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Eriksen, R. S.

Publications and source records attributed to Eriksen, R. S..

6 recordsLinked to original sources

The dynamics of phage predation on a microcolony

Phage predation is an important factor for controlling the bacterial biomass. At face value, dense microbial habitats are expected to be vulnerable to phage epidemics due to the abundance of fresh hosts immediately next to any infected bacteria. Despite this, the bacterial microcolony is a common habitat for bacteria in nature. Here we experimentally quantify the fate of microcolonies of Escherichia coli exposed to virulent phage T4. It has been proposed that the outer bacterial layers of the colony will shield the inner layers from the phage invasion and thereby constrain the phage to the colonys surface. We develop a dynamical model that incorporates this shielding mechanism and fits the results with experimental measurements to extract important phage-bacteria interaction parameters. The analysis suggests that, while the shielding mechanism delays phage attack,T4 phage are able to diffuse so deep into the dense bacterial environment that colony level survival of the bacterial community is challenged. SignificanceThe shielding mechanism of bacterial microcolonies against phage invasion has been experimentally quantified, and the result was analyzed by using a mathematical model. The analysis suggests that while forming a dense colony delays phage attack by limiting the infection closer to the colony surface,T4 phage can diffuse so deep into the dense bacterial environment that colony-level survival of the bacterial community is challenged. This finding highlights the importance of the interplay between the phage infection dynamics and the physical structure of bacterial colonies in controlling the microbial population.

microbiology↗

Emergence of networks of shared restriction-modification systems in phage-bacteria ecosystems

1Restriction-modification (RM) systems are the most ubiquitous bacterial defense system against bacteriophages and an important part of controlling phage predation. Using genomic sequence data, we show that RM systems are often shared among bacterial strains in a structured way. Examining the network of interconnections between bacterial strains within each genus, we find that in many genera strains share more RM systems than expected from a random network. We also find that many genera have a larger than expected number of bacterial strains with unique RM systems. We use population dynamics models of closed and open phage-bacteria ecosystems to qualitatively understand the selection pressures that could lead to these non-random network structures with enhanced overlap or uniqueness. In our models we find that the phages impose a pressure that favours bacteria with more RM systems, and more overlap of RM systems with other strains, but in bacteria dominated states this is opposed by the increased cost to the growth rate of these bacteria. Similar to what we observe in the genome data, we find that two distinct bacterial strategies emerge - strains either have a larger overlap than expected, or they have more unique RM systems than one expects from a null model. The former strategy appears to dominate when the repertoire of available RM systems is smaller but the average number of RM systems per strain is larger.

microbiology↗

On phage adsorption to bacterial chains

Bacteria often arrange themselves in various spatial configurations which changes how they interact with their surroundings. In this paper, we investigate in silico how the structure of the bacterial arrangements influences the adsorption of bacteriophages. We quantify how the adsorption rate scales with the number of bacteria in the arrangement, and show that the adsorption rates for microcolonies (increasing with exponent [~]1/3) and bacterial chains (increasing with exponent [~]0.5 - 0.8) are substantially lower than for well-mixed bacteria (increasing with exponent 1). We further show that, after infection, the spatially clustered arrangements reduce the effective burst size by more than 50 % and cause substantial superinfections in a very short time interval after phage lysis. SIGNIFICANCEWhen bacteria forms clusters they substantially change their exposure to invading phages and other external agents from the well-mixed scenario. Despite this fact, much research has focused on and is focusing on using well-mixed bacteria. Understanding the kinetics of the spatial structures is paramount to developing robust analyses and theories of experimental results. We carefully investigate how the clusters lower the adsorption rate of external phages and how the clustering modifies the hit probabilities for the bacteria.

biophysics↗

Defense versus growth in a hostile world - Lessons from phage and bacteria

Bacterial communities are often highly diverse with several closely related species (or strains) coexisting together. These bacteria compete for resources and the competitive exclusion principle predicts that all but the fastest-growing bacteria will go extinct. When exposed to phage, it is predicted that bacterial strains with restriction-modification (RM) systems can circumvent the competitive exclusion principle and reach diversity on the order of the phage burst size. We show that with a trade-off between bacterial growth rates and the strength of their RM systems, the diversity of such an ecosystem can further increase several fold beyond the burst size limit. Moreover, we find that the ratio of the growth rate of a bacterial strain to the imperfection of its RM system is an excellent predictor of (i) whether the strain will go extinct or not, and (ii) the biomass of the strain if it survives. In contrast, the growth rate alone is not a determinant of either of these properties. Our work provides a quantitative example of a model ecosystem where the fitness of a species is determined not by growth rate, but by a trade-off between growth and defence against predators.

ecology↗

Sustainability of spatially distributed bacteria-phage systems

Virulent phages can expose their bacterial hosts to devastating epidemics, in principle opening for a complete elimination of their hosts. Although experiments indeed confirm large reduction of susceptible bacteria, there is no reports of complete extinctions. We here address this phenomenon from the perspective of spatial organization of bacteria and how this can influence the final survival of them. By modeling the transient dynamics of bacteria and phages when they are introduced into an environment with finite resources, we quantify how the spatial separation of initial bacterial positions and the self-protection of bacteria growing in spherical colonies favor bacterial survival. This suggest that spatial structures on the millimeter scale plays an important role in maintaining microbial diversity.

ecology↗

A Growing Microcolony can Survive and Support Persistent Propagation of Virulent Phages

Bacteria form colonies and secrete extracellular polymeric substances that surround the individual cells. These spatial structures are often associated with collaboration and quorum sensing between the bacteria. Here we investigate the mutual protection provided by spherical growth of a monoclonal colony during exposure to phages that proliferate on its surface. As a proof of concept we exposed growing colonies of Escherichia coli to a virulent mutant of phage P1. When the colony consists of less than ~ 50000 members it is eliminated, while larger initial colonies allow long-term survival because the growth of bacteria throughout the spherical colony exceeds the killing of bacteria on the surface. A mathematical model pinpoints how this critical colony size depends on key parameters in the phage infection cycle. Surprisingly, we predict that a higher phage adsorption rate would allow substantially smaller colonies to survive a virulent phage.\n\nSignificance StatementBacteria are repeatedly exposed to an excess of phages, and carry evidence of this in terms of multiple defense mechanisms encoded in their genome. In addition to molecular mechanisms, bacteria may exploit the defense of spatial refuges. Here we demonstrate how bacteria can limit the impact of a virulent phage attack by growing as a colony which only exposes its surface to phages. We identify a critical size of the initial colony, below which the phages entirely eliminates the colony, and above which the colony continues to grow despite the presence of phages. Our study suggests that coexistence of phages and bacteria is strongly influenced by the spatial composition of microcolonies of susceptible bacteria.

microbiology↗