Biology subjects

Sneppen, K.

Publications and source records attributed to Sneppen, K..

5 recordsLinked to original sources

bioRxiv2018

Hitchhiking, collapse and contingency in phage infections of migrating bacterial populations

Natural bacterial populations are subject to constant predation pressure by phages. Bacteria use a variety of well-studied molecular mechanisms to defend themselves from phage predation. However, since phage are non-motile, perhaps the simplest defense against phage would be for bacteria to outrun their predators. In particular, chemotaxis, the active migration of bacteria up attractant gradients, may help the bacteria escape slowly diffusing phages. Here we study phage infection dynamics in migrating bacterial populations driven by chemotaxis through low viscosity agar plates. We find that expanding phage-bacteria populations support two migrating fronts, an outermost \"bacterial\" front driven by nutrient uptake and chemotaxis and an inner \"phage\" front at which bacterial population collapses due to phage predation. We show that with increasing adsorption rate and initial phage population, the rate of migration of the phage front increases, eventually overtaking the bacterial front and driving the system across a \"phage transition\" from a regime where bacteria outrun a phage infection to one where they must evolve phage resistance to survive. We confirm experimentally that this process requires phages to \"surf\" the bacterial front by repeatedly reinfecting the fastest moving bacteria. A deterministic model recapitulates the transition. Macroscopic fluctuations in bacterial densities at the phage front suggest that a feedback mechanism, possibly due to growth rate dependent phage infection rates, drives millimeter scale spatial structure in phage-bacteria populations. Our work opens a new, spatiotemporal, line of investigation into the eco-evolutionary struggle between bacteria and their phage predators.\n\nSignificance StatementThe infection of bacteria by phage requires physical contact. This fact means that motile bacteria may avoid non-motile phage by simply running away. By this mechanism bacterial chemotaxis may help bacteria to escape phages. Here we show that when phage infect bacteria moving in soft agar plates, high phage populations or infectivity rates result in phages stopping and killing all bacteria. Conversely, when initial phage numbers or infectivity rates are low, bacteria are able to migrate away from phage successfully, despite phage ability to \"surf\" bacterial fronts for more than 24 hours. Between these regimes we document a \"phage transition\" where bacterial physiology and contingency in phage infection manifest through large-scale fluctuations in spatio-temporal dynamics.

ecology↗

bioRxiv2018

Theory bridging cell polarities with development of robust complex morphologies

Despite continual renewal and damages, a multicellular organism is able to maintain its complex morphology. How is this stability compatible with the complexity and diversity of living forms? Looking for answers at protein level may be limiting as diverging protein sequences can result in similar morphologies. Inspired by the progressive role of apical-basal and planar cell polarity in development, we propose that stability, complexity, and diversity are emergent properties in populations of proliferating polarized cells. We support our hypothesis by a theoretical approach, developed to effectively capture both types of polar cell adhesions. When applied to specific cases of development gastrulation and the origins of folds and tubes our theoretical tool suggests experimentally testable predictions pointing to the strength of polar adhesion, restricted directions of cell polarities, and the rate of cell proliferation to be major determinants of morphological diversity and stability.

biophysics↗

bioRxiv2017

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↗

bioRxiv2017

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.

epidemiology↗

bioRxiv2017

Existence and construction of large stable food webs

Ecological diversity is ubiquitous despite the restrictions imposed by competitive exclusion and apparent competition. To explain the observed richness of species in a given habitat, food web theory has explored nonlinear functional responses, self-interaction or spatial structure and dispersal -- model ingredients that have proven to promote stability and diversity. We here instead return to classical Lotka-Volterra equations, where species-species interaction is characterized by a simple product and spatial restrictions are ignored. We quantify how this idealization imposes constraints on coexistence and diversity for many species. To this end, we introduce the concept of free and controlled species and use this to demonstrate how stable food webs can be constructed by sequential addition of species. When we augment the resulting network by additional weak interactions we are able to show that it is possible to construct large food webs of arbitrary connectivity. Our model thus serves as a formal starting point for the study of sustainable interaction patterns between species.

ecology↗