Two very basic ideas in sexual selection are heavily influenced by numbers of potential mates: the evolution of anisogamy, leading to sex role differentiation, and the frequency dependence of reproductive success that tends to equalize primary sex ratios. However, being explicit about the numbers of potential mates is not typical to most evolutionary theory of sexual selection. Here, we argue that this may prevent us from finding the appropriate ecological equilibria that determine the evolutionary endpoints of selection. We review both theoretical and empirical advances on how population density may influence aspects of mating systems such as intrasexual competition, female choice or resistance, and parental care. Density can have strong effects on selective pressures, whether or not there is phenotypic plasticity in individual strategies with respect to density. Mating skew may either increase or decrease with density, which may be aided or counteracted by changes in female behaviour. Switchpoints between alternative mating strategies can be density dependent, and mate encounter rates may influence mate choice (including mutual mate choice), multiple mating, female resistance to male mating attempts, mate searching, mate guarding, parental care, and the probability of divorce. Considering density-dependent selection may be essential for understanding how populations can persist at all despite sexual conflict, but simple models seem to fail to predict the diversity of observed responses in nature. This highlights the importance of considering the interaction between mating systems and population dynamics, and we strongly encourage further work in this area.

1Garrett Hardin's tragedy of the commons is an analogy that shows how 2 individuals driven by self-interest can end up destroying the resource 3 upon which they all depend. The proposed solutions for humans rely on 4 highly advanced skills such as negotiation, which raises the question 5 of how non-human organisms manage to resolve similar tragedies. In recent 6 years, this question has promoted evolutionary biologists to apply the 7 tragedy of the commons to a wide range of biological systems. Here we 8 provide tools to categorize different types of tragedies, and review 9 different mechanisms that can resolve conflicts that could otherwise end 10 in tragedy, including kinship, policing and diminishing returns. A 11 central open question, however, is how often biological systems are able 12 to resolve these scenarios rather than drive themselves extinct through 13 individual-level selection favouring self-interested behaviours. 14 15

SummaryBackgroundMicrobes engage in a remarkable array of cooperative behaviors, secreting shared proteins that are essential for foraging, shelter, microbial warfare, and virulence. These proteins are costly, rendering populations of cooperators vulnerable to exploitation by nonproducing cheaters arising by gene loss or migration. In such conditions, how can cooperation persist?ResultsOur model predicts that differential gene mobility drives intragenomic variation in investment in cooperative traits. More mobile loci generate stronger among-individual genetic correlations at these loci (higher relatedness) and thereby allow the maintenance of more cooperative traits via kin selection. By analyzing 21 Escherichia genomes, we confirm that genes coding for secreted proteins—the secretome—are very frequently lost and gained and are associated with mobile elements. We show that homologs of the secretome are overrepresented among human gut metagenomics samples, consistent with increased relatedness at secretome loci across multiple species. The biosynthetic cost of secreted proteins is shown to be under intense selective pressure, even more than for highly expressed proteins, consistent with a cost of cooperation driving social dilemmas. Finally, we demonstrate that mobile elements are in conflict with their chromosomal hosts over the chimeric ensemble's social strategy, with mobile elements enforcing cooperation on their otherwise selfish hosts via the cotransfer of secretome genes with “mafia strategy” addictive systems (toxin-antitoxin and restriction-modification).ConclusionOur analysis matches the predictions of our model suggesting that horizontal transfer promotes cooperation, as transmission increases local genetic relatedness at mobile loci and enforces cooperation on the resident genes. As a consequence, horizontal transfer promoted by agents such as plasmids, phages, or integrons drives microbial cooperation.

No abstract

No abstract

Abstract1 Models of population dynamics generally neglect the presence of males. While this 2 assumption holds under many circumstances, behavioural ecology increasingly tells 3 us that the presence (or absence) of males may have an impact on female fitness, and 4 hence population sizes. Here we ask the question of whether males matter to 5 population dynamics, operationally defined as a dependency of population growth on 6 the relative density of males. We provide simple models, and evaluate the current 7 empirical evidence for them, that illustrate various mechanisms of such male 8 influence: mate searching behavior, male resource use (including effects of sexual 9 dimorphism), sexual harassment and sexual segregation. In each case, theory predicts 10 that males can have an effect on population densities, and in some extreme cases a 11 positive feedback between an increasingly male-biased sex ratio and the effects on 12 female harassment may theoretically even bring about population extinction. The 13 results of this study, and the literature reviewed, show that the males can have a 14 substantial effect on population dynamics, particularly so when human influences 15 result in biased sex ratios. 16

It is widely understood that the costs and benefits of mating can affect the fecundity and survival of individuals. Sexual conflict may have profound consequences for populations, due to the negative effects it causes males and females to have on one another"s fitness. Here we present a model describing the evolution of sexual conflict, in which males inflict a direct cost on female fitness. We show that these costs can drive the entire population to extinction. To males, females are an essential, but finite, resource over which they have to compete. Population extinction owing to sexual conflict can therefore be seen as an evolutionary "tragedy of the commons". Our model shows that a positive feedback between harassment and the operational sex ratio is responsible for the demise of females, and thus for population extinction. We further show that the evolution of female resistance to counter harassment can prevent a tragedy of the commons. Our findings not only demonstrate that sexual conflict can drive a population extinct, but also highlight how simple mechanisms, such as harassment costs to males and females and the coevolution between harassment and resistance, can help avert a tragedy of the commons caused by sexual conflict.

BackgroundAntibiotic resistance represents a significant public health problem. When resistance genes are mobile, being carried on plasmids or phages, their spread can be greatly accelerated. Plasmids in particular have been implicated in the spread of antibiotic resistance genes. However, the selective pressures which favour plasmid-carried resistance genes have not been fully established. Here we address this issue with mathematical models of plasmid dynamics in response to different antibiotic treatment regimes.ResultsWe show that transmission of plasmids is a key factor influencing plasmid-borne antibiotic resistance, but the dosage and interval between treatments is also important. Our results also hold when plasmids carrying the resistance gene are in competition with other plasmids that do not carry the resistance gene. By altering the interval between antibiotic treatments, and the dosage of antibiotic, we show that different treatment regimes can select for either plasmid-carried, or chromosome-carried, resistance.ConclusionsOur research addresses the effect of environmental variation on the evolution of plasmid-carried antibiotic resistance.