Filamentous prophage capsid proteins contribute to superinfection exclusion and phage defence in <i>Pseudomonas aeruginosa</i>

Wang, Weiquan; Li, Yangmei; Tang, Kaihao; Lin, Jianzhong; Gao, Xinyu; Guo, Yunxue

doi:10.1111/1462-2920.15991

Cited by 21 publications

(7 citation statements)

References 62 publications

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“…The phage adsorption assay we performed as we reported recently with minor modification 53 . Briefly, 2 ml of culture was collected at OD 600 ∼ 1 and mixed with different amounts of phages (10 7 -10 9 PFU/ml) to reach a MOI of 0.01.…”

Section: Methodsmentioning

confidence: 99%

Dual control of lysogeny and phage defense by a phosphorylation-based toxin/antitoxin system

Guo

Tang

Sit

et al. 2022

Preprint

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Regulatory systems that maintain prophage quiescence integrate phage and host gene expression with environmental conditions1,2. In the opportunistic bacterial pathogen Pseudomonas aeruginosa, Pf filamentous bacteriophages play critical roles in biofilm formation and virulence3-5, but mechanisms governing Pf prophage activation in biofilms are largely unknown. Here, we report a new type of prophage regulatory module in a widely-distributed P. aeruginosa lineage that not only controls virion production of co-resident Pf prophages, but also mediates defense against diverse lytic phages. By comparing two lineages of the prototype P. aeruginosa strain PAO1 that harbor different Pf prophages, we identified a prophage-encoded kinase-kinase-phosphatase (KKP) system that controls Pf production in biofilms. KKP components exhibit dynamic stoichiometry, where high kinase levels in planktonic conditions maintain phosphorylation of the host H-NS protein MvaU, repressing prophage activation. During biofilm formation, phosphatase expression is heightened, leading to MvaU dephosphorylation and alleviating repression of prophage gene expression. KKP clusters are present in hundreds of diverse temperate prophages and other mobile elements across Gram-negative bacteria. Characterization of KKP modules from different species revealed that, in addition to regulating Pf phage lysogeny, KKP functions as a tripartite toxin-antitoxin system that mediates host defense from predatory lytic phages. KKP represents a new phosphorylation-based mechanism for prophage regulation and for phage defense. The dual function of this module raises the question of whether other newly described phage defense systems6-9 also regulate intrinsic prophage biology in diverse hosts.

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Section: Methodsmentioning

confidence: 99%

Dual control of lysogeny and phage defense by a phosphorylation-based toxin/antitoxin system

Guo

Tang

Sit

et al. 2022

Preprint

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“…T4P repression in these strains could be ascribed to the loss of transcriptional activation, as both Pf4r 31 and PA0715 33 in the L region were recently demonstrated to promote transcription of T4P-essential genes. Additionally, Pf4 minor capsid proteins pVII and pIII also interfered with T4P assembly and contributed to Pf4 superinfection exclusion 34,35 . Furthermore, we examined whether XisF4 had an additional effect on twitching motility, as it was upregulated more than 64-fold in those T4P-defective strains (Fig.…”

Section: Superinfection Of Pseudomonas Lamentous (Pf4) Bacteriophage ...mentioning

confidence: 99%

Divergent molecular strategies drive convergent evolutionary adaptation to kin competition in biofilms

Tang,

Yang,

Han

et al. 2024

Preprint

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Biofilms are a hotspot of bacterial social interactions that are characterized by cooperation and competition. Even a mono-species biofilm would evolve and diversify into polymorphic subpopulations so that bacterial kins of different genotypes would compete for limited nutrient and space. However, the specific biological functions underlying biofilm diversification and competition adaptation are poorly demonstrated. Here, we launched and monitored the experimental evolution of Pseudomonas aeruginosa biofilms, finding that two competition-adaptive derivatives rapidly emerged with variable capacities in forming biofilm. Further investigations identified that two novel divergent molecular trajectories were adopted for convergent adaptation to kin competition: one involved hijacking bacteriophage superinfection to aggressively inhibit kin competitors, while the other induced a subtle change in c-di-GMP signaling to gain a positional advantage via enhanced early biofilm adhesion. Bioinformatics analyses implicated that similar evolutionary strategies were prevalent among clinical P. aeruginosa strains, indicative of parallelism between natural and experimental evolution. Divergence in the molecular bases illustrated the adaptive values of genomic plasticity for gaining competitive fitness in the biofilm. Finally, we demonstrated that these competition-adaptive mutations reduced bacterial virulence. Our findings showed how kin competition shaped the P. aeruginosa biofilm evolution. More importantly, it revealed new insights into molecular targets for the treatment of recalcitrant biofilm infections formed by this clinically relevant pathogen.

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“…To compete for host cell resources, many phages have evolved superinfection exclusion mechanisms that enable the host’s resistance to repeated infection by other phage. Pf phages in P. aeruginosa can exclude infection of other phages by interfering with the function of type IV pili (T4P), which may reduce the efficacy of phages in treating pseudomonas-associated infections [ 34 ]. Escherichia coli abolishes further infection by bacteriophage T5 via the jamming of TonB-dependent transporters by small phage lipoproteins [ 35 ].…”

Section: Underlying Mechanisms Of Phages In Chronic Liver Diseasesmentioning

confidence: 99%

The Novel Role of Phage Particles in Chronic Liver Diseases

2023

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The gut microbiome is made up of bacteria, fungi, viruses and archaea, all of which are closely related with human health. As the main component of enterovirus, the role of bacteriophages (phages) in chronic liver disease has been gradually recognized. Chronic liver diseases, including alcohol-related liver disease and nonalcoholic fatty liver disease, exhibited alterations of the enteric phages. Phages shape intestinal bacterial colonization and regulate bacterial metabolism. Phages adjoining to intestinal epithelial cells prevent bacteria from invading the intestinal barrier, and mediate intestinal inflammatory response. Phages are also observed increasing intestinal permeability and migrating to peripheral blood and organs, likely contributing to inflammatory injury in chronic liver diseases. By preying on harmful bacteria, phages can improve the gut microbiome of patients with chronic liver disease and thus act as an effective treatment method.

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Filamentous prophage capsid proteins contribute to superinfection exclusion and phage defence in Pseudomonas aeruginosa

Cited by 21 publications

References 62 publications

Dual control of lysogeny and phage defense by a phosphorylation-based toxin/antitoxin system

Dual control of lysogeny and phage defense by a phosphorylation-based toxin/antitoxin system

Divergent molecular strategies drive convergent evolutionary adaptation to kin competition in biofilms

The Novel Role of Phage Particles in Chronic Liver Diseases

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