scholarly journals Cooperation and Cheating through a Secreted Aminopeptidase in the Pseudomonas aeruginosa RpoS Response

mBio ◽  
2020 ◽  
Vol 11 (2) ◽  
Author(s):  
Tanner Robinson ◽  
Parker Smith ◽  
Erin R. Alberts ◽  
Mariana Colussi-Pelaez ◽  
Martin Schuster
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Stress Response ◽  
Public Good ◽  
Proteolytic Enzymes ◽  
Cooperative Behavior ◽  
Enteric Bacteria ◽  
Wild Type ◽  
Content Type ◽  
Metabolic Costs ◽  
Extracellular Proteolysis

ABSTRACT The global stress response controlled by the alternative sigma factor RpoS protects enteric bacteria from a variety of environmental stressors. The role of RpoS in other, nonenteric bacteria, such as the opportunistic pathogen Pseudomonas aeruginosa, is less well understood. Here, we employed experimental social evolution to reveal that cooperative behavior via secreted public goods is an important function in the RpoS response of P. aeruginosa. Using whole-genome sequencing, we identified rpoS loss-of-function mutants among isolates evolved in a protein growth medium that requires extracellular proteolysis. We found that rpoS mutants comprise up to 25% of the evolved population and that they behave as social cheaters, with low fitness in isolation but high fitness in mixed culture with the cooperating wild type. We conclude that rpoS mutants cheat because they exploit an RpoS-controlled public good produced by the wild type, the secreted aminopeptidase PaAP, and because they do not carry the metabolic costs of expressing PaAP and many other gene products in the large RpoS regulon. Our results suggest that PaAP is an integral part of a proteolytic sequence in P. aeruginosa that permits the utilization of protein as a nutrient source. Our work broadens the scope of stress response functions in bacteria. IMPORTANCE Bacterial stress responses are generally considered protective measures taken by individual cells. Enabled by an experimental evolution approach, we describe a contrasting property, collective nutrient acquisition, in the RpoS-dependent stress response of the opportunistic human pathogen P. aeruginosa. Specifically, we identify the secreted P. aeruginosa aminopeptidase (PaAP) as an essential RpoS-controlled function in extracellular proteolysis. As a secreted “public good,” PaAP permits cheating by rpoS mutants that save the metabolic costs of expressing RpoS-controlled genes dispensable under the given growth conditions. Proteolytic enzymes are important virulence factors in P. aeruginosa pathogenesis and constitute a potential target for antimicrobial therapy. More broadly, our work contributes to recent findings in higher organisms that stress affects not only individual fitness and competitiveness but also cooperative behavior.

scholarly journals Indole Production Promotes Escherichia coli Mixed-Culture Growth with Pseudomonas aeruginosa by Inhibiting Quorum Signaling

2011 ◽  
Vol 78 (2) ◽  
pp. 411-419 ◽  
Author(s):  
Weihua Chu ◽  
Tesfalem R. Zere ◽  
Mary M. Weber ◽  
Thomas K. Wood ◽  
Marvin Whiteley ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Pseudomonas Aeruginosa ◽  
Mixed Culture ◽  
Receptor Gene ◽  
Enteric Bacteria ◽  
Wild Type ◽  
Content Type ◽  
E Coli ◽  
Culture Growth ◽  
Indole Production

ABSTRACTIndole production byEscherichia coli, discovered in the early 20th century, has been used as a diagnostic marker for distinguishingE. colifrom other enteric bacteria. By using transcriptional profiling and competition studies with defined mutants, we show that cyclic AMP (cAMP)-regulated indole formation is a major factor that enablesE. coligrowth in mixed biofilm and planktonic populations withPseudomonas aeruginosa. Mutants deficient in cAMP production (cyaA) or the cAMP receptor gene (crp), as well as indole production (tnaA), were not competitive in coculture withP. aeruginosabut could be restored to wild-type competitiveness by supplementation with a physiologically relevant indole concentration.E. colisdiAmutants, which lacked the receptor for both indole andN-acyl-homoserine lactones (AHLs), showed no change in competitive fitness, suggesting that indole acted directly onP. aeruginosa. AnE. colitnaAmutant strain regained wild-type competiveness if grown withP. aeruginosaAHL synthase (rhlIandrhlI lasI) mutants. In contrast to the wild type,P. aeruginosaAHL synthase mutants were unable to degrade indole. Indole produced during mixed-culture growth inhibited pyocyanin production and other AHL-regulated virulence factors inP. aeruginosa. Mixed-culture growth withP. aeruginosastimulated indole formation inE. colicpdA, which is unable to regulate cAMP levels, suggesting the potential for mixed-culture gene activation via cAMP. These findings illustrate how indole, an early described feature ofE. colicentral metabolism, can play a significant role in mixed-culture survival by inhibiting quorum-regulated competition factors inP. aeruginosa.

scholarly journals Quorum Sensing Protects Pseudomonas aeruginosa against Cheating by Other Species in a Laboratory Coculture Model

2015 ◽  
Vol 197 (19) ◽  
pp. 3154-3159 ◽  
Author(s):  
Nicole E. Smalley ◽  
Dingding An ◽  
Matthew R. Parsek ◽  
Josephine R. Chandler ◽  
Ajai A. Dandekar
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Quorum Sensing ◽  
Public Goods ◽  
Public Good ◽  
Hydrogen Cyanide ◽  
Cooperative Behavior ◽  
Bacterial Species ◽  
Cell Communication ◽  
Content Type ◽  
Burkholderia Multivorans

ABSTRACTMany species of bacteria use a cell-cell communication system called quorum sensing (QS) to coordinate group activities. QS systems frequently regulate the production of exoproducts. Some of these products, such as proteases, are “public goods” that are shared among the population and vulnerable to cheating by nonproducing members of the population. Because the QS system of the opportunistic pathogenPseudomonas aeruginosaregulates several public goods, it can serve as a model for studying cooperation. Bacteria also commonly regulate antimicrobial production through QS. In this study, we focused on the hypothesis that QS-regulated antimicrobials may be important forP. aeruginosato protect against cheating by another bacterial species,Burkholderia multivorans.We assessed laboratory cocultures ofP. aeruginosaandB. multivoransand investigated the importance of threeP. aeruginosaQS-regulated antimicrobials, hydrogen cyanide, rhamnolipids, and phenazines, for competition. We found thatP. aeruginosadominates cocultures withB. multivoransand that the three antimicrobials together promoteP. aeruginosacompetitiveness, with hydrogen cyanide contributing the greatest effect. We show that these QS-regulated antimicrobials are also critical forP. aeruginosato preventB. multivoransfrom cheating under nutrient conditions where both species require aP. aeruginosaquorum-regulated protease for growth. Together our results highlight the importance of antimicrobials in protecting cooperating populations from exploitation by other species that can act as cheaters.IMPORTANCECooperative behaviors are threatened by social cheating, wherein individuals do not produce but nonetheless benefit from shared public goods. Bacteria have been shown to use several genetic mechanisms to restrain the emergence of cheaters from within the population, but public goods might also be used by other bacterial species in the vicinity. We demonstrate that a public good produced byPseudomonas aeruginosacan be used by another species,Burkholderia multivorans, to obtain carbon and energy. We also show thatP. aeruginosaantimicrobials that are coregulated with the public good prevent invasion by the cheating species. Our results demonstrate that cross-species cheating can occur and that coregulation of public goods with antimicrobials may stabilize cooperative behavior in mixed microbial communities.

scholarly journals Bactericidal Activity, Absence of Serum Effect, and Time-Kill Kinetics of Ceftazidime-Avibactam against β-Lactamase-Producing Enterobacteriaceae and Pseudomonas aeruginosa

2014 ◽  
Vol 58 (9) ◽  
pp. 5297-5305 ◽  
Author(s):  
Tiffany R. Keepers ◽  
Marcela Gomez ◽  
Chris Celeri ◽  
Wright W. Nichols ◽  
Kevin M. Krause
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Human Serum ◽  
Bactericidal Activity ◽  
Minimum Bactericidal Concentration ◽  
Wild Type ◽  
Content Type ◽  
Positive Isolate ◽  
New Treatment ◽  
Time Kill ◽  
Kinetics Of

ABSTRACTAvibactam, a non-β-lactam β-lactamase inhibitor with activity against extended-spectrum β-lactamases (ESBLs), KPC, AmpC, and some OXA enzymes, extends the antibacterial activity of ceftazidime against most ceftazidime-resistant organisms producing these enzymes. In this study, the bactericidal activity of ceftazidime-avibactam against 18Pseudomonas aeruginosaisolates and 15Enterobacteriaceaeisolates, including wild-type isolates and ESBL, KPC, and/or AmpC producers, was evaluated. Ceftazidime-avibactam MICs (0.016 to 32 μg/ml) were lower than those for ceftazidime alone (0.06 to ≥256 μg/ml) against all isolates except for 2P. aeruginosaisolates (1blaVIM-positive isolate and 1blaOXA-23-positive isolate). The minimum bactericidal concentration/MIC ratios of ceftazidime-avibactam were ≤4 for all isolates, indicating bactericidal activity. Human serum and human serum albumin had a minimal effect on ceftazidime-avibactam MICs. Ceftazidime-avibactam time-kill kinetics were evaluated at low MIC multiples and showed time-dependent reductions in the number of CFU/ml from 0 to 6 h for all strains tested. A ≥3-log10decrease in the number of CFU/ml was observed at 6 h for allEnterobacteriaceae, and a 2-log10reduction in the number of CFU/ml was observed at 6 h for 3 of the 6P. aeruginosaisolates. Regrowth was noted at 24 h for some of the isolates tested in time-kill assays. These data demonstrate the potent bactericidal activity of ceftazidime-avibactam and support the continued clinical development of ceftazidime-avibactam as a new treatment option for infections caused byEnterobacteriaceaeandP. aeruginosa, including isolates resistant to ceftazidime by mechanisms dependent on avibactam-sensitive β-lactamases.

scholarly journals Effect of Nitroxides on Swarming Motility and Biofilm Formation, Multicellular Behaviors in Pseudomonas aeruginosa

2013 ◽  
Vol 57 (10) ◽  
pp. 4877-4881 ◽  
Author(s):  
César de la Fuente-Núñez ◽  
Fany Reffuveille ◽  
Kathryn E. Fairfull-Smith ◽  
Robert E. W. Hancock
Keyword(s):  
Nitric Oxide ◽  
Pseudomonas Aeruginosa ◽  
Biofilm Formation ◽  
Wild Type ◽  
Planktonic Cells ◽  
Swarming Motility ◽  
Content Type ◽  
Exogenous Addition ◽  
Biofilm Dispersion ◽  
Dispersal Activity

ABSTRACTThe ability of nitric oxide (NO) to induce biofilm dispersion has been well established. Here, we investigated the effect of nitroxides (sterically hindered nitric oxide analogues) on biofilm formation and swarming motility inPseudomonas aeruginosa. A transposon mutant unable to produce nitric oxide endogenously (nirS) was deficient in swarming motility relative to the wild type and the complemented strain. Moreover, expression of thenirSgene was upregulated by 9.65-fold in wild-type swarming cells compared to planktonic cells. Wild-type swarming levels were substantially restored upon the exogenous addition of nitroxide containing compounds, a finding consistent with the hypothesis that NO is necessary for swarming motility. Here, we showed that nitroxides not only mimicked the dispersal activity of NO but also prevented biofilms from forming in flow cell chambers. In addition, anirStransposon mutant was deficient in biofilm formation relative to the wild type and the complemented strain, thus implicating NO in the formation of biofilms. Intriguingly, despite its stand-alone action in inhibiting biofilm formation and promoting dispersal, a nitroxide partially restored the ability of anirSmutant to form biofilms.

scholarly journals Overproduction of the AlgT Sigma Factor Is Lethal to Mucoid Pseudomonas aeruginosa

2020 ◽  
Vol 202 (20) ◽  
Author(s):  
Ashley R. Cross ◽  
Vishnu Raghuram ◽  
Zihuan Wang ◽  
Debayan Dey ◽  
Joanna B. Goldberg
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Sigma Factor ◽  
Continuous Production ◽  
Common Mutation ◽  
Wild Type ◽  
Chronic Infections ◽  
Truncated Form ◽  
Content Type ◽  
Lung Infections

ABSTRACT Pseudomonas aeruginosa isolates from chronic lung infections often overproduce alginate, giving rise to the mucoid phenotype. Isolation of mucoid strains from chronic lung infections correlates with a poor patient outcome. The most common mutation that causes the mucoid phenotype is called mucA22 and results in a truncated form of the anti-sigma factor MucA that is continuously subjected to proteolysis. When a functional MucA is absent, the cognate sigma factor, AlgT, is no longer sequestered and continuously transcribes the alginate biosynthesis operon, leading to alginate overproduction. In this work, we report that in the absence of wild-type MucA, providing exogenous AlgT is toxic. This is intriguing, since mucoid strains endogenously possess high levels of AlgT. Furthermore, we show that suppressors of toxic AlgT production have mutations in mucP, a protease involved in MucA degradation, and provide the first atomistic model of MucP. Based on our findings, we speculate that mutations in mucP stabilize the truncated form of MucA22, rendering it functional and therefore able to reduce toxicity by properly sequestering AlgT. IMPORTANCE Pseudomonas aeruginosa is an opportunistic bacterial pathogen capable of causing chronic lung infections. Phenotypes important for the long-term persistence and adaption to this unique lung ecosystem are largely regulated by the AlgT sigma factor. Chronic infection isolates often contain mutations in the anti-sigma factor mucA, resulting in uncontrolled AlgT and continuous production of alginate in addition to the expression of ∼300 additional genes. Here, we report that in the absence of wild-type MucA, AlgT overproduction is lethal and that suppressors of toxic AlgT production have mutations in the MucA protease, MucP. Since AlgT contributes to the establishment of chronic infections, understanding how AlgT is regulated will provide vital information on how P. aeruginosa is capable of causing long-term infections.

scholarly journals Pseudomonas aeruginosa Ethanol Oxidation by AdhA in Low-Oxygen Environments

2019 ◽  
Vol 201 (23) ◽  
Author(s):  
Alex W. Crocker ◽  
Colleen E. Harty ◽  
John H. Hammond ◽  
Sven D. Willger ◽  
Pedro Salazar ◽  
...  
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Alcohol Dehydrogenase ◽  
Ethanol Oxidation ◽  
Physiological Role ◽  
Wild Type ◽  
Low Oxygen ◽  
Content Type ◽  
Anoxic Conditions ◽  
Oxygen Conditions ◽  
Acetate Accumulation

ABSTRACT Pseudomonas aeruginosa has a broad metabolic repertoire that facilitates its coexistence with different microbes. Many microbes secrete products that P. aeruginosa can then catabolize, including ethanol, a common fermentation product. Here, we show that under oxygen-limiting conditions P. aeruginosa utilizes AdhA, an NAD-linked alcohol dehydrogenase, as a previously undescribed means for ethanol catabolism. In a rich medium containing ethanol, AdhA, but not the previously described PQQ-linked alcohol dehydrogenase, ExaA, oxidizes ethanol and leads to the accumulation of acetate in culture supernatants. AdhA-dependent acetate accumulation and the accompanying decrease in pH promote P. aeruginosa survival in LB-grown stationary-phase cultures. The transcription of adhA is elevated by hypoxia and under anoxic conditions, and we show that it is regulated by the Anr transcription factor. We have shown that lasR mutants, which lack an important quorum sensing regulator, have higher levels of Anr-regulated transcripts under low-oxygen conditions than their wild-type counterparts. Here, we show that a lasR mutant, when grown with ethanol, has an even larger decrease in pH than the wild type (WT) that is dependent on both anr and adhA. The large increase in AdhA activity is similar to that of a strain expressing a hyperactive Anr-D149A variant. Ethanol catabolism in P. aeruginosa by AdhA supports growth on ethanol as a sole carbon source and electron donor in oxygen-limited settings and in cells growing by denitrification under anoxic conditions. This is the first demonstration of a physiological role for AdhA in ethanol oxidation in P. aeruginosa. IMPORTANCE Ethanol is a common product of microbial fermentation, and the Pseudomonas aeruginosa response to and utilization of ethanol are relevant to our understanding of its role in microbial communities. Here, we report that the putative alcohol dehydrogenase AdhA is responsible for ethanol catabolism and acetate accumulation under low-oxygen conditions and that it is regulated by Anr.

scholarly journals PQS Produced by the Pseudomonas aeruginosa Stress Response Repels Swarms Away from Bacteriophage and Antibiotics

2019 ◽  
Vol 201 (23) ◽  
Author(s):  
Jean-Louis Bru ◽  
Brandon Rawson ◽  
Calvin Trinh ◽  
Katrine Whiteson ◽  
Nina Molin Høyland-Kroghsbo ◽  
...  
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Stress Response ◽  
Antibiotic Treatment ◽  
Bacterial Pathogen ◽  
Warning Signal ◽  
Opportunistic Pathogen ◽  
Evolutionary Strategy ◽  
Swarming Motility ◽  
Content Type ◽  
Bacteriophage Infection

ABSTRACT We investigate the effect of bacteriophage infection and antibiotic treatment on the coordination of swarming, a collective form of flagellum- and pilus-mediated motility in bacteria. We show that phage infection of the opportunistic bacterial pathogen Pseudomonas aeruginosa abolishes swarming motility in the infected subpopulation and induces the release of the Pseudomonas quinolone signaling molecule PQS, which repulses uninfected subpopulations from approaching the infected area. These mechanisms have the overall effect of limiting the infection to a subpopulation, which promotes the survival of the overall population. Antibiotic treatment of P. aeruginosa elicits the same response, abolishing swarming motility and repulsing approaching swarms away from the antibiotic-treated area through a PQS-dependent mechanism. Swarms are entirely repelled from the zone of antibiotic-treated P. aeruginosa, consistent with a form of antibiotic evasion, and are not repelled by antibiotics alone. PQS has multiple functions, including serving as a quorum-sensing molecule, activating an oxidative stress response, and regulating the release of virulence and host-modifying factors. We show that PQS serves additionally as a stress warning signal that causes the greater population to physically avoid cell stress. The stress response at the collective level observed here in P. aeruginosa is consistent with a mechanism that promotes the survival of bacterial populations. IMPORTANCE We uncover a phage- and antibiotic-induced stress response in the clinically important opportunistic pathogen Pseudomonas aeruginosa. Phage-infected P. aeruginosa subpopulations are isolated from uninfected subpopulations by the production of a stress-induced signal. Activation of the stress response by antibiotics causes P. aeruginosa to physically be repelled from the area containing antibiotics altogether, consistent with a mechanism of antibiotic evasion. The stress response observed here could increase P. aeruginosa resilience against antibiotic treatment and phage therapy in health care settings, as well as provide a simple evolutionary strategy to avoid areas containing stress.

scholarly journals Changes to Its Peptidoglycan-Remodeling Enzyme Repertoire Modulate β-Lactam Resistance in Pseudomonas aeruginosa

2013 ◽  
Vol 57 (7) ◽  
pp. 3078-3084 ◽  
Author(s):  
Joseph F. Cavallari ◽  
Ryan P. Lamers ◽  
Edie M. Scheurwater ◽  
Andrea L. Matos ◽  
Lori L. Burrows
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Penicillin Binding Protein ◽  
Wild Type ◽  
Content Type ◽  
Lytic Transglycosylases ◽  
Phenotypic Screen ◽  
Simultaneous Activation ◽  
Mutant Phenotypes ◽  
High Level ◽  
Hospital Acquired

ABSTRACTPseudomonas aeruginosais a leading cause of hospital-acquired infections and is resistant to many antibiotics. Among its primary mechanisms of resistance is expression of a chromosomally encoded AmpC β-lactamase that inactivates β-lactams. The mechanisms leading to AmpC expression inP. aeruginosaremain incompletely understood but are intricately linked to cell wall metabolism. To better understand the roles of peptidoglycan-active enzymes in AmpC expression—and consequent β-lactam resistance—a phenotypic screen ofP. aeruginosamutants lacking such enzymes was performed. Mutants lacking one of four lytic transglycosylases (LTs) or the nonessential penicillin-binding protein PBP4 (dacB) had altered β-lactam resistance.mltFandsltmutants with reduced β-lactam resistance were designated WIMPs (wall-impaired mutant phenotypes), while highly resistantdacB,sltB1, andmltBmutants were designated HARMs (high-level AmpC resistant mutants). Double mutants lackingdacBandsltB1had extreme piperacillin resistance (>256 μg/ml) compared to either of the single knockouts (64 μg/ml for adacBmutant and 12 μg/ml for ansltB1mutant). Inactivation ofampCreverted these mutants to wild-type susceptibility, confirming that AmpC expression underlies resistance.dacBmutants had constitutively elevated AmpC expression, but the LT mutants had wild-type levels of AmpC in the absence of antibiotic exposure. These data suggest that there are at least two different pathways leading to AmpC expression inP. aeruginosaand that their simultaneous activation leads to extreme β-lactam resistance.

scholarly journals TheprrF-Encoded Small Regulatory RNAs Are Required for Iron Homeostasis and Virulence of Pseudomonas aeruginosa

2014 ◽  
Vol 83 (3) ◽  
pp. 863-875 ◽  
Author(s):  
Alexandria A. Reinhart ◽  
Daniel A. Powell ◽  
Angela T. Nguyen ◽  
Maura O'Neill ◽  
Louise Djapgne ◽  
...  
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Iron Homeostasis ◽  
Opportunistic Pathogen ◽  
Wild Type ◽  
Content Type ◽  
Genes Encoding ◽  
Small Regulatory Rnas ◽  
Regulatory Rnas ◽  
Heme Regulation ◽  
Heme Binding Protein

Pseudomonas aeruginosais an opportunistic pathogen that requires iron to cause infection, but it also must regulate the uptake of iron to avoid iron toxicity. The iron-responsive PrrF1 and PrrF2 small regulatory RNAs (sRNAs) are part ofP. aeruginosa'siron regulatory network and affect the expression of at least 50 genes encoding iron-containing proteins. The genes encoding the PrrF1 and PrrF2 sRNAs are encoded in tandem inP. aeruginosa, allowing for the expression of a distinct, heme-responsive sRNA named PrrH that appears to regulate genes involved in heme metabolism. Using a combination of growth, mass spectrometry, and gene expression analysis, we showed that the ΔprrF1,2mutant, which lacks expression of the PrrF and PrrH sRNAs, is defective for both iron and heme homeostasis. We also identifiedphuS, encoding a heme binding protein involved in heme acquisition, andvreR, encoding a previously identified regulator ofP. aeruginosavirulence genes, as novel targets ofprrF-mediated heme regulation. Finally, we showed that theprrFlocus encoding the PrrF and PrrH sRNAs is required forP. aeruginosavirulence in a murine model of acute lung infection. Moreover, we showed that inoculation with a ΔprrF1,2deletion mutant protects against future challenge with wild-typeP. aeruginosa. Combined, these data demonstrate that theprrF-encoded sRNAs are critical regulators ofP. aeruginosavirulence.

scholarly journals The Sociomicrobiology of Antivirulence Drug Resistance: a Proof of Concept

mBio ◽  
2011 ◽  
Vol 2 (5) ◽  
Author(s):  
Brett Mellbye ◽  
Martin Schuster
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Social Interactions ◽  
Proof Of Concept ◽  
Wild Type ◽  
Content Type ◽  
Future Studies ◽  
Cooperative Behaviors ◽  
The Impact ◽  
Virulence Factor Production ◽  
Proof Of Principle

ABSTRACTAntivirulence drugs disarm rather than kill pathogens and are thought to alleviate the problem of resistance, although there is no evidence to support this notion. Quorum sensing (QS) often controls cooperative virulence factor production and is therefore an attractive antivirulence target, for which inhibitors (QSI) have been developed. We designed a proof-of-principle experiment to investigate the impact of bacterial social interactions on the evolution of QSI resistance. We coculturedPseudomonas aeruginosaQS-deficient mutants with small proportions of the QS-proficient wild type, which in the absence of QSI mimic QSI-sensitive and -resistant variants, respectively. We employed two different QS-dependent nutrients that are degraded by extracellular (public) and cell-associated (private) enzymes. QS mutants (QSI-sensitive mimics) behaved as social cheaters that delayed population growth and prevented enrichment of wild-type cooperators (QSI-resistant mimics) only when nutrient acquisition was public, suggesting that QSI resistance would not spread. This highlights the potential for antivirulence strategies that target cooperative behaviors and provides a conceptual framework for future studies.

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