Population dynamics of the rat tapeworm, 'Hymenolepis Diminuta'

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Expansion, Exploitation and Extinction: Niche Construction in Ephemeral Landscapes

We aim to understand general consequences of niche construction on metapopulation dynamics in ephemeral landscapes. To this effect, a contact process-like stochastic spatial model is introduced where local populations colonize and go extinct on a dynamic landscape of habitable and destroyed patches. In contrast to previous models, where the extinction threshold is a consequence of available niche rendered by global rates of patch destruction/renewal, here we investigate how the metapopulation persists when they are the sole generators of their own niche. Niche construction is full-filled by localized populations through the transformation of destroyed patches in their neighborhood to viable habitat for future colonization. With this theoretical framework we are able to address the dual nature of niche construction by investigating the ephemerality of the landscape (destruction rate) and the continuum of population level strategies, where construction comes at a cost to colonization. Using mean field theory and Monte Carlo simulations of the model, we are able to quantify optimal population level strategies in a wide range of ephemeral landscapes. Interestingly, we observe qualitative differences at the extinction threshold between analytic and numeric results. Investigating this discrepancy further, we find that increasing niche construction neighborhood in the spatial model leads to two interrelated effects i) an increased rate in range expansion ii) a loss in resiliency and return of the discontinuous transition at the extinction threshold. Furthermore, in the discontinuous regime of the model, spatial clustering prior to a critical transition disappears. This is a significant finding as spatial clustering has been considered to be an early warning signal before ecosystems reach their 'tipping point'. In addition to maintaining stability, we find local niche construction strategies have an advantage when in scramble competition with an exploiter strategy because of their ability to monopolize the constructed niche due to spatial adjacency. As the niche construction neighborhood expands this advantage disappears and the exploiter strategy out-competes the niche constructor. In some cases the exploiter pushes the niche constructor to extinction, thus a tragedy of the commons ensues leading to 'ecological suicide' and a collapse of the niche

Variance in Landscape Connectivity Shifts Microbial Population Scaling

Understanding mechanisms shaping distributions and interactions of soil microbes is essential for determining their impact on large scale ecosystem services, such as carbon sequestration, climate regulation, waste decomposition, and nutrient cycling. As the functional unit of soil ecosystems, we focus our attention on the spatial structure of soil macroaggregates. Emulating this complex physico-chemical environment as a patchy habitat landscape we investigate on-chip the effect of changing the connectivity features of this landscape as Escherichia coli forms a metapopulation. We analyze the distributions of E. coli occupancy using Taylor's law, an empirical law in ecology which asserts that the fluctuations in populations is a power law function of the mean. We provide experimental evidence that bacterial metapopulations in patchy habitat landscapes on microchips follow this law. Furthermore, we find that increased variance of patch-corridor connectivity leads to a qualitative transition in the fluctuation scaling. We discuss these results in the context of the spatial ecology of microbes in soil

Adaptive response and enlargement of dynamic range

Many membrane channels and receptors exhibit adaptive, or desensitized, response to a strong sustained input stimulus, often supported by protein activity-dependent inactivation. Adaptive response is thought to be related to various cellular functions such as homeostasis and enlargement of dynamic range by background compensation. Here we study the quantitative relation between adaptive response and background compensation within a modeling framework. We show that any particular type of adaptive response is neither sufficient nor necessary for adaptive enlargement of dynamic range. In particular a precise adaptive response, where system activity is maintained at a constant level at steady state, does not ensure a large dynamic range neither in input signal nor in system output. A general mechanism for input dynamic range enlargement can come about from the activity-dependent modulation of protein responsiveness by multiple biochemical modification, regardless of the type of adaptive response it induces. Therefore hierarchical biochemical processes such as methylation and phosphorylation are natural candidates to induce this property in signaling systems.Comment: Corrected typos, minor text revision

Ecological Succession and the Competition-Colonization Trade-Off in Microbial Communities

BACKGROUND: During range expansion in spatially distributed habitats, organisms differ from one another in terms of their patterns of localization versus propagation. To exploit locations or explore the landscape? This is the competition-colonization trade-off, a dichotomy at the core of ecological succession. In bacterial communities, this trade-off is a fundamental mechanism towards understanding spatio-temporal fluxes in microbiome composition. RESULTS: Using microfluidics devices as structured bacterial habitats, we show that, in a synthetic two-species community of motile strains, Escherichia coli is a fugitive species, whereas Pseudomonas aeruginosa is a slower colonizer but superior competitor. We provide evidence highlighting the role of succession and the relevance of this trade-off in the community assembly of bacteria in spatially distributed patchy landscapes. Furthermore, aggregation-dependent priority effects enhance coexistence which is not possible in well-mixed environments. CONCLUSIONS: Our findings underscore the interplay between micron-scale landscape structure and dispersal in shaping biodiversity patterns in microbial ecosystems. Understanding this interplay is key to unleash the technological revolution of microbiome applications. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s12915-022-01462-5

Self-Organization, Layered Structure, and Aggregation Enhance Persistence of a Synthetic Biofilm Consortium

Microbial consortia constitute a majority of the earth’s biomass, but little is known about how these cooperating communities persist despite competition among community members. Theory suggests that non-random spatial structures contribute to the persistence of mixed communities; when particular structures form, they may provide associated community members with a growth advantage over unassociated members. If true, this has implications for the rise and persistence of multi-cellular organisms. However, this theory is difficult to study because we rarely observe initial instances of non-random physical structure in natural populations. Using two engineered strains of Escherichia coli that constitute a synthetic symbiotic microbial consortium, we fortuitously observed such spatial self-organization. This consortium forms a biofilm and, after several days, adopts a defined layered structure that is associated with two unexpected, measurable growth advantages. First, the consortium cannot successfully colonize a new, downstream environment until it selforganizes in the initial environment; in other words, the structure enhances the ability of the consortium to survive environmental disruptions. Second, when the layered structure forms in downstream environments the consortium accumulates significantly more biomass than it did in the initial environment; in other words, the structure enhances the global productivity of the consortium. We also observed that the layered structure only assembles in downstream environments that are colonized by aggregates from a previous, structured community. These results demonstrate roles for self-organization and aggregation in persistence of multi-cellular communities, and also illustrate a role for the techniques of synthetic biology in elucidating fundamental biological principles

Mathematical description of bacterial traveling pulses

The Keller-Segel system has been widely proposed as a model for bacterial waves driven by chemotactic processes. Current experiments on {\em E. coli} have shown precise structure of traveling pulses. We present here an alternative mathematical description of traveling pulses at a macroscopic scale. This modeling task is complemented with numerical simulations in accordance with the experimental observations. Our model is derived from an accurate kinetic description of the mesoscopic run-and-tumble process performed by bacteria. This model can account for recent experimental observations with {\em E. coli}. Qualitative agreements include the asymmetry of the pulse and transition in the collective behaviour (clustered motion versus dispersion). In addition we can capture quantitatively the main characteristics of the pulse such as the speed and the relative size of tails. This work opens several experimental and theoretical perspectives. Coefficients at the macroscopic level are derived from considerations at the cellular scale. For instance the stiffness of the signal integration process turns out to have a strong effect on collective motion. Furthermore the bottom-up scaling allows to perform preliminary mathematical analysis and write efficient numerical schemes. This model is intended as a predictive tool for the investigation of bacterial collective motion

Robust Signal Processing in Living Cells

Cellular signaling networks have evolved an astonishing ability to function reliably and with high fidelity in uncertain environments. A crucial prerequisite for the high precision exhibited by many signaling circuits is their ability to keep the concentrations of active signaling compounds within tightly defined bounds, despite strong stochastic fluctuations in copy numbers and other detrimental influences. Based on a simple mathematical formalism, we identify topological organizing principles that facilitate such robust control of intracellular concentrations in the face of multifarious perturbations. Our framework allows us to judge whether a multiple-input-multiple-output reaction network is robust against large perturbations of network parameters and enables the predictive design of perfectly robust synthetic network architectures. Utilizing the Escherichia coli chemotaxis pathway as a hallmark example, we provide experimental evidence that our framework indeed allows us to unravel the topological organization of robust signaling. We demonstrate that the specific organization of the pathway allows the system to maintain global concentration robustness of the diffusible response regulator CheY with respect to several dominant perturbations. Our framework provides a counterpoint to the hypothesis that cellular function relies on an extensive machinery to fine-tune or control intracellular parameters. Rather, we suggest that for a large class of perturbations, there exists an appropriate topology that renders the network output invariant to the respective perturbations

Mathematical analysis of the Escherichia coli chemotaxis signalling pathway

We undertake a detailed mathematical analysis of a recent nonlinear ordinary differential equation (ODE) model describing the chemotactic signalling cascade within an {\it Escherichia coli} cell. The model includes a detailed description of the cell signalling cascade and an average approximation of the receptor activity. A steady-state stability analysis reveals the system exhibits one positive real steady-state which is shown to be asymptotically stable. Given the occurrence of a negative feedback between phosphorylated CheB (CheB-P) and the receptor state, we ask under what conditions, the system may exhibit oscillatory type behaviour. A detailed analysis of parameter space reveals that whilst variation in kinetic rate parameters within known biological limits is unlikely to lead to such behaviour, changes in the total concentration of the signalling proteins does. We postulate that experimentally observed overshoot behaviour can actually be described by damped oscillatory dynamics and consider the relationship between overshoot amplitude, total cell protein concentration and the magnitude of the external ligand stimulus. Model reductions of the full ODE model allow us to understand the link between phosphorylation events and the negative feedback between CheB-P and receptor methylation, as well as elucidate why some mathematical models exhibit overshoot and others do not. Our manuscript closes by discussing intercell variability of total protein concentration as means of ensuring the overall survival of a population as cells are subjected to different environments