scholarly journals The role of ‘soaking’ in spiteful toxin production in Pseudomonas aeruginosa

2013 ◽  
Vol 9 (1) ◽  
pp. 20120569 ◽  
Author(s):  
R. Fredrik Inglis ◽  
Alex R. Hall ◽  
Angus Buckling
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Individual Cell ◽  
Toxin Production ◽  
Wild Type ◽  
Low Frequencies ◽  
Direct Benefit ◽  
Indirect Fitness ◽  
Fitness Benefits ◽  
Significant Class

The ubiquitous production of antibacterial toxins, such as bacteriocins, is an ecologically significant class of interbacterial interactions that have primarily evolved through their indirect fitness benefits to the producer. Bacteria release bacteriocins into the environment at a cost to individual cell, but individual bacteriocin-producing cells are unlikely to gain any direct benefit from their own toxin; indeed, cell lysis is required in many species. There is a growing body of research describing the ecological conditions that can favour the evolution of bacteriocin production. However, an important aspect of many bacteriocins has yet to be investigated: the ability of bacteriocin-producing cells to neutralize toxin (‘soaking’) produced by other clonemates. By competing Pseudomonas aeruginosa bacteriocin-producing wild-type and ‘non-soaking’ strains against a bacteriocin-susceptible strain, we find that soaking markedly reduces the fitness of a bacteriocin-producing strain at both high and low frequencies.

scholarly journals The value of oviposition timing, queen presence and kinship in a social insect

2013 ◽  
Vol 280 (1766) ◽  
pp. 20131231 ◽  
Author(s):  
Martina Ozan ◽  
Heikki Helanterä ◽  
Liselotte Sundström
Keyword(s):  
Social Insect ◽  
Breeding Phenology ◽  
Reproductive Competition ◽  
Formica Fusca ◽  
Indirect Fitness ◽  
Fitness Benefits ◽  
Reproductive Conflicts

Reproductive cooperation confers benefits, but simultaneously creates conflicts among cooperators. Queens in multi-queen colonies of ants share a nest and its resources, but reproductive competition among queens often results in unequal reproduction. Two mutually non-exclusive factors may produce such inequality in reproduction: worker intervention or queen traits. Workers may intervene by favouring some queens over others, owing to either kinship or queen signals. Queens may differ in their intrinsic fecundity at the onset of oviposition or in their timing of the onset of oviposition, leading to their unequal representation in the brood. Here, we test the role of queen kin value (relatedness) to workers, timing of the onset of oviposition and signals of presence by queens in determining the maternity of offspring. We show that queens of the ant Formica fusca gained a significantly higher proportion of sexuals in the brood when ovipositing early, and that the presence of a caged queen resulted in a significant increase in both her share of sexual brood and her overall reproductive share. Moreover, the lower the kin value of the queen, the more the workers invested in their own reproduction by producing males. Our results show that both kinship and breeding phenology influence the outcome of reproductive conflicts, and the balance of direct and indirect fitness benefits in the multi-queen colonies of F. fusca .

scholarly journals Pseudomonas aeruginosa Keratitis in Knockout Mice Deficient in Intercellular Adhesion Molecule 1

1999 ◽  
Vol 67 (2) ◽  
pp. 972-975 ◽  
Author(s):  
Jeffery A. Hobden ◽  
Sharon Masinick-McClellan ◽  
Ronald P. Barrett ◽  
Kenneth S. Bark ◽  
Linda D. Hazlett
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Adhesion Molecule ◽  
Knockout Mice ◽  
Severe Disease ◽  
Intercellular Adhesion ◽  
Intercellular Adhesion Molecule ◽  
Wild Type ◽  
Intercellular Adhesion Molecule 1 ◽  
Disease Response

ABSTRACT In this study, the role of intercellular adhesion molecule 1 (ICAM-1) in the pathogenesis of Pseudomonas aeruginosakeratitis was examined by using inbred ICAM-1-deficient knockout mice. These mice had significantly less (P ≤ 0.02) ocular disease than wild-type mice, suggesting that ICAM-1 contributes to a more severe disease response following P. aeruginosainfection.

scholarly journals Discovery of an inhibitor of the production of the Pseudomonas aeruginosa virulence factor pyocyanin in wild-type cells

2016 ◽  
Vol 12 ◽  
pp. 1428-1433 ◽  
Author(s):  
Bernardas Morkunas ◽  
Balint Gal ◽  
Warren R J D Galloway ◽  
James T Hodgkinson ◽  
Brett M Ibbeson ◽  
...  
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Quorum Sensing ◽  
Cell Signalling ◽  
Opportunistic Pathogen ◽  
Wild Type ◽  
Wide Range ◽  
Potential Applications ◽  
Therapeutic Context ◽  
Pyocyanin Production

Pyocyanin is a small molecule produced by Pseudomonas aeruginosa that plays a crucial role in the pathogenesis of infections by this notorious opportunistic pathogen. The inhibition of pyocyanin production has been identified as an attractive antivirulence strategy for the treatment of P. aeruginosa infections. Herein, we report the discovery of an inhibitor of pyocyanin production in cultures of wild-type P. aeruginosa which is based around a 4-alkylquinolin-2(1H)-one scaffold. To the best of our knowledge, this is the first reported example of pyocyanin inhibition by a compound based around this molecular framework. The compound may therefore be representative of a new structural sub-class of pyocyanin inhibitors, which could potentially be exploited in in a therapeutic context for the development of critically needed new antipseudomonal agents. In this context, the use of wild-type cells in this study is notable, since the data obtained are of direct relevance to native situations. The compound could also be of value in better elucidating the role of pyocyanin in P. aeruginosa infections. Evidence suggests that the active compound reduces the level of pyocyanin production by inhibiting the cell–cell signalling mechanism known as quorum sensing. This could have interesting implications; quorum sensing regulates a range of additional elements associated with the pathogenicity of P. aeruginosa and there is a wide range of other potential applications where the inhibition of quorum sensing is desirable.

scholarly journals Role of TonB1 in Pyoverdine-Mediated Signaling in Pseudomonas aeruginosa

2009 ◽  
Vol 191 (18) ◽  
pp. 5634-5640 ◽  
Author(s):  
Matt Shirley ◽  
Iain L. Lamont
Keyword(s):  
Gene Expression ◽  
Pseudomonas Aeruginosa ◽  
Sigma Factor ◽  
Phenylacetic Acid ◽  
Cytoplasmic Membrane ◽  
Receptor Protein ◽  
Wild Type ◽  
Membrane Spanning ◽  
Signaling Process

ABSTRACT Pyoverdines are siderophores secreted by Pseudomonas aeruginosa. Uptake of ferripyoverdine in P. aeruginosa PAO1 occurs via the FpvA receptor protein and requires the energy-transducing protein TonB1. Interaction of (ferri)pyoverdine with FpvA activates pyoverdine gene expression in a signaling process involving the cytoplasmic-membrane-spanning anti-sigma factor FpvR and the sigma factor PvdS. Here, we show that mutation of a region of FpvA that interacts with TonB1 (the TonB box) prevents this signaling process, as well as inhibiting bacterial growth in the presence of the iron-chelating compound ethylenediamine-di(o-hydroxy-phenylacetic acid). Signaling via wild-type FpvA was also eliminated in strains lacking TonB1 but was unaffected in strains lacking either (or both) of two other TonB proteins in P. aeruginosa, TonB2 and TonB3. An absence of pyoverdine-mediated signaling corresponded with proteolysis of PvdS. These data show that interactions between FpvA and TonB1 are required for (ferri)pyoverdine signal transduction, as well as for ferripyoverdine transport, consistent with a mechanistic link between the signaling and transport functions of FpvA.

scholarly journals Induction of Systemic Resistance to Botrytis cinerea in Tomato by Pseudomonas aeruginosa 7NSK2: Role of Salicylic Acid, Pyochelin, and Pyocyanin

2002 ◽  
Vol 15 (11) ◽  
pp. 1147-1156 ◽  
Author(s):  
Kris Audenaert ◽  
Theresa Pattery ◽  
Pierre Cornelis ◽  
Monica Höfte
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Salicylic Acid ◽  
Botrytis Cinerea ◽  
Induced Resistance ◽  
Mammalian Cells ◽  
Cell Damage ◽  
Systemic Resistance ◽  
Wild Type ◽  
Induce Resistance

The rhizobacterium Pseudomonas aeruginosa 7NSK2 produces secondary metabolites such as pyochelin (Pch), its precursor salicylic acid (SA), and the phenazine compound pyocyanin. Both 7NSK2 and mutant KMPCH (Pch-negative, SA-positive) induced resistance to Botrytis cinerea in wild-type but not in transgenic NahG tomato. SA-negative mutants of both strains lost the capacity to induce resistance. On tomato roots, KMPCH produced SA and induced phenylalanine ammonia lyase activity, while this was not the case for 7NSK2. In 7NSK2, SA is probably very efficiently converted to Pch. However, Pch alone appeared not to be sufficient to induce resistance. In mammalian cells, Fe-Pch and pyocyanin can act synergistically to generate highly reactive hydroxyl radicals that cause cell damage. Reactive oxygen species are known to play an important role in plant defense. To study the role of pyocyanin in induced resistance, a pyocyanin-negative mutant of 7NSK2, PHZ1, was generated. PHZ1 is mutated in the phzM gene encoding an O-methyltransferase. PHZ1 was unable to induce resistance to B. cinerea, whereas complementation for pyocyanin production or co-inoculation with mutant 7NSK2-562 (Pch-negative, SA-negative, pyocyanin-positive) restored induced resistance. These results suggest that pyocyanin and Pch, rather than SA, are the determinants for induced resistance in wild-type P. aeruginosa 7NSK2.

scholarly journals Protective Role of Catalase in Pseudomonas aeruginosa Biofilm Resistance to Hydrogen Peroxide

1999 ◽  
Vol 65 (10) ◽  
pp. 4594-4600 ◽  
Author(s):  
James G. Elkins ◽  
Daniel J. Hassett ◽  
Philip S. Stewart ◽  
Herbert P. Schweizer ◽  
Timothy R. McDermott
Keyword(s):  
Hydrogen Peroxide ◽  
Pseudomonas Aeruginosa ◽  
Single Dose ◽  
Cell Viability ◽  
Catalase Activity ◽  
Type Strain ◽  
Wild Type Strain ◽  
Wild Type ◽  
Planktonic Cells

ABSTRACT The role of the two known catalases in Pseudomonas aeruginosa in protecting planktonic and biofilm cells against hydrogen peroxide (H2O2) was investigated. Planktonic cultures and biofilms formed by the wild-type strain PAO1 and the katA and katB catalase mutants were compared for their susceptibility to H2O2. Over the course of 1 h, wild-type cell viability decreased steadily in planktonic cells exposed to a single dose of 50 mM H2O2, whereas biofilm cell viability remained at approximately 90% when cells were exposed to a flowing stream of 50 mM H2O2. The katB mutant, lacking the H2O2-inducible catalase KatB, was similar to the wild-type strain with respect to H2O2 resistance. The katA mutant possessed undetectable catalase activity. PlanktonickatA mutant cultures were hypersusceptible to a single dose of 50 mM H2O2, while biofilms displayed a 10-fold reduction in the number of culturable cells after a 1-h exposure to 50 mM H2O2. Catalase activity assays, activity stains in nondenaturing polyacrylamide gels, andlacZ reporter genes were used to characterize the oxidative stress responses of planktonic cultures and biofilms. Enzyme assays and catalase activity bands in nondenaturing polyacrylamide gels showed significant KatB catalase induction occurred in biofilms after a 20-min exposure to H2O2, suggesting that biofilms were capable of a rapid adaptive response to the oxidant. Reporter gene data obtained with a katB::lacZtranscriptional reporter strain confirmed katB induction and that the increase in total cellular catalase activity was attributable to KatB. Biofilms upregulated the reporter in the constant presence of 50 mM H2O2, while planktonic cells were overwhelmed by a single 50 mM dose and were unable to make detectable levels of β-galactosidase. The results of this study demonstrated the following: the constitutively expressed KatA catalase is important for resistance of planktonic and biofilm P. aeruginosa to H2O2, particularly at high H2O2 concentrations; KatB is induced in both planktonic and biofilm cells in response to H2O2 insult, but plays a relatively small role in biofilm resistance; and KatB is important to either planktonic cells or biofilm cells for acquired antioxidant resistance when initial levels of H2O2 are sublethal.

scholarly journals Large Crystal Toxin Formation in Chromosomally Engineered Bacillus thuringiensis subsp. aizawai Due to σEAccumulation

2012 ◽  
Vol 78 (6) ◽  
pp. 1682-1691 ◽  
Author(s):  
Wasin Buasri ◽  
Watanalai Panbangred
Keyword(s):  
Bacillus Thuringiensis ◽  
Expression Profiles ◽  
Toxin Production ◽  
Wild Type ◽  
Large Crystal ◽  
Content Type ◽  
Crystal Toxin ◽  
Cat Expression ◽  
Toxin Formation

ABSTRACTSeven distinctBacillus thuringiensissubsp.aizawaiintegrants were constructed that carried the chitinase (chiBlA) gene fromB. licheniformisunder the control of thecry11Aapromoter and terminator with and withoutp19andp20genes. The toxicity ofB. thuringiensissubsp.aizawaiintegrants against second-instarSpodoptera lituralarvae was increased 1.8- to 4.6-fold compared to that of the wild-type strain (BTA1). Surprisingly, the enhanced toxicity in some strains ofB. thuringiensissubsp.aizawaiintegrants (BtaP19CS,BtaP19CSter, andBtaCAT) correlated with an increase in toxin formation. To investigate the role of these genes in toxin production, the expression profiles of the toxin genes,cry1AaandchiBlA, as well as their transcriptional regulators (sigKandsigE), were analyzed by quantitative real-time RT-PCR (qPCR) from BTA1,BtaP19CS, andBtaCAT. Expression levels ofcry1Aain these two integrants increased about 2- to 3-fold compared to those of BTA1. The expression of the transcription factorsigKalso was prolonged in the integrants compared to that of the wild type; however,sigEexpression was unchanged. Western blot analysis of σEand σKshowed the prolonged accumulation of σEin the integrants compared to that of BTA1, resulting in the increased synthesis of pro-σKup toT17after the onset of sporulation in bothBtaP19CS andBtaCAT compared to that ofT13in BTA1. The results from qPCR indicate clearly that thecry1Aapromoter activity was influenced most strongly by σE, whereascry11Aadepended mostly on σK. These results on large-crystal toxin formation with enhanced toxicity should provide useful information for the generation of strains with improved insecticidal activity.

scholarly journals Role of Pseudomonas aeruginosa Low-Molecular-Mass Penicillin-Binding Proteins in AmpC Expression, β-Lactam Resistance, and Peptidoglycan Structure

2015 ◽  
Vol 59 (7) ◽  
pp. 3925-3934 ◽  
Author(s):  
Alaa Ropy ◽  
Gabriel Cabot ◽  
Irina Sánchez-Diener ◽  
Cristian Aguilera ◽  
Bartolome Moya ◽  
...  
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Molecular Mass ◽  
Binding Proteins ◽  
Wild Type ◽  
Content Type ◽  
Penicillin Binding Proteins ◽  
Peptidoglycan Structure ◽  
The Impact ◽  
Pao1 Strain

ABSTRACTThis study aimed to characterize the role ofPseudomonas aeruginosalow-molecular-mass penicillin-binding proteins (LMM PBPs), namely, PBP4 (DacB), PBP5 (DacC), and PBP7 (PbpG), in peptidoglycan composition, β-lactam resistance, andampCregulation. For this purpose, we constructed all single and multiple mutants ofdacB,dacC,pbpG, andampCfrom the wild-typeP. aeruginosaPAO1 strain. Peptidoglycan composition was determined by high-performance liquid chromatography (HPLC),ampCexpression by reverse transcription-PCR (RT-PCR), PBP patterns by a Bocillin FL-binding test, and antimicrobial susceptibility by MIC testing for a panel of β-lactams. Microscopy and growth rate analyses revealed no apparent major morphological changes for any of the mutants compared to the wild-type PAO1 strain. Of the single mutants, onlydacCmutation led to significantly increased pentapeptide levels, showing that PBP5 is the majordd-carboxypeptidase inP. aeruginosa. Moreover, our results indicate that PBP4 and PBP7 play a significant role asdd-carboxypeptidase only if PBP5 is absent, and theirdd-endopeptidase activity is also inferred. As expected, the inactivation of PBP4 led to a significant increase inampCexpression (around 50-fold), but, remarkably, the sequential inactivation of the three LMM PBPs produced a much greater increase (1,000-fold), which correlated with peptidoglycan pentapeptide levels. Finally, the β-lactam susceptibility profiles of the LMM PBP mutants correlated well with theampCexpression data. However, the inactivation ofampCin these mutants also evidenced a role of LMM PBPs, especially PBP5, in intrinsic β-lactam resistance. In summary, in addition to assessing the effect ofP. aeruginosaLMM PBPs on peptidoglycan structure for the first time, we obtained results that represent a step forward in understanding the impact of these PBPs on β-lactam resistance, apparently driven by the interplay between their roles in AmpC induction, β-lactam trapping, anddd-carboxypeptidase/β-lactamase activity.

scholarly journals Virulence Gene Regulation by the agr System in Clostridium perfringens

2009 ◽  
Vol 191 (12) ◽  
pp. 3919-3927 ◽  
Author(s):  
Kaori Ohtani ◽  
Yonghui Yuan ◽  
Sufi Hassan ◽  
Ruoyu Wang ◽  
Yun Wang ◽  
...  
Keyword(s):  
Mutant Strain ◽  
Clostridium Perfringens ◽  
Culture Supernatant ◽  
Toxin Production ◽  
Toxin Gene ◽  
Wild Type ◽  
Knockout Mutant ◽  
Double Knockout ◽  
Signal Molecule

ABSTRACT A gram-positive anaerobic pathogen, Clostridium perfringens, causes clostridial myonecrosis or gas gangrene in humans by producing numerous extracellular toxins and enzymes that act in concert to degrade host tissue. The agr system is known to be important for the regulation of virulence genes in a quorum-sensing manner in Staphylococcus aureus. A homologue for S. aureus agrBD (agrBDSa ) was identified in the C. perfringens strain 13 genome, and the role of C. perfringens agrBD (agrBDCp ) was examined. The agrBDCp knockout mutant did not express the theta-toxin gene, and transcription of the alpha- and kappa-toxin genes was also significantly decreased in the mutant strain. The mutant strain showed a recovery of toxin production after the addition of the culture supernatant of the wild-type strain, indicating that the agrBDCp mutant lacks a signal molecule in the culture supernatant. An agr-virR double-knockout mutant was constructed to examine the role of the VirR/VirS two-component regulatory system, a key virulence regulator, in agrBDCp -mediated regulation of toxin production. The double-mutant strain could not be stimulated for toxin production with the wild-type culture supernatant. These results indicate that the agrBDCp system plays an important role in virulence regulation and also suggest that VirR/VirS is required for sensing of the extracellular signal and activation of toxin gene transcription in C. perfringens.

scholarly journals FlhA, a Component of the Flagellum Assembly Apparatus of Pseudomonas aeruginosa, Plays a Role in Internalization by Corneal Epithelial Cells

2001 ◽  
Vol 69 (8) ◽  
pp. 4931-4937 ◽  
Author(s):  
Suzanne M. J. Fleiszig ◽  
Shiwani K. Arora ◽  
Rajana Van ◽  
Reuben Ramphal
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Epithelial Cell ◽  
Epithelial Cells ◽  
Vector Control ◽  
Plasmid Vector ◽  
Wild Type ◽  
Corneal Epithelial Cells ◽  
Corneal Epithelial

ABSTRACT Pseudomonas aeruginosa invades various epithelial cell types in vitro and in vivo. The P. aeruginosa genome possesses a gene (flhA) which encodes a protein that is believed to be part of the export apparatus for flagellum assembly and which is homologous to invA of Salmonella spp. Because invA is required for invasion ofSalmonella spp., a role for flhA in P. aeruginosa invasion was explored using cultured rabbit corneal epithelial cells. An flhA mutant of P. aeruginosa strain PAO1 was constructed and was shown to be nonmotile. Complementation with flhA in transrestored motility. Corneal cells were infected for 3 h with the wild type (PAO1), the flhA mutant, the flhA mutant complemented with flhA in trans, anflhA mutant containing the plasmid vector control, or anfliC mutant (nonmotile mutant control). Invasion was quantified by amikacin exclusion assays. Both the flhA and the fliC mutants invaded at a lower level than the wild-type strain did, suggesting that both fliC andflhA played roles in invasion. However, loss of motility was not sufficient to explain the reduced invasion by flhAmutants, since centrifugation of bacteria onto cells did not restore invasion to wild-type levels. Unexpectedly, the flhA mutant adhered significantly better to corneal epithelial cells than wild-type bacteria or the fliC mutant did. The percentage of adherent bacteria that invaded was reduced by ∼80% for the flhAmutant and ∼50% for the fliC mutant, showing that only part of the role of flhA in invasion involvesfliC. Invasion was restored by complementing theflhA mutant with flhA in trans but not by the plasmid vector control. Intracellular survival assays, in which intracellular bacteria were enumerated after continued incubation in the presence of antibiotics, showed that although flhAand fliC mutants had a reduced capacity for epithelial cell entry, they were not defective in their ability to survive within those cells after entry. These results suggest that the flagellum assembly type III secretion system plays a role in P. aeruginosainvasion of epithelial cells. Since the flhA mutants were not defective in their ability to adhere to corneal epithelial cells, to retain viability at the cell surface, or to survive inside epithelial cells after entry, the role of flhA in invasion of epithelial cells is likely to occur during the process of bacterial internalization.

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