Cost and conflict in animal signals and human language.

The "costly signaling" hypothesis proposes that animal signals are kept honest by appropriate signal costs. We show that to the contrary, signal cost is unnecessary for honest signaling even when interests conflict. We illustrate this principle by constructing examples of cost-free signaling equilibria for the two paradigmatic signaling games of Grafen (1990) and Godfray (1991). Our findings may explain why some animal signals use cost to ensure honesty whereas others do not and suggest that empirical tests of the signaling hypothesis should focus not on equilibrium cost but, rather, on the cost of deviation from equilibrium. We use these results to apply costly signaling theory to the low-cost signals that make up human language. Recent game theoretic models have shown that several key features of language could plausibly arise and be maintained by natural selection when individuals have coincident interests. In real societies, however, individuals do not have fully coincident interests. We show that coincident interests are not a prerequisite for linguistic communication, and find that many of the results derived previously can be expected also under more realistic models of society.

Natural selection, infectious transfer and the existence conditions for bacterial plasmids.

Despite the near-ubiquity of plasmids in bacterial populations and the profound contribution of infectious gene transfer to the adaptation and evolution of bacteria, the mechanisms responsible for the maintenance of plasmids in bacterial populations are poorly understood. In this article, we address the question of how plasmids manage to persist over evolutionary time. Empirical studies suggest that plasmids are not infectiously transmitted at a rate high enough to be maintained as genetic parasites. In part i, we present a general mathematical proof that if this is the case, then plasmids will not be able to persist indefinitely solely by carrying genes that are beneficial or sometimes beneficial to their host bacteria. Instead, such genes should, in the long run, be incorporated into the bacterial chromosome. If the mobility of host-adaptive genes imposes a cost, that mobility will eventually be lost. In part ii, we illustrate a pair of mechanisms by which plasmids can be maintained indefinitely even when their rates of transmission are too low for them to be genetic parasites. First, plasmids may persist because they can transfer locally adapted genes to newly arriving strains bearing evolutionary innovations, and thereby preserve the local adaptations in the face of background selective sweeps. Second, plasmids may persist because of their ability to shuttle intermittently favored genes back and forth between various (noncompeting) bacterial strains, ecotypes, or even species.

Bacteria are different: observations, interpretations, speculations, and opinions about the mechanisms of adaptive evolution in prokaryotes.

To some extent, the genetic theory of adaptive evolution in bacteria is a simple extension of that developed for sexually reproducing eukaryotes. In other, fundamental ways, the process of adaptive evolution in bacteria is quantitatively and qualitatively different from that of organisms for which recombination is an integral part of the reproduction process. In this speculative and opinionated discussion, we explore these differences. In particular, we consider (i) how, as a consequence of the low rates of recombination, "ordinary" chromosomal gene evolution in bacteria is different from that in organisms where recombination is frequent and (ii) the fundamental role of the horizontal transmission of genes and accessory genetic elements as sources of variation in bacteria. We conclude with speculations about the evolution of accessory elements and their role in the adaptive evolution of bacteria.

The epidemiology of antibiotic resistance in hospitals: paradoxes and prescriptions.

A simple mathematical model of bacterial transmission within a hospital was used to study the effects of measures to control nosocomial transmission of bacteria and reduce antimicrobial resistance in nosocomial pathogens. The model predicts that: (i) Use of an antibiotic for which resistance is not yet present in a hospital will be positively associated at the individual level (odds ratio) with carriage of bacteria resistant to other antibiotics, but negatively associated at the population level (prevalence). Thus inferences from individual risk factors can yield misleading conclusions about the effect of antibiotic use on resistance to another antibiotic. (ii) Nonspecific interventions that reduce transmission of all bacteria within a hospital will disproportionately reduce the prevalence of colonization with resistant bacteria. (iii) Changes in the prevalence of resistance after a successful intervention will occur on a time scale of weeks to months, considerably faster than in community-acquired infections. Moreover, resistance can decline rapidly in a hospital even if it does not carry a fitness cost. The predictions of the model are compared with those of other models and published data. The implications for resistance control and study design are discussed, along with the limitations and assumptions of the model.

Risky business: sexual and asexual reproduction in variable environments.

Patterns of reproductive uncertainty can have an important influence on population dynamics. There is a crucial distinction between what we describe here as aggregate uncertainty (in which reproductive output in each generation is correlated among the individuals in a population) and idiosyncratic risk (in which reproductive output is independent across individuals). All else being equal, populations experiencing idiosyncratic risk enjoy a higher asymptotic growth rate than do those experiencing aggregate uncertainty. Therefore individuals in populations of the former type will have a competitive advantage over individuals in populations of the latter type. Applying this distinction to models of randomly fluctuating environments, we point out that genetic variation among offspring can serve to reduce aggregate uncertainty, transforming it into a more idiosyncratic form of risk. We show that this transformation underlies the dynamics observed in several previous models of the role of outcrossing in the evolution of sex.

Transmission bottlenecks as determinants of virulence in rapidly evolving pathogens.

Transmission bottlenecks occur in pathogen populations when only a few individual pathogens are transmitted from one infected host to another in the initiation of a new infection. Transmission bottlenecks can dramatically affect the evolution of virulence in rapidly evolving pathogens such as RNA viruses. Characterizing pathogen diversity with the quasispecies concept, we use analytical and simulation methods to demonstrate that severe bottlenecks are likely to drive down the virulence of a pathogen because of stochastic loss of the most virulent pathotypes, through a process analogous to Muller's ratchet. We investigate in this process the roles of host population size, duration of within-host viral replication, and transmission bottleneck size. We argue that the patterns of accumulation of deleterious mutation may explain differing levels of virulence in vertically and horizontally transmitted diseases.

Signalling among relatives. II. Beyond the tower of Babel.

Models of costly signalling are commonly employed in evolutionary biology in order to explain how honest communication between individuals with conflicting interests can be stable. These models have focused primarily on a single type of honest signalling equilibrium, the separating equilibrium in which any two different signallers send distinct signals, thereby providing signal receivers with complete information. In this paper, we demonstrate that in signalling among relatives (modelled using the Sir Philip Sidney game), there is not one but a large number of possible signalling equilibria, most of which are pooling equilibria in which different types of signallers may share a common signal. We prove that in a general Sir Philip Sidney game, any partition of signallers into equi-signalling classes can have a stable signalling equilibrium if and only if it is a contiguous partition, and provide examples of such partitions. A similar (but slightly stricter) condition is shown to hold when signals are transmitted through a medium with signalling error. These results suggest a solution to a problem faced by previous signalling theory models: when we consider the separating equilibrium, signal cost is independent of the frequency of individuals sending that signal and, consequently, even very rare signaller types can drastically affect signal cost. Here, we show that by allowing these rare signallers to pool with more common signallers, signal cost can be greatly reduced.

Germline bottlenecks and the evolutionary maintenance of mitochondrial genomes.

Several features of the biology of mitochondria suggest that mitochondria might be susceptible to Muller's ratchet and other forms of evolutionary degradation: Mitochondria have predominantly uniparental inheritance, appear to be nonrecombining, and have high mutation rates producing significant deleterious variation. We demonstrate that the persistence of mitochondria may be explained by recent data that point to a severe "bottleneck" in the number of mitochondria passing through the germline in humans and other mammals. We present a population-genetic model in which deleterious mutations arise within individual mitochondria, while selection operates on assemblages of mitochondria at the level of their eukaryotic hosts. We show that a bottleneck increases the efficacy of selection against deleterious mutations by increasing the variance in fitness among eukaryotic hosts. We investigate both the equilibrium distribution of deleterious variation in large populations and the dynamics of Muller's ratchet in small populations. We find that in the absence of the ratchet, a bottleneck leads to improved mitochondrial performance and that, over a longer time scale, a bottleneck acts to slow the progression of the ratchet.

Signaling among relatives. III. Talk is cheap.

The Sir Philip Sidney game has been used by numerous authors to show how signal cost can facilitate honest signaling among relatives. Here, we demonstrate that, in this game, honest cost-free signals are possible as well, under very general conditions. Moreover, these cost-free signals are better for all participants than the previously explored alternatives. Recent empirical evidence suggests that begging is energetically inexpensive for nestling birds; this finding led some researchers to question the applicability of the costly signaling framework to nestling begging. Our results show that cost-free or inexpensive signals, as observed empirically, fall within the framework of signaling theory.