Does the Red Queen reign in the kingdom of digital organisms?

In competition experiments between two RNA viruses of equal or almost equal fitness, often both strains gain in fitness before one eventually excludes the other. This observation has been linked to the Red Queen effect, which describes a situation in which organisms have to constantly adapt just to keep their status quo. I carried out experiments with digital organisms (self-replicating computer programs) in order to clarify how the competing strains' location in fitness space influences the Red-Queen effect. I found that gains in fitness during competition were prevalent for organisms that were taken from the base of a fitness peak, but absent or rare for organisms that were taken from the top of a peak or from a considerable distance away from the nearest peak. In the latter two cases, either neutral drift and loss of the fittest mutants or the waiting time to the first beneficial mutation were more important factors. Moreover, I found that the Red-Queen dynamic in general led to faster exclusion than the other two mechanisms.Comment: 10 pages, 5 eps figure

Evolution Equation of Phenotype Distribution: General Formulation and Application to Error Catastrophe

An equation describing the evolution of phenotypic distribution is derived using methods developed in statistical physics. The equation is solved by using the singular perturbation method, and assuming that the number of bases in the genetic sequence is large. Applying the equation to the mutation-selection model by Eigen provides the critical mutation rate for the error catastrophe. Phenotypic fluctuation of clones (individuals sharing the same gene) is introduced into this evolution equation. With this formalism, it is found that the critical mutation rate is sometimes increased by the phenotypic fluctuations, i.e., noise can enhance robustness of a fitted state to mutation. Our formalism is systematic and general, while approximations to derive more tractable evolution equations are also discussed.Comment: 22 pages, 2 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

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

Scaling laws in bacterial genomes: A side-effect of selection of mutational robustness?

In the past few years, numerous research projects have focused on identifying and understanding scaling properties in the gene content of prokaryote genomes and the intricacy of their regulation networks. Yet, and despite the increasing amount of data available, the origins of these scalings remain an open question. The RAevol model, a digital genetics model, provides us with an insight into the mechanisms involved in an evolutionary process. The results we present here show that (i) our model reproduces qualitatively these scaling laws and that (ii) these laws are not due to differences in lifestyles but to differences in the spontaneous rates of mutations and rearrangements. We argue that this is due to an indirect selective pressure for robustness that constrains the genome size

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

Evolutionary trajectories in rugged fitness landscapes

We consider the evolutionary trajectories traced out by an infinite population undergoing mutation-selection dynamics in static, uncorrelated random fitness landscapes. Starting from the population that consists of a single genotype, the most populated genotype \textit{jumps} from a local fitness maximum to another and eventually reaches the global maximum. We use a strong selection limit, which reduces the dynamics beyond the first time step to the competition between independent mutant subpopulations, to study the dynamics of this model and of a simpler one-dimensional model which ignores the geometry of the sequence space. We find that the fit genotypes that appear along a trajectory are a subset of suitably defined fitness \textit{records}, and exploit several results from the record theory for non-identically distributed random variables. The genotypes that contribute to the trajectory are those records that are not \textit{bypassed} by superior records arising further away from the initial population. Several conjectures concerning the statistics of bypassing are extracted from numerical simulations. In particular, for the one-dimensional model, we propose a simple relation between the bypassing probability and the dynamic exponent which describes the scaling of the typical evolution time with genome size. The latter can be determined exactly in terms of the extremal properties of the fitness distribution.Comment: Figures in color; minor revisions in tex

Knowledge politics and new converging technologies: a social epistemological perspective

The “new converging technologies” refers to the prospect of advancing the human condition by the integrated study and application of nanotechnology, biotechnology, information technology and the cognitive sciences - or “NBIC”. In recent years, it has loomed large, albeit with somewhat different emphases, in national science policy agendas throughout the world. This article considers the political and intellectual sources - both historical and contemporary - of the converging technologies agenda. Underlying it is a fluid conception of humanity that is captured by the ethically challenging notion of “enhancing evolution”

A soluble model of evolution and extinction dynamics in a rugged fitness landscape

We consider a continuum version of a previously introduced and numerically studied model of macroevolution (PRL 75, 2055, (1995)) in which agents evolve by an optimization process in a rugged fitness landscape and die due to their competitive interactions. We first formulate dynamical equations for the fitness distribution and the survival probability. Secondly we analytically derive the $t^{-2}$ law which characterizes the life time distribution of biological genera. Thirdly we discuss other dynamical properties of the model such as the rate of extinction and conclude with a brief discussion.Comment: 6 pages LaTeX source with 2 figures. Submitted to PRL (Jan. 97

Sociobiological Control of Plasmid copy number

Background:
All known mechanisms and genes responsible for the regulation of plasmid replication lie with the plasmid rather than the chromosome. It is possible therefore that there can be copy-up mutants. Copy-up mutants will have within host selective advantage. This would eventually result into instability of bacteria-plasmid association. In spite of this possibility low copy number plasmids appear to exist stably in host populations. We examined this paradox using a computer simulation model.

Model:
Our multilevel selection model assumes a wild type with tightly regulated replication to ensure low copy number. A mutant with slightly relaxed replication regulation can act as a “cheater” or “selfish” plasmid and can enjoy a greater within-host-fitness. However the host of a cheater plasmid has to pay a greater cost. As a result, in host level competition, host cell with low copy number plasmid has a greater fitness. Furthermore, another mutant that has lost the genes required for conjugation was introduced in the model. The non-conjugal mutant was assumed to undergo conjugal transfer in the presence of another conjugal plasmid in the host cell.

Results:
The simulatons showed that if the cost of carrying a plasmid was low, the copy-up mutant could drive the wild type to extinction or very low frequencies. Consequently, another mutant with a higher copy number could invade the first invader. This process could result into an increasing copy number. However above a certain copy number within-host selection was overcompensated by host level selection leading to a rock-paper-scissor (RPS) like situation. The RPS situation allowed the coexistence of high and low copy number plasmids. The non-conjugal “hypercheaters” could further arrest the copy numbers to a substantially lower level.

Conclusions:
These sociobiological interactions might explain the stability of copy numbers better than molecular mechanisms of replication regulation alone