The Diverse Impacts of Phage Morons on Bacterial Fitness and Virulence

Taylor, Véronique L.; Fitzpatrick, Alexa; Islam, Zafrin; Maxwell, Karen L.

doi:10.1016/bs.aivir.2018.08.001

Cited by 100 publications

(92 citation statements)

References 149 publications

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“…Beyond virulence factors and antibiotic resistance genes, temperate phages encode many other morons, defined as phage genes unnecessary for the phage lytic or lysogenic cycles, but believed to confer improved fitness to their host. Many of them have been characterized over the years (for a recent review, see 50 ). We took advantage of our collection of 19 lambda to search for additional moron genes (Fig.…”

Section: Resultsmentioning

confidence: 99%

Virulent coliphages in 1-year-old children fecal samples are fewer, but more infectious than temperate coliphages

et al. 2020

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Bacteriophages constitute an important part of the human gut microbiota, but their impact on this community is largely unknown. Here, we cultivate temperate phages produced by 900 E. coli strains isolated from 648 fecal samples from 1-year-old children and obtain coliphages directly from the viral fraction of the same fecal samples. We find that 63% of strains hosted phages, while 24% of the viromes contain phages targeting E. coli. 150 of these phages, half recovered from strain supernatants, half from virome (73% temperate and 27% virulent) were tested for their host range on 75 E. coli strains isolated from the same cohort. Temperate phages barely infected the gut strains, whereas virulent phages killed up to 68% of them. We conclude that in fecal samples from children, temperate coliphages dominate, while virulent ones have greater infectivity and broader host range, likely playing a role in gut microbiota dynamics.

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Section: Resultsmentioning

confidence: 99%

Virulent coliphages in 1-year-old children fecal samples are fewer, but more infectious than temperate coliphages

et al. 2020

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“…For example, recent studies highlighted the evidence of subdued phage resistance in the natural environment, probably because of the fitness cost associated with resistance mechanisms [89,[204][205][206][207][208][209]. In addition, these methods have the capability to identify fitness costs associated with broadly seen phage resistance phenotypes in a competitive natural environment, and thus improve our understanding of microbial ecology in general [13,114,206,207,[210][211][212]. Such systems-level insights will be valuable both in uncovering new mechanisms in host-phage interaction and perhaps in developing different design strategies for targeted microbial community interventions, engineering highly virulent or extended host-range phages and rationally formulated phage-cocktails for therapeutic applications [89,204,208,[213][214][215][216][217][218][219][220][221][222][223][224][225][226].…”

Section: Discussionmentioning

confidence: 99%

High-throughput mapping of the phage resistance landscape inE. coli

Mutalik¹,

Adler²,

Rishi³

et al. 2020

Preprint

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Bacteriophages (phages) are critical players in the dynamics and function of microbial communities and drive processes as diverse as global biogeochemical cycles and human health. Phages tend to be predators finely tuned to attack specific hosts, even down to the strain level, which in turn defend themselves using an array of mechanisms. However, to date, efforts to rapidly and comprehensively identify bacterial host factors important in phage infection and resistance have yet to be fully realized. Here, we globally map the host genetic determinants involved in resistance to 14 phylogenetically diverse double-stranded DNA phages using two model Escherichia coli strains (K-12 and BL21) with known sequence divergence to demonstrate strain-specific differences. Using genome-wide loss-of-function and gain-of-function genetic technologies, we are able to confirm previously described phage receptors as well as uncover a number of previously unknown host factors that confer resistance to one or more of these phages. We uncover differences in resistance factors that strongly align with the susceptibility of K-12 and BL21 to specific phage. We also identify both phage specific mechanisms, such as the unexpected role of cyclic-di-GMP in host sensitivity to phage N4, and more generic defenses, such as the overproduction of colanic acid capsular polysaccharide that defends against a wide array of phages. Our results indicate that host responses to phages can occur via diverse cellular mechanisms. Our systematic and highthroughput genetic workflow to characterize phage-host interaction determinants can be extended to diverse bacteria to generate datasets that allow predictive models of how phagemediated selection will shape bacterial phenotype and evolution. The results of this study and future efforts to map the phage resistance landscape will lead to new insights into the coevolution of hosts and their phage, which can ultimately be used to design better phage therapeutic treatments and tools for precision microbiome engineering.3 Introduction:

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“…A number of LPS-specific phages that target P. aeruginosa have been described in the literature as well as phage-resistant mutants arising from mutations in LPS biosynthesis genes [138][139][140][141][142][143][144][145][146][147]. In other cases, phage resistance may arise when temperate bacteriophages encode proteins that modify the O antigen, conferring resistance to superinfection [148]. The P. aeruginosa temperate bacteriophage D3 encodes a peptide that inhibits the host O antigen polymerase, allowing a separate phage polymerase to dominate and produce O antigen with a β linkage instead of an α linkage between O units, resulting in seroconversion [141,149,150].…”

Section: Phages and Pyocinsmentioning

confidence: 99%

The Role of Pseudomonas aeruginosa Lipopolysaccharide in Bacterial Pathogenesis and Physiology

2019

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The major constituent of the outer membrane of Gram-negative bacteria is lipopolysaccharide (LPS), which is comprised of lipid A, core oligosaccharide, and O antigen, which is a long polysaccharide chain extending into the extracellular environment. Due to the localization of LPS, it is a key molecule on the bacterial cell wall that is recognized by the host to deploy an immune defence in order to neutralize invading pathogens. However, LPS also promotes bacterial survival in a host environment by protecting the bacteria from these threats. This review explores the relationship between the different LPS glycoforms of the opportunistic pathogen Pseudomonas aeruginosa and the ability of this organism to cause persistent infections, especially in the genetic disease cystic fibrosis. We also discuss the role of LPS in facilitating biofilm formation, antibiotic resistance, and how LPS may be targeted by new antimicrobial therapies.

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The Diverse Impacts of Phage Morons on Bacterial Fitness and Virulence

Cited by 100 publications

References 149 publications

Virulent coliphages in 1-year-old children fecal samples are fewer, but more infectious than temperate coliphages

Virulent coliphages in 1-year-old children fecal samples are fewer, but more infectious than temperate coliphages

High-throughput mapping of the phage resistance landscape inE. coli

The Role of Pseudomonas aeruginosa Lipopolysaccharide in Bacterial Pathogenesis and Physiology

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