No Arabic abstract
A central goal of evolutionary biology is to explain the origins and distribution of diversity across life. Beyond species or genetic diversity, we also observe diversity in the circuits (genetic or otherwise) underlying complex functional traits. However, while the theory behind the origins and maintenance of genetic and species diversity has been studied for decades, theory concerning the origin of diverse functional circuits is still in its infancy. It is not known how many different circuit structures can implement any given function, which evolutionary factors lead to different circuits, and whether the evolution of a particular circuit was due to adaptive or non-adaptive processes. Here, we use digital experimental evolution to study the diversity of neural circuits that encode motion detection in digital (artificial) brains. We find that evolution leads to an enormous diversity of potential neural architectures encoding motion detection circuits, even for circuits encoding the exact same function. Evolved circuits vary in both redundancy and complexity (as previously found in genetic circuits) suggesting that similar evolutionary principles underlie circuit formation using any substrate. We also show that a simple (designed) motion detection circuit that is optimally-adapted gains in complexity when evolved further, and that selection for mutational robustness led this gain in complexity.
By challenging E. coli with sublethal norfloxacin for 10 days, Henry Lee and James Collins suggests the bacterial altruism leads to the population-wide resistance. By detailedly analyzing experiment data, we suggest that bacterial cooperation leads to population-wide resistance under norfloxacin pressure and simultaneously propose the bacteria shield is the possible feedback mechanism of less resistant bacteria. The bacteria shield is that the less resistant bacteria sacrifice the large number of themselves to consume norfloxacin and then to relieve the norfloxacin burden from highly resistant bacteria. Thus, due to highly resistant bacteria and less resistant bacteria extracted from the same bacteria population, bacterial cooperation leads to heteroresistance.
Community ecology has traditionally relied on the competitive exclusion principle, a piece of common wisdom in conceptual frameworks developed to describe species assemblages. Key concepts in community ecology, such as limiting similarity and niche partitioning, are based on competitive exclusion. However, this classical paradigm in ecology relies on implications derived from simple, deterministic models. Here we show how the predictions of a symmetric, deterministic model about the way extinctions proceed can be utterly different from the results derived from the same model when ecological drift (demographic stochasticity) is explicitly considered. Using analytical approximations to the steady-state conditional probabilities for assemblages with two and three species, we demonstrate that stochastic competitive exclusion leads to a cascade of extinctions, whereas the symmetric, deterministic model predicts a multiple collapse of species. To test the robustness of our results, we have studied the effect of environmental stochasticity and relaxed the species symmetry assumption. Our conclusions highlight the crucial role of stochasticity when deriving reliable theoretical predictions for species community assembly.
Cancer cell population dynamics often exhibit remarkably replicable, universal laws despite their underlying heterogeneity. Mechanistic explanations of universal cell population growth remain partly unresolved to this day, whereby population feedback between the microscopic and mesoscopic configurations can lead to macroscopic growth laws. We here present a unification under density-dependent birth events via contact inhibition. We consider five classical tumor growth laws: exponential, generalized logistic, Gompertz, radial growth, and fractal growth, which can be seen as manifestations of a single microscopic model. Our theory is substantiated by agent based simulations and can explain growth curve differences in experimental data from in vitro cancer cell population growth. Thus, our framework offers a possible explanation for the large number of mean-field laws that can adequately capture seemingly unrelated cancer or microbial growth dynamics.
Flies that walk in a covered planar arena on straight paths avoid colliding with each other, but which of the two flies stops is not random. High-throughput video observations, coupled with dedicated experiments with controlled robot flies have revealed that flies utilize the type of optic flow on their retina as a determinant of who should stop, a strategy also used by ship captains to determine which of two ships on a collision course should throw engines in reverse. We use digital evolution to test whether this strategy evolves when collision avoidance is the sole penalty. We find that the strategy does indeed evolve in a narrow range of cost/benefit ratios, for experiments in which the regressive motion cue is error free. We speculate that these stringent conditions may not be sufficient to evolve the strategy in real flies, pointing perhaps to auxiliary costs and benefits not modeled in our study
It is well recognized that population heterogeneity plays an important role in the spread of epidemics. While individual variations in social activity are often assumed to be persistent, i.e. constant in time, here we discuss the consequences of dynamic heterogeneity. By integrating the stochastic dynamics of social activity into traditional epidemiological models we demonstrate the emergence of a new long timescale governing the epidemic in broad agreement with empirical data. Our model captures multiple features of real-life epidemics such as COVID-19, including prolonged plateaus and multiple waves, which are transiently suppressed due to the dynamic nature of social activity. The existence of the long timescale due to the interplay between epidemic and social dynamics provides a unifying picture of how a fast-paced epidemic typically will transition to the endemic state.