to OmpR/PhoB family regulator function. Thus, our global analysis of CovR-D53E indicates dimerization-dependent and dimerization-independent modes of CovR-mediated repression, thereby establishing distinct mechanisms by which this critical regulator coordinates virulence gene expression. IMPORTANCE Streptococcus pyogenes causes a wide variety of diseases, ranging from superficial skin and throat infections to life-threatening invasive infections. To establish these various disease manifestations, Streptococcus pyogenes requires tightly coordinated production of its virulence factor repertoire. Here, the response regulator CovR plays a crucial role. As an OmpR/PhoB family member, CovR is activated by phosphorylation on a conserved aspartate residue, leading to protein dimerization and subsequent binding to operator sites. Our transcriptome analysis using the monomeric phosphorylation mimic mutant CovR-D53E broadens this general notion by revealing dimerization-independent repression of a subset of CovR-regulated genes. Combined with promoter analyses, these data suggest distinct mechanisms of CovR transcriptional control, which allow for differential expression of virulence genes in response to environmental cues.

scholarly journals The Cpx System Regulates Virulence Gene Expression in Vibrio cholerae

2015 ◽  
Vol 83 (6) ◽  
pp. 2396-2408 ◽  
Author(s):  
Nicole Acosta ◽  
Stefan Pukatzki ◽  
Tracy L. Raivio
Keyword(s):  
Vibrio Cholerae ◽  
Response Regulator ◽  
Bacterial Species ◽  
Virulence Gene ◽  
Receptor Protein ◽  
Virulence Determinants ◽  
Content Type ◽  
Virulence Gene Expression ◽  
Envelope Stress ◽  
El Tor

Bacteria possess signal transduction pathways capable of sensing and responding to a wide variety of signals. The Cpx envelope stress response, composed of the sensor histidine kinase CpxA and the response regulator CpxR, senses and mediates adaptation to insults to the bacterial envelope. The Cpx response has been implicated in the regulation of a number of envelope-localized virulence determinants across bacterial species. Here, we show that activation of the Cpx pathway inVibrio choleraeEl Tor strain C6706 leads to a decrease in expression of the major virulence factors in this organism, cholera toxin (CT) and the toxin-coregulated pilus (TCP). Our results indicate that this occurs through the repression of production of the ToxT regulator and an additional upstream transcription factor, TcpP. The effect of the Cpx response on CT and TCP expression is mostly abrogated in a cyclic AMP receptor protein (CRP) mutant, although expression of thecrpgene is unaltered. Since TcpP production is controlled by CRP, our data suggest a model whereby the Cpx response affects CRP function, which leads to diminished TcpP, ToxT, CT, and TCP production.

scholarly journals Regulation of fixLJ by Hfq Controls Symbiotically Important Genes in Sinorhizobium meliloti

2016 ◽  
Vol 29 (11) ◽  
pp. 844-853 ◽  
Author(s):  
Mengsheng Gao ◽  
Hahn Nguyen ◽  
Isai Salas González ◽  
Max Teplitski
Keyword(s):  
Sinorhizobium Meliloti ◽  
Rna Binding ◽  
Response Regulator ◽  
Sensor Kinase ◽  
In Planta ◽  
Symbiotic Efficiency ◽  
Posttranscriptional Control ◽  
Nitrogenase Genes ◽  
Regulatory Effects

The RNA-binding chaperone Hfq plays critical roles in the establishment and functionality of the symbiosis between Sinorhizobium meliloti and its legume hosts. A mutation in hfq reduces symbiotic efficiency resulting in a Fix− phenotype, characterized by the inability of the bacterium to fix nitrogen. At least in part, this is due to the ability of Hfq to regulate the fixLJ operon, which encodes a sensor kinase–response regulator pair that controls expression of the nitrogenase genes. The ability of Hfq to bind fixLJ in vitro and in planta was demonstrated with gel shift and coimmunoprecipitation experiments. Two (ARN)2 motifs in the fixLJ message were the likely sites through which Hfq exerted its posttranscriptional control. Consistent with the regulatory effects of Hfq, downstream genes controlled by FixLJ (such as nifK, noeB) were also subject to Hfq regulation in planta.

scholarly journals The response regulator ResD modulates virulence gene expression in response to carbohydrates in Listeria monocytogenes

2006 ◽  
Vol 61 (6) ◽  
pp. 1622-1635 ◽  
Author(s):  
Marianne H. Larsen ◽  
Birgitte H. Kallipolitis ◽  
Janne K. Christiansen ◽  
John E. Olsen ◽  
Hanne Ingmer
Keyword(s):  
Gene Expression ◽  
Listeria Monocytogenes ◽  
Response Regulator ◽  
Virulence Gene ◽  
Virulence Gene Expression

scholarly journals The infection cushion: a fungal “weapon” of plant-biomass destruction

2020 ◽  
Author(s):  
Mathias Choquer ◽  
Christine Rascle ◽  
Isabelle R Gonçalves ◽  
Amélie de Vallée ◽  
Cécile Ribot ◽  
...  
Keyword(s):  
Cell Wall ◽  
Plant Cell Wall ◽  
Plant Biomass ◽  
Ornamental Plants ◽  
Sugar Transport ◽  
Differential Staining ◽  
List Type ◽  
In Planta ◽  
Cell Wall Degrading Enzymes

SummaryGrey mold disease affects fruits, vegetables and ornamental plants around the world, causing considerable losses every year. Its causing agent, the necrotrophic fungus Botrytis cinerea, produces infection cushions (IC) that are compound appressorial structures dedicated to the penetration of the plant tissues.A microarray analysis was performed to identify genes up-regulated in mature IC. The expression data were supported by RT-qPCR analysis performed in vitro and in planta, proteomic analysis of the IC secretome and mutagenesis of two candidate genes.1,231 up-regulated genes and 79 up-accumulated proteins were identified. They highlight a secretion of ROS, secondary metabolites including phytotoxins, and proteins involved in virulence: proteases, plant cell wall degrading enzymes and necrosis inducers. The role in pathogenesis was confirmed for two up-regulated fasciclin genes. DHN-melanin pathway and chitin deacetylases genes are up-regulated and the conversion of chitin into chitosan was confirmed by differential staining of the IC cell wall. In addition, up-regulation of sugar transport and sugar catabolism encoding genes was found.These results support a role for the B. cinerea IC in plant penetration and suggest other unexpected roles for this fungal organ, in camouflage, necrotrophy or nutrition of the pathogen.

scholarly journals Identification of Novel Thermosensors in Gram-Positive Pathogens

2020 ◽  
Vol 7 ◽  
Author(s):  
Pilar Fernández ◽  
Alejandra Raquel Díaz ◽  
María Florencia Ré ◽  
Lucía Porrini ◽  
Diego de Mendoza ◽  
...  
Keyword(s):  
Pathogenic Bacteria ◽  
Response Regulator ◽  
Physiological Mechanism ◽  
Virulence Gene ◽  
Membrane Lipid ◽  
Gram Positive ◽  
Virulence Gene Expression ◽  
Cognate Response Regulator

Temperature is a crucial variable that every living organism, from bacteria to humans, need to sense and respond to in order to adapt and survive. In particular, pathogenic bacteria exploit host-temperature sensing as a cue for triggering virulence gene expression. Here, we have identified and characterized two integral membrane thermosensor histidine kinases (HKs) from Gram-positive pathogens that exhibit high similarity to DesK, the extensively characterized cold sensor histidine kinase from Bacillus subtilis. Through in vivo experiments, we demonstrate that SA1313 from Staphylococcus aureus and BA5598 from Bacillus anthracis, which likely control the expression of putative ATP binding cassette (ABC) transporters, are regulated by environmental temperature. We show here that these HKs can phosphorylate the non-cognate response regulator DesR, partner of DesK, both in vitro and in vivo, inducing in B. subtilis the expression of the des gene upon a cold shock. In addition, we report the characterization of another DesK homolog from B. subtilis, YvfT, also closely associated to an ABC transporter. Although YvfT phosphorylates DesR in vitro, this sensor kinase can only induce des expression in B. subtilis when overexpressed together with its cognate response regulator YvfU. This finding evidences a physiological mechanism to avoid cross talk with DesK after a temperature downshift. Finally, we present data suggesting that the HKs studied in this work appear to monitor different ranges of membrane lipid properties variations to mount adaptive responses upon cooling. Overall, our findings point out that bacteria have evolved sophisticated mechanisms to assure specificity in the response to environmental stimuli. These findings pave the way to understand thermosensing mediated by membrane proteins that could have important roles upon host invasion by bacterial pathogens.

scholarly journals Identification of an Orphan Response Regulator Required for the Virulence of Francisella spp. and Transcription of Pathogenicity Island Genes

2007 ◽  
Vol 75 (7) ◽  
pp. 3305-3314 ◽  
Author(s):  
Nrusingh P. Mohapatra ◽  
Shilpa Soni ◽  
Brian L. Bell ◽  
Richard Warren ◽  
Robert K. Ernst ◽  
...  
Keyword(s):  
Gene Expression ◽  
Mutant Strain ◽  
Lipid A ◽  
Response Regulator ◽  
Model Organism ◽  
Virulence Gene ◽  
Pathogenicity Island ◽  
Effective Vaccine ◽  
Gene Encoding ◽  
Virulence Gene Expression

ABSTRACT Francisella tularensis is a category A agent of biowarfare/biodefense. Little is known about the regulation of virulence gene expression in Francisella spp. Comparatively few regulatory factors exist in Francisella, including those belonging to two-component systems (TCS). However, orphan members of typical TCS can be identified. To determine if orphan TCS members affect Francisella gene expression, a gene encoding a product with high similarity to the Salmonella PmrA response regulator (FTT1557c/FNU0663.2) was deleted in Francisella novicida (a model organism for F. tularensis). The F. novicida pmrA mutant was defective in survival/growth within human and murine macrophage cell lines and was 100% defective in virulence in mice at a dose of up to 108 CFU. In addition, the mutant strain demonstrated increased susceptibility to antimicrobial peptide killing, but no differences were observed between the lipid A of the mutant and the parental strain, as has been observed with pmrA mutants of other microbes. The F. novicida pmrA mutant was 100% protective as a single-dose vaccine when challenge was with 106 CFU of F. novicida but did not protect against type A Schu S4 wild-type challenge. DNA microarray analysis identified 65 genes regulated by PmrA. The majority of these genes were located in the region surrounding pmrA or within the Francisella pathogenicity island (FPI). These FPI genes are also regulated by MglA, but MglA does not regulate pmrA, nor does PmrA regulate MglA. Thus, the orphan response regulator PmrA is an important factor in controlling virulence in F. novicida, and a pmrA mutant strain is an effective vaccine against homologous challenge.

scholarly journals Inactivation of pecS restores the virulence of mutants devoid of osmoregulated periplasmic glucans in the phytopathogenic bacterium Dickeya dadantii

Microbiology ◽  
2014 ◽  
Vol 160 (4) ◽  
pp. 766-777 ◽  
Author(s):  
Sébastien Bontemps-Gallo ◽  
Edwige Madec ◽  
Jean-Marie Lacroix
Keyword(s):  
Plant Cell Wall ◽  
Transcriptional Regulator ◽  
Soft Rot ◽  
Cellular Functions ◽  
Cell Wall Degrading Enzymes ◽  
Dickeya Dadantii ◽  
Phytopathogenic Bacterium ◽  
Wide Range ◽  
Severe Reduction ◽  
Rot Disease

Dickeya dadantii is a phytopathogenic enterobacterium that causes soft rot disease in a wide range of plant species. Maceration, an apparent symptom of the disease, is the result of the synthesis and secretion of a set of plant cell wall-degrading enzymes (PCWDEs), but many additional factors are required for full virulence. Among these, osmoregulated periplasmic glucans (OPGs) and the PecS transcriptional regulator are essential virulence factors. Several cellular functions are controlled by both OPGs and PecS. Strains devoid of OPGs display a pleiotropic phenotype including total loss of virulence, loss of motility and severe reduction in the synthesis of PCWDEs. PecS is one of the major regulators of virulence in D. dadantii, acting mainly as a repressor of various cellular functions including virulence, motility and synthesis of PCWDEs. The present study shows that inactivation of the pecS gene restored virulence in a D. dadantii strain devoid of OPGs, indicating that PecS cannot be de-repressed in strains devoid of OPGs.

scholarly journals Potato Plants Genetically Modified to Produce N-Acylhomoserine Lactones Increase Susceptibility to Soft Rot Erwiniae

2004 ◽  
Vol 17 (8) ◽  
pp. 880-887 ◽  
Author(s):  
I. K. Toth ◽  
J. A. Newton ◽  
L. J. Hyman ◽  
A. K. Lees ◽  
M. Daykin ◽  
...  
Keyword(s):  
Plant Cell Wall ◽  
Erwinia Carotovora ◽  
Soft Rot ◽  
Transgenic Potato ◽  
Homoserine Lactone ◽  
In Planta ◽  
Susceptibility To Infection ◽  
Potato Plants ◽  
Physiological Processes ◽  
Transgenic Potato Plants

Many gram-negative bacteria employ N-acylhomoserine lactones (AHL) to regulate diverse physiological processes in concert with cell population density (quorum sensing [QS]). In the plant pathogen Erwinia carotovora, the AHL synthesized via the carI/expI genes are responsible for regulating the production of secreted plant cell wall-degrading exoenzymes and the antibiotic carbapen-3-em carboxylic acid. We have previously shown that targeting the product of an AHL synthase gene (yenI) from Yersinia enterocolitica to the chloroplasts of transgenic tobacco plants caused the synthesis in planta of the cognate AHL signaling molecules N-(3-oxohexanoyl)-L-homoserine lactone (3-oxo-C6-HSL) and N-hexanoylhomoserine lactone (C6-HSL), which in turn, were able to complement a carI¯ QS mutant. In the present study, we demonstrate that transgenic potato plants containing the yenI gene are also able to express AHL and that the presence and level of these AHL in the plant increases susceptibility to infection by E. carotovora. Susceptibility is further affected by both the bacterial level and the plant tissue under investigation.

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