Applying allometric scaling to predator-prey systems

In population dynamics, mathematical models often contain too many parameters to be easily testable. A way to reliably estimate parameters for a broad range of systems would help us obtain clearer predictions from theory. In this paper, we examine how the allometric scaling of a number of biological quantities with animal mass may be useful to parameterise population dynamical models. Using this allometric scaling, we make predictions about the ratio of prey to predators in real ecosystems, and we attempt to estimate the length of animal population cycles as a function of mass. Our analytical and numerical results turn out to compare reasonably to data from a number of ecosystems. This paves the way for a wider usage of allometric scaling to simplify mathematical models in population dynamics and make testable predictions.Comment: 9 pages, 3 figure

Well-temperate phage: optimal bet-hedging against local environmental collapses

Upon infection of their bacterial hosts temperate phages must chose between lysogenic and lytic developmental strategies. Here we apply the game-theoretic bet-hedging strategy introduced by Kelly to derive the optimal lysogenic fraction of the total population of phages as a function of frequency and intensity of environmental downturns affecting the lytic subpopulation. "Well-temperate" phage from our title is characterized by the best long-term population growth rate. We show that it is realized when the lysogenization frequency is approximately equal to the probability of lytic population collapse. We further predict the existence of sharp boundaries in system's environmental, ecological, and biophysical parameters separating the regions where this temperate strategy is optimal from those dominated by purely virulent or} dormant (purely lysogenic) strategies. We show that the virulent strategy works best for phages with large diversity of hosts, and access to multiple independent environments reachable by diffusion. Conversely, progressively more temperate or even dormant strategies are favored in the environments, that are subject to frequent and severe temporal downturns.Comment: 26 pages, 3 figure

Severe population collapses and species extinctions in multi-host epidemic dynamics

Most infectious diseases including more than half of known human pathogens are not restricted to just one host, yet much of the mathematical modeling of infections has been limited to a single species. We investigate consequences of a single epidemic propagating in multiple species and compare and contrast it with the endemic steady state of the disease. We use the two-species Susceptible-Infected-Recovered (SIR) model to calculate the severity of post-epidemic collapses in populations of two host species as a function of their initial population sizes, the times individuals remain infectious, and the matrix of infection rates. We derive the criteria for a very large, extinction-level, population collapse in one or both of the species. The main conclusion of our study is that a single epidemic could drive a species with high mortality rate to local or even global extinction provided that it is co-infected with an abundant species. Such collapse-driven extinctions depend on factors different than those in the endemic steady state of the disease

Diversity waves in collapse-driven population dynamics

Populations of species in ecosystems are often constrained by availability of resources within their environment. In effect this means that a growth of one population, needs to be balanced by comparable reduction in populations of others. In neutral models of biodiversity all populations are assumed to change incrementally due to stochastic births and deaths of individuals. Here we propose and model another redistribution mechanism driven by abrupt and severe collapses of the entire population of a single species freeing up resources for the remaining ones. This mechanism may be relevant e.g. for communities of bacteria, with strain-specific collapses caused e.g. by invading bacteriophages, or for other ecosystems where infectious diseases play an important role. The emergent dynamics of our system is cyclic "diversity waves" triggered by collapses of globally dominating populations. The population diversity peaks at the beginning of each wave and exponentially decreases afterwards. Species abundances are characterized by a bimodal time-aggregated distribution with the lower peak formed by populations of recently collapsed or newly introduced species, while the upper peak - species that has not yet collapsed in the current wave. In most waves both upper and lower peaks are composed of several smaller peaks. This self-organized hierarchical peak structure has a long-term memory transmitted across several waves. It gives rise to a scale-free tail of the time-aggregated population distribution with a universal exponent of 1.7. We show that diversity wave dynamics is robust with respect to variations in the rules of our model such as diffusion between multiple environments, species-specific growth and extinction rates, and bet-hedging strategies.Comment: 15 pages (including SI), 6 figures + 7 supplementary figure

Longevity of orders is related to the longevity of their constituent genera rather than genus richness

Longevity of a taxonomic group is an important issue in understanding the dynamics of evolution. In this respect a key observation is that genera, families or orders can each be assigned a characteristic average lifetime [Van Valen, L., (1973) Evolutionary Theory 1, 1-30]. Using the fossil marine animal genera database [Sepkoski, J.J.Jr. (2002) A Compendium of Fossil Marine Animal Genera, Bull. Am. Paleontol. 363, 563 pp.] we here examine key determinants for robustness of a higher taxonomic group in terms of the characteristics of its constituents. We find insignificant correlation between the size of an order and its stability against extinction, whereas we observe amazingly large correlation between the lifetime of an order and the lifetime of its constituent genera.Comment: 9 pages, 6 figure

Ribosome collisions and Translation efficiency: Optimization by codon usage and mRNA destabilization

Individual mRNAs are translated by multiple ribosomes that initiate translation with a few seconds interval. The ribosome speed is codon dependant, and ribosome queuing has been suggested to explain specific data for translation of some mRNAs in vivo. By modelling the stochastic translation process as a traffic problem, we here analyze conditions and consequences of collisions and queuing. The model allowed us to determine the on-rate (0.8 to 1.1 initiations per sec) and the time (1 sec) the preceding ribosome occludes initiation for Escherichia coli lacZ mRNA in vivo. We find that ribosome collisions and queues are inevitable consequences of a stochastic translation mechanism that reduce the translation efficiency substantially on natural mRNAs. The cells minimize collisions by having its mRNAs being unstable and by a highly selected codon usage in the start of the mRNA. The cost of mRNA breakdown is offset by the concomitant increase in translational efficiency.Comment: 5 figures, 3 table