1,040 research outputs found
Sustained coevolution of phage Lambda and Escherichia coli involves inner- as well as outer- membrane defences and counter- defences
Bacteria often evolve resistance to phage through the loss or modification of cell surface receptors. In Escherichia coli and phage λ, such resistance can catalyze a coevolutionary arms race focused on host and phage structures that interact at the outer membrane. Here, we analyse another facet of this arms race involving interactions at the inner membrane, whereby E. coli evolves mutations in mannose permease- encoding genes manY and manZ that impair λ’s ability to eject its DNA into the cytoplasm. We show that these man mutants arose concurrently with the arms race at the outer membrane. We tested the hypothesis that λ evolved an additional counter- defence that allowed them to infect bacteria with deleted man genes. The deletions severely impaired the ancestral λ, but some evolved phage grew well on the deletion mutants, indicating that they regained infectivity by evolving the ability to infect hosts independently of the mannose permease. This coevolutionary arms race fulfils the model of an inverse gene- for- gene infection network. Taken together, the interactions at both the outer and inner membranes reveal that coevolutionary arms races can be richer and more complex than is often appreciated
Frequency-dependent complex conductivity of an organic thin-film transistor
We measure the complex impedance between source/drain electrodes and the gate
electrode of a pentacene thin-film transistor (TFT) at frequencies 50 Hz <
omega/2pi < 20 kHz. Modeling the TFT as a distributed RC network (RC
transmission line), we find that the data cannot be explained by a model
including only a real, frequency-independent sheet conductivity. Instead, we
use the RC transmission line model to extract the frequency-dependent complex
sheet conductivity sigma(omega) = sigma'(omega) + jsigma"(omega) of the
pentacene film. At high frequencies, sigma(omega) increases with frequency,
sigma'(omega) and sigma"(omega) become similar in magnitude, and the on/off
ratio is significantly reduced.Comment: 13 pages, 4 figure
Diversity in CRISPR-based immunity protects susceptible genotypes by restricting phage spread and evolution.
This is the final version. Available from the publisher via the DOI in this record.Data deposited at dryad: https://doi.org/10.5061/dryad.66t1g1k00.Diversity in host resistance often associates with reduced pathogen spread. This may result from ecological and evolutionary processes, likely with feedback between them. Theory and experiments on bacteria-phage interactions have shown that genetic diversity of the bacterial adaptive immune system can limit phage evolution to overcome resistance. Using the CRISPR-Cas bacterial immune system and lytic phage, we engineered a host-pathogen system where each bacterial host genotype could be infected by only one phage genotype. With this model system, we explored how CRISPR diversity impacts the spread of phage when they can overcome a resistance allele, how immune diversity affects the evolution of the phage to increase its host range, and if there was feedback between these processes. We show that increasing CRISPR diversity benefits susceptible bacteria via a dilution effect, which limits the spread of the phage. We suggest that this ecological effect impacts the evolution of novel phage genotypes, which then feeds back into phage population dynamics
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Coevolution Drives the Emergence of Complex Traits and Promotes Evolvability
The evolution of complex organismal traits is obvious as a historical fact, but the underlying causes—including the role of natural selection—are contested. Gould argued that a random walk from a necessarily simple beginning would produce the appearance of increasing complexity over time. Others contend that selection, including coevolutionary arms races, can systematically push organisms toward more complex traits. Methodological challenges have largely precluded experimental tests of these hypotheses. Using the Avida platform for digital evolution, we show that coevolution of hosts and parasites greatly increases organismal complexity relative to that otherwise achieved. As parasites evolve to counter the rise of resistant hosts, parasite populations retain a genetic record of past coevolutionary states. As a consequence, hosts differentially escape by performing progressively more complex functions. We show that coevolution's unique feedback between host and parasite frequencies is a key process in the evolution of complexity. Strikingly, the hosts evolve genomes that are also more phenotypically evolvable, similar to the phenomenon of contingency loci observed in bacterial pathogens. Because coevolution is ubiquitous in nature, our results support a general model whereby antagonistic interactions and natural selection together favor both increased complexity and evolvability
Fitness in time-dependent environments includes a geometric contribution
Phenotypic evolution implies sequential fixations of new genomic sequences.
The speed at which these mutations fixate depends, in part, on the relative
fitness (selection coefficient) of the mutant vs. the ancestor. Using a simple
population dynamics model we show that the relative fitness in dynamical
environments is not equal to the fitness averaged over individual environments.
Instead it includes a term that explicitly depends on the sequence of the
environments. This term is geometric in nature and depends only on the oriented
area enclosed by the trajectory taken by the system in the environment state
space. It is related to the well-studied geometric phases in classical and
quantum physical systems. We discuss possible biological implications of these
observations, focusing on evolution of novel metabolic or stress-resistant
functions
Mutator Dynamics on a Smooth Evolutionary Landscape
We investigate a model of evolutionary dynamics on a smooth landscape which
features a ``mutator'' allele whose effect is to increase the mutation rate. We
show that the expected proportion of mutators far from equilibrium, when the
fitness is steadily increasing in time, is governed solely by the transition
rates into and out of the mutator state. This results is a much faster rate of
fitness increase than would be the case without the mutator allele. Near the
fitness equilibrium, however, the mutators are severely suppressed, due to the
detrimental effects of a large mutation rate near the fitness maximum. We
discuss the results of a recent experiment on natural selection of E. coli in
the light of our model.Comment: 4 pages, 3 figure
Evolutionary instability of Zero Determinant strategies demonstrates that winning isn't everything
Zero Determinant (ZD) strategies are a new class of probabilistic and
conditional strategies that are able to unilaterally set the expected payoff of
an opponent in iterated plays of the Prisoner's Dilemma irrespective of the
opponent's strategy, or else to set the ratio between a ZD player's and their
opponent's expected payoff. Here we show that while ZD strategies are weakly
dominant, they are not evolutionarily stable and will instead evolve into less
coercive strategies. We show that ZD strategies with an informational advantage
over other players that allows them to recognize other ZD strategies can be
evolutionarily stable (and able to exploit other players). However, such an
advantage is bound to be short-lived as opposing strategies evolve to
counteract the recognition.Comment: 14 pages, 4 figures. Change in title (again!) to comply with Nature
Communications requirements. To appear in Nature Communication
Live to cheat another day: bacterial dormancy facilitates the social exploitation of beta-lactamases
The breakdown of antibiotics by β-lactamases may be cooperative, since resistant cells can detoxify their environment and facilitate the growth of susceptible neighbours. However, previous studies of this phenomenon have used artificial bacterial vectors or engineered bacteria to increase the secretion of β-lactamases from cells. Here, we investigated whether a broad-spectrum β-lactamase gene carried by a naturally occurring plasmid (pCT) is cooperative under a range of conditions. In ordinary batch culture on solid media, there was little or no evidence that resistant bacteria could protect susceptible cells from ampicillin, although resistant colonies could locally detoxify this growth medium. However, when susceptible cells were inoculated at high densities, late-appearing phenotypically susceptible bacteria grew in the vicinity of resistant colonies. We infer that persisters, cells that have survived antibiotics by undergoing a period of dormancy, founded these satellite colonies. The number of persister colonies was positively correlated with the density of resistant colonies and increased as antibiotic concentrations decreased. We argue that detoxification can be cooperative under a limited range of conditions: if the toxins are bacteriostatic rather than bacteridical; or if susceptible cells invade communities after resistant bacteria; or if dormancy allows susceptible cells to avoid bactericides. Resistance and tolerance were previously thought to be independent solutions for surviving antibiotics. Here, we show that these are interacting strategies: the presence of bacteria adopting one solution can have substantial effects on the fitness of their neighbours
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