Plasmid co-infection: linking biological mechanisms to ecological and evolutionary dynamics

Igler, Claudia; Huisman, Jana S.; Siedentop, Berit; Bonhoeffer, Sebastian; Lehtinen, Sonja

doi:10.1098/rstb.2020.0478

Cited by 14 publications

(11 citation statements)

References 108 publications

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“…25–50% of colonized hosts depending on setting [21–23]), although whether such co-colonization is possible between strains with different bacteriocin profiles is not clear. Furthermore, previous theoretical work suggests that assumptions about within-host dynamics and competition can have considerable impact on predictions about strain diversity at the between-host scale [37–39]. We tested the impact of allowing slower within-host dynamics and thus co-colonization in all three models (bacteriocin dynamics, pherotype and antibiotic resistance) and find our results are qualitatively robust (electronic supplementary material, section 2.1).…”

Section: Discussionmentioning

confidence: 75%

Epidemiological dynamics of bacteriocin competition and antibiotic resistance

et al. 2022

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Bacteriocins, toxic peptides involved in the competition between bacterial strains, are extremely diverse. Previous work on bacteriocin dynamics has highlighted the role of non-transitive ‘rock–paper–scissors’ competition in maintaining the coexistence of different bacteriocin profiles. The focus to date has primarily been on bacteriocin interactions at the within-host scale (i.e. within a single bacterial population). Yet in species such as Streptococcus pneumoniae , with relatively short periods of colonization and limited within-host diversity, ecological outcomes are also shaped by processes at the epidemiological (between-host) scale. Here, we first investigate bacteriocin dynamics and diversity in epidemiological models. We find that in these models, bacteriocin diversity is more readily maintained than in within-host models, and with more possible combinations of coexisting bacteriocin profiles. Indeed, maintenance of diversity in epidemiological models does not require rock–paper–scissors dynamics; it can also occur through a competition–colonization trade-off. Second, we investigate the link between bacteriocin diversity and diversity at antibiotic resistance loci. Previous work has proposed that bacterial duration of colonization modulates the fitness of antibiotic resistance. Due to their inhibitory effects, bacteriocins are a plausible candidate for playing a role in the duration of colonization episodes. We extend the epidemiological model of bacteriocin dynamics to incorporate an antibiotic resistance locus and demonstrate that bacteriocin diversity can indeed maintain the coexistence of antibiotic-sensitive and -resistant strains.

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Section: Discussionmentioning

confidence: 75%

Epidemiological dynamics of bacteriocin competition and antibiotic resistance

et al. 2022

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“…Postsegregational killing can also lead to loss of a coinfecting plasmid over time [120]. Some plasmids also actively destroy other potentially coinfecting plasmids with plasmid-borne CRISPR/Cas [183][184][185] or restriction-modification systems [118,119,186] (see Fig. 2c), which work analogously to their chromosomal counterparts.…”

Section: Interactions With Other Plasmids and Mobile Genetic Elementsmentioning

confidence: 99%

A mathematician’s guide to plasmids: an introduction to plasmid biology for modellers

Dewan,

Uecker

2023

Microbiology

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Plasmids, extrachromosomal DNA molecules commonly found in bacterial and archaeal cells, play an important role in bacterial genetics and evolution. Our understanding of plasmid biology has been furthered greatly by the development of mathematical models, and there are many questions about plasmids that models would be useful in answering. In this review, we present an introductory, yet comprehensive, overview of the biology of plasmids suitable for modellers unfamiliar with plasmids who want to get up to speed and to begin working on plasmid-related models. In addition to reviewing the diversity of plasmids and the genes they carry, their key physiological functions, and interactions between plasmid and host, we also highlight selected plasmid topics that may be of particular interest to modellers and areas where there is a particular need for theoretical development. The world of plasmids holds a great variety of subjects that will interest mathematical biologists, and introducing new modellers to the subject will help to expand the existing body of plasmid theory.

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“…Our model is based on the model for type I/II CRISPR-Cas systems of Chabas et al, 2022 [18], with the addition of basic plasmid processes incorporated along the lines of Igler et al, 2022 [19]. We chose to limit our analysis on type I CRISPR-Cas systems because type I CRISPR-Cas systems are the most frequent on bacterial chromosomes and plasmids [11, 20].…”

Section: Model Of Plasmid Crispr-cas and Phage Dynamicsmentioning

confidence: 99%

My host’s enemy is my enemy: plasmids carrying CRISPR-Cas as a defence against phages

Siedentop,

Rüegg,

Bonhoeffer

et al. 2023

Preprint

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Bacteria are infected by mobile genetic elements like plasmids and virulent phages, and those infections significantly impact bacterial ecology and evolution. Recent discoveries reveal that some plasmids carry anti-phage immune systems like CRISPR-Cas, suggesting that plasmids may participate in the coevolutionary arms-race between virulent phages and bacteria. Intuitively, this seems reasonable as virulent phages kill the plasmid’s obligate host. However, the efficiency of CRISPR-Cas systems carried by plasmids can be expected to be lower than those carried by the chromosome due to continuous segregation loss, creating susceptible cells for phage amplification. To evaluate the anti-phage protection efficiency of CRISPR-Cas on plasmids, we develop a stochastic model describing the dynamics of a virulent phage infection against which a conjugative plasmid defends using CRISPR-Cas. We show that CRISPR-Cas on plasmids provides robust protection, except in limited parameter-sets. In these cases, high segregation favours phage outbreaks by generating a population of defenceless cells on which the phage can evolve and escape CRISPR-Cas immunity. We show that the phage’s ability to exploit segregation loss depends strongly on the evolvability of both CRISPR-Cas and the phage itself.

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Plasmid co-infection: linking biological mechanisms to ecological and evolutionary dynamics

Cited by 14 publications

References 108 publications

Epidemiological dynamics of bacteriocin competition and antibiotic resistance

Epidemiological dynamics of bacteriocin competition and antibiotic resistance

A mathematician’s guide to plasmids: an introduction to plasmid biology for modellers

My host’s enemy is my enemy: plasmids carrying CRISPR-Cas as a defence against phages

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