Bacterial chemotaxis, the directed movement of cells along "chemoattractant" gradients, is among the best-characterized subjects of molecular biology 1-10. Much less is known about its physiological roles 11. Commonly, it is seen as starvation response when nutrients run out, or as escape response from harmful situations 12-16. Here, we establish an alternative role of chemotaxis by systematically examining the spatiotemporal dynamics of Escherichia coli in soft agar 12,17,18 : Chemotaxis in nutrient-replete conditions promotes the expansion of bacterial populations into unoccupied territories well before nutrients run out in the current environment. We show how low levels of chemoattractants act as aroma-like cues in this process, establishing the direction and enhancing the speed of population movement along the self-generated attractant gradients. This navigated range expansion process spreads faster and yields larger population gains than unguided expansion following the canonical Fisher-Kolmogorov dynamics 19,20 and is therefore a general strategy to promote population growth in spatially extended, nutrient-replete environments.
The human gut harbors a dynamic microbial community whose composition bears great importance for the health of the host. Here, we investigate how colonic physiology impacts bacterial growth, which ultimately dictates microbiota composition. Combining measurements of bacterial physiology with analysis of published data on human physiology into a quantitative, comprehensive modeling framework, we show how water flow in the colon, in concert with other physiological factors, determine the abundances of the major bacterial phyla. Mechanistically, our model shows that local pH values in the lumen, which differentially affect the growth of different bacteria, drive changes in microbiota composition. It identifies key factors influencing the delicate regulation of colonic pH, including epithelial water absorption, nutrient inflow, and luminal buffering capacity, and generates testable predictions on their effects. Our findings show that a predictive and mechanistic understanding of microbial ecology in the gut is possible. Such predictive understanding is needed for the rational design of intervention strategies to actively control the microbiota. T he human gut microbiota is composed of trillions of bacterial cells (1-4) from several hundred species (1-3, 5, 6). Over the last two decades, a multitude of studies have shown a strong impact of human health status on the composition of this microbiota, and in turn a strong effect of microbiota composition on host physiology has also been confirmed (7-9). Various intervention strategies are being investigated to modify the microbiota composition via prebiotics and probiotics (10). Despite this importance for human health, little is known about how the microbiota composition is shaped by the interplay between human and bacterial physiology in the gut.In this study, we present a physiological model that quantitatively describes this host-microbiota interplay. Our model is based on a hydrodynamic perspective, which posits that bacterial densities reached in the colon result from a dynamic balance between bacterial growth, flow through the colon, and peristaltic mixing (11). To build the present model, we extensively analyzed literature data on human gut physiology to obtain quantitative estimates for a range of relevant host parameters. We further characterized the rates of bacterial growth, carbohydrate consumption, and fermentation product excretion for representatives of the two dominant bacteria phyla, Bacteroidetes and Firmicutes, that typically make up more than 90% of the bacterial cells observed in the gut (6).Combining these aspects of human and bacterial physiology into a coarse-grained mathematical model allowed us to study bacterial growth dynamics in the human gut. Without resorting to ad hoc fitting parameters, model results are in quantitative agreement with available data on key observables of human gut physiology. We find that changes in pH values in the colon that are due to the secretion of acidic fermentation products and shaped by human physiology (such a...
Existing theoretical models of evolution focus on the relative fitness advantages of different mutants in a population while the dynamic behavior of the population size is mostly left unconsidered. We here present a generic stochastic model which combines the growth dynamics of the population and its internal evolution. Our model thereby accounts for the fact that both evolutionary and growth dynamics are based on individual reproduction events and hence are highly coupled and stochastic in nature. We exemplify our approach by studying the dilemma of cooperation in growing populations and show that genuinely stochastic events can ease the dilemma by leading to a transient but robust increase in cooperation.
The ecology of microbes in the gut has been shown to play important roles in the health of the host. To better understand microbial growth and population dynamics in the proximal colon, the primary region of bacterial growth in the gut, we built and applied a fluidic channel that we call the "minigut." This is a channel with an array of membrane valves along its length, which allows mimicking active contractions of the colonic wall. Repeated contraction is shown to be crucial in maintaining a steady-state bacterial population in the device despite strong flow along the channel that would otherwise cause bacterial washout. Depending on the flow rate and the frequency of contractions, the bacterial density profile exhibits varying spatial dependencies. For a synthetic cross-feeding community, the species abundance ratio is also strongly affected by mixing and flow along the length of the device. Complex mixing dynamics due to contractions is described well by an effective diffusion term. Bacterial dynamics is captured by a simple reaction-diffusion model without adjustable parameters. Our results suggest that flow and mixing play a major role in shaping the microbiota of the colon.
Microbes providing public goods are widespread in nature despite running the risk of being exploited by free-riders. However, the precise ecological factors supporting cooperation are still puzzling. Following recent experiments, we consider the role of population growth and the repetitive fragmentation of populations into new colonies mimicking simple microbial life-cycles. Individual-based modeling reveals that demographic fluctuations, which lead to a large variance in the composition of colonies, promote cooperation. Biased by population dynamics these fluctuations result in two qualitatively distinct regimes of robust cooperation under repetitive fragmentation into groups. First, if the level of cooperation exceeds a threshold, cooperators will take over the whole population. Second, cooperators can also emerge from a single mutant leading to a robust coexistence between cooperators and free-riders. We find frequency and size of population bottlenecks, and growth dynamics to be the major ecological factors determining the regimes and thereby the evolutionary pathway towards cooperation.
We study the interplay of population growth and evolutionary dynamics using a stochastic model based on birth and death events. In contrast to the common assumption of an independent population size, evolution can be strongly affected by population dynamics in general. Especially for fast reproducing microbes which are subject to selection, both types of dynamics are often closely intertwined. We illustrate this by considering different growth scenarios. Depending on whether microbes die or stop to reproduce (dormancy), qualitatively different behaviors emerge. For cooperating bacteria, a permanent increase of costly cooperation can occur. Even if not permanent, cooperation can still increase transiently due to demographic fluctuations. We validate our analysis via stochastic simulations and analytic calculations. In particular, we derive a condition for an increase in the level of cooperation.
The ability of a species to colonize newly available habitas is crucial to its overall fitness. Generally, motility and fast expansion is expected to be beneficial to the colonization process and hence to organismal fitness. Here we apply a unique evolution protocol to investigate phenotypical requirements for colonizing habitats of different sizes during range expansion of chemotaxing bacteria. Contrary to the intuitive expectation that faster is better, we show the existence of an optimal expansion speed associated with a given habitat size. Our analysis showed this effect to arise from interactions among pioneering cells at the front of the expanding population, and revealed a simple, evolutionary stable strategy for colonizing a habitat of a specific size: to expand at a speed given by the product of the growth rate and habitat size. These results illustrates stability-to-invasion as a powerful principle for the selection of phenotypes in complex ecological processes. Users may view, print, copy, and download text and data-mine the content in such documents, for the purposes of academic research, subject always to the full Conditions of use:
The physical interactions of growing bacterial cells with each other and with their surroundings significantly affect the structure and dynamics of biofilms. Here a 3D agent-based model is formulated to describe the establishment of simple bacterial colonies expanding by the physical force of their growth. With a single set of parameters, the model captures key dynamical features of colony growth by non-motile, non EPS-producing E. coli cells on hard agar. The model, supported by experiment on colony growth in different types and concentrations of nutrients, suggests that radial colony expansion is not limited by nutrients as commonly believed, but by mechanical forces. Nutrient penetration instead governs vertical colony growth, through thin layers of vertically oriented cells lifting up their ancestors from the bottom. Overall, the model provides a versatile platform to investigate the influences of metabolic and environmental factors on the growth and morphology of bacterial colonies.
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