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Hamilton's rule provides the cornerstone for our understanding of the evolution of all forms of social behavior, from altruism to spite, across all organisms, from viruses to humans. In contrast to the standard prediction from Hamilton's rule, recent studies have suggested that altruistic helping can be favored even if it does not benefit relatives, as long as it decreases the environmentally induced variance of their reproductive success ("altruistic bet-hedging"). However, previous predictions both rely on an approximation and focus on variance-reducing helping behaviors. We derived a version of Hamilton's rule that fully captures environmental variability. This shows that decreasing (or increasing) the variance in the absolute reproductive success of relatives does not have a consistent effect--it can either favor or disfavor the evolution of helping. We then empirically quantified the effect of helping on the variance in reproductive success across 15 species of cooperatively breeding birds. We found that a) helping did not consistently decrease the variance of reproductive success and often increased it, and b) the mean benefits of helping across environments consistently outweighed other variability components of reproductive success. Altogether, our theoretical and empirical results suggest that the effects of helping on the variability components of reproductive success have not played a consistent or strong role in favoring helping. [ABSTRACT FROM AUTHOR]

Pangenomes vary across bacteria. Some species have fluid pangenomes, with a high proportion of genes varying between individual genomes. Other species have less fluid pangenomes, with different genomes tending to contain the same genes. Two main hypotheses have been suggested to explain this variation: differences in species' bacterial lifestyle and effective population size. However, previous studies have not been able to test between these hypotheses because the different features of lifestyle and effective population size are highly correlated with each other, and phylogenetically conserved, making it hard to disentangle their relative importance. We used phylogeny-based analyses, across 126 bacterial species, to tease apart the causal role of different factors. We found that pangenome fluidity was lower in i) host-associated compared with free-living species and ii) host-associated species that are obligately dependent on a host, live inside cells, and are more pathogenic and less motile. In contrast, we found no support for the competing hypothesis that larger effective population sizes lead to more fluid pangenomes. Effective population size appears to correlate with pangenome variation because it is also driven by bacterial lifestyle, rather than because of a causal relationship. [ABSTRACT FROM AUTHOR]

Cooperation is prevalent across bacteria, but risks being exploited by non-cooperative cheats. Horizontal gene transfer, particularly via plasmids, has been suggested as a mechanism to stabilize cooperation. A key prediction of this hypothesis is that genes which are more likely to be transferred, such as those on plasmids, should be more likely to code for cooperative traits. Testing this prediction requires identifying all genes for cooperation in bacterial genomes. However, previous studies used a method which likely misses some of these genes for cooperation. To solve this, we used a new genomics tool, SOCfinder, which uses three distinct modules to identify all kinds of genes for cooperation. We compared where these genes were located across 4648 genomes from 146 bacterial species. In contrast to the prediction of the hypothesis, we found no evidence that plasmid genes are more likely to code for cooperative traits. Instead, we found the opposite—that genes for cooperation were more likely to be carried on chromosomes. Overall, the vast majority of genes for cooperation are not located on plasmids, suggesting that the more general mechanism of kin selection is sufficient to explain the prevalence of cooperation across bacteria. [ABSTRACT FROM AUTHOR]

Cooperative societies can be threatened by cheats, who invest less in cooperation and exploit the contributions of others. The impact of cheats depends on the extent to which they are maintained in the population. However, different empirical studies, across organisms ranging from RNA replicators to bacteria, have shown diverse cheat-cooperator dynamics. These vary from approaching a stable equilibrium to dynamic cyclical oscillations. The reason for this variation remains unclear. Here, we develop a theoretical model to identify the factors that determine whether dynamics should tend toward stable equilibria or cyclical oscillations. Our analyses show that (1) a combination of both periodic population bottlenecks and density-dependent selection on cheating is required to produce cyclical oscillations and (2) the extent of frequency-dependent selection for cheating can influence the amplitude of these oscillations but does not lead to oscillations alone. Furthermore, we show that stochastic group formation (demographic stochasticity) can generate different forms of oscillation, over a longer time scale, across growth cycles. Our results provide experimentally testable hypotheses for the processes underlying cheat-cooperator dynamics. [ABSTRACT FROM AUTHOR]

Laboratory experiments have suggested that bacteria perform a range of cooperative behaviors, which are favored because they are directed toward relatives (kin selection). However, there is a lack of evidence for cooperation and kin selection in natural bacterial populations. Molecular population genetics offers a promising method to study natural populations because the theory predicts that kin selection will lead to relaxed selection, which will result in increased polymorphism and divergence at cooperative genes. Examining a natural population of Bacillus subtilis, we found consistent evidence that putatively cooperative traits have higher polymorphism and greater divergence than putatively private traits expressed at the same rate. In addition, we were able to eliminate alternative explanations for these patterns and found more deleterious mutations in genes controlling putatively cooperative traits. Overall, our results suggest that cooperation is favored by kin selection, with an average relatedness of r = .79 between interacting individuals. [ABSTRACT FROM AUTHOR]

Crozier’s paradox suggests that genetic kin recognition will not be evolutionarily stable. The problem is that more common tags (markers) are more likely to be recognized and helped. This causes common tags to increase in frequency, eliminating the genetic variability that is required for genetic kin recognition. Two potential solutions to this problem have been suggested: host–parasite coevolution and multiple social encounters. We show that the host–parasite coevolution hypothesis does not work as commonly assumed. Host–parasite coevolution only stabilizes kin recognition at a parasite resistance locus if parasites adapt rapidly to hosts and cause intermediate or high levels of damage (virulence). Additionally, when kin recognition is stabilized at a parasite resistance locus, this can have an additional cost of making hosts more susceptible to parasites. However, we show that if the genetic architecture is allowed to evolve, meaning natural selection can choose the recognition locus, genetic kin recognition is more likely to be stable. The reason for this is that host–parasite coevolution can maintain tag diversity at another (neutral) locus by genetic hitchhiking, allowing that other locus to be used for genetic kin recognition. These results suggest a way that host–parasite coevolution can resolve Crozier’s paradox, without making hosts more susceptible to parasites. However, the opportunity for multiple social encounters may provide a more robust resolution of Crozier’s paradox. [ABSTRACT FROM AUTHOR]

It has been hypothesized that horizontal gene transfer on plasmids can facilitate the evolution of cooperation, by allowing genes to jump between bacteria, and hence increase genetic relatedness at the cooperative loci. However, we show theoretically that horizontal gene transfer only appreciably increases relatedness when plasmids are rare, where there are many plasmid-free cells available to infect (many opportunities for horizontal gene transfer). In contrast, when plasmids are common, there are few opportunities for horizontal gene transfer, meaning relatedness is not appreciably increased, and so cooperation is not favored. Plasmids, therefore, evolve to be rare and cooperative, or common and noncooperative, meaning plasmid frequency and cooperativeness are never simultaneously high. The overall level of plasmid-mediated cooperation, given by the product of plasmid frequency and cooperativeness, is therefore consistently negligible or low. [ABSTRACT FROM AUTHOR]

In multipartite viruses, the genome is split into multiple segments, each of which is transmitted via a separate capsid. The existence of multipartite viruses poses a problem, because replication is only possible when all segments are present within the same host. Given this clear cost, why is multipartitism so common in viruses? Most previous hypotheses try to explain how multipartitism could provide an advantage. In so doing, they require scenarios that are unrealistic and that cannot explain viruses with more than 2 multipartite segments. We show theoretically that selection for cheats, which avoid producing a shared gene product, but still benefit from gene products produced by other genomes, can drive the evolution of both multipartite and segmented viruses. We find that multipartitism can evolve via cheating under realistic conditions and does not require unreasonably high coinfection rates or any group-level benefit. Furthermore, the cheating hypothesis is consistent with empirical patterns of cheating and multipartitism across viruses. More broadly, our results show how evolutionary conflict can drive new patterns of genome organisation in viruses and elsewhere. In multipartite viruses, the genome is split into multiple segments, each of which is transmitted via a separate capsid. This seems costly, so why is this form of genome organization so widespread? This theoretical study shows that selection for cheats can drive the evolution of multipartite viruses under realistic conditions. [ABSTRACT FROM AUTHOR]

The black box method was developed as an "asocial control" to allow for payoff-based learning while eliminating social responses in repeated public goods games. Players are told they must decide how many virtual coins they want to input into a virtual black box that will provide uncertain returns. However, in truth, they are playing with each other in a repeated social game. By "black boxing" the game's social aspects and payoff structure, the method creates a population of self-interested but ignorant or confused individuals that must learn the game's payoffs. This low-information environment, stripped of social concerns, provides an alternative, empirically derived null hypothesis for testing social behaviours, as opposed to the theoretical predictions of rational self-interested agents (Homo economicus). However, a potential problem is that participants can unwittingly affect the learning of other participants. Here, we test a solution to this problem in a range of public goods games by making participants interact, unknowingly, with simulated players ("computerised black box"). We find no significant differences in rates of learning between the original and the computerised black box, therefore either method can be used to investigate learning in games. These results, along with the fact that simulated agents can be programmed to behave in different ways, mean that the computerised black box has great potential for complementing studies of how individuals and groups learn under different environments in social dilemmas. [ABSTRACT FROM AUTHOR]

Crozier's paradox suggests that genetic kin recognition will not be evolutionarily stable. The problem is that more common tags (markers) are more likely to be recognised and helped. This causes common tags to increase in frequency, and hence eliminates the genetic variability that is required for genetic kin recognition. It has therefore been assumed that genetic kin recognition can only be stable if there is some other factor maintaining tag diversity, such as the advantage of rare alleles in host-parasite interactions. We show that allowing for multiple social encounters before each social interaction can eliminate Crozier's paradox, because it allows individuals with rare tags to find others with the same tag. We also show that rare tags are better indicators of relatedness, and hence better at helping individuals avoid interactions with non-cooperative cheats. Consequently, genetic kin recognition provides an advantage to rare tags that maintains tag diversity, and stabilises itself. Crozier's paradox suggests that genetic kin recognition will not be evolutionarily stable. Here, the authors show that allowing for multiple social encounters before each social interaction can eliminate Crozier's paradox and stabilise genetic kin recognition. [ABSTRACT FROM AUTHOR]

Bacteria produce a range of molecules that are secreted from the cell and can provide a benefit to the local population of cells. Laboratory experiments have suggested that these “public goods” molecules represent a form of cooperation, favored because they benefit closely related cells (kin selection). However, there is a relative lack of data demonstrating kin selection for cooperation in natural populations of bacteria. We used molecular population genetics to test for signatures of kin selection at the genomic level in natural populations of the opportunistic pathogen Pseudomonas aeruginosa. We found consistent evidence from multiple traits that genes controlling putatively cooperative traits have higher polymorphism and greater divergence and are more likely to harbor deleterious mutations relative to genes controlling putatively private traits, which are expressed at similar rates. These patterns suggest that cooperative traits are controlled by kin selection, and we estimate that the relatedness for social interactions in P. aeruginosa is r = 0.84. More generally, our results demonstrate how molecular population genetics can be used to study the evolution of cooperation in natural populations. [ABSTRACT FROM AUTHOR]

In bacteria and other microorganisms, the cells within a population often show extreme phenotypic variation. Different species use different mechanisms to determine how distinct phenotypes are allocated between individuals, including coordinated, random, and genetic determination. However, it is not clear if this diversity in mechanisms is adaptive—arising because different mechanisms are favoured in different environments—or is merely the result of non-adaptive artifacts of evolution. We use theoretical models to analyse the relative advantages of the two dominant mechanisms to divide labour between reproductives and helpers in microorganisms. We show that coordinated specialisation is more likely to evolve over random specialisation in well-mixed groups when: (i) social groups are small; (ii) helping is more "essential"; and (iii) there is a low metabolic cost to coordination. We find analogous results when we allow for spatial structure with a more detailed model of cellular filaments. More generally, this work shows how diversity in the mechanisms to produce phenotypic heterogeneity could have arisen as adaptations to different environments. In microorganisms, the cells within a population often show extreme phenotypic variation with different mechanisms used to determine how distinct phenotypes are allocated. This study uses theoretical models to examine the relative advantages of the two dominant mechanisms, coordinated and random determination, in dividing labour between reproductives and helpers in microorganisms. [ABSTRACT FROM AUTHOR]

The success of many viruses depends upon cooperative interactions between viral genomes. However, whenever cooperation occurs, there is the potential for 'cheats' to exploit that cooperation. We suggest that: (1) the biology of viruses makes viral cooperation particularly susceptible to cheating; (2) cheats are common across a wide range of viruses, including viral entities that are already well studied, such as defective interfering genomes, and satellite viruses. Consequently, the evolutionary theory of cheating could help us understand and manipulate viral dynamics, while viruses also offer new opportunities to study the evolution of cheating. Cooperation is vulnerable to cheating, and both cooperation and cheating may be especially common in viruses. Here, Leeks et al. place diverse examples of viral cooperation and cheating within an evolutionary framework, highlighting opportunities emerging from greater synthesis of virology and evolutionary theory. [ABSTRACT FROM AUTHOR]

Division of labor occurs when cooperating individuals specialize to perform different tasks. In bacteria and other microorganisms, some species divide labor by random specialization, where an individual's role is determined by random fluctuations in biochemical reactions within the cell. Other species divide labor by coordinating across individuals to determine which cells will perform which task, using mechanisms such as between‐cell signaling. However, previous theory, examining the evolution of mechanisms to divide labor between reproductives and sterile helpers, has only considered clonal populations, where there is no potential for conflict between individuals. We used a mixture of analytical and simulation models to examine nonclonal populations and found that: (a) intermediate levels of coordination can be favored, between the extreme of no coordination (random) and full coordination; (b) as relatedness decreases, coordinated division of labor is less likely to be favored. Our results can help explain why coordinated division of labor is relatively rare in bacteria, where groups may frequently be nonclonal. [ABSTRACT FROM AUTHOR]

Hamilton's local mate competition theory provided an explanation for extraordinary female‐biased sex ratios in a range of organisms. When mating takes place locally, in structured populations, a female‐biased sex ratio is favored to reduce competition between related males, and to provide more mates for males. However, there are a number of wasp species in which the sex ratios appear to more female biased than predicted by Hamilton's theory. It has been hypothesized that the additional female bias in these wasp species results from cooperative interactions between females. We investigated theoretically the extent to which cooperation between related females can interact with local mate competition to favor even more female‐biased sex ratios. We found that (i) cooperation between females can lead to sex ratios that are more female biased than predicted by local competition theory alone, and (ii) sex ratios can be more female biased when the cooperation occurs from offspring to mothers before dispersal, rather than cooperation between siblings after dispersal. Our models formally confirm the verbal predictions made in previous experimental studies, which could be applied to a range of organisms. Specifically, cooperation can help explain sex ratio biases in Sclerodermus and Melittobia wasps, although quantitative comparisons between predictions and data suggest that some additional factors may be operating. [ABSTRACT FROM AUTHOR]

The article offers information on how compartmentalization drives the evolution of symbiotic cooperation. Topics include the evolution of physical structures that allow hosts to spatially separate symbionts, interacting with multiple partners creates a potential tragedy of the commons where less beneficial individuals can share in the collective benefits the host provides, and the symbiosis research being conflicts among symbionts, and between host and symbionts has avoided.

Spiteful behaviors occur when an actor harms its own fitness to inflict harm on the fitness of others. Several papers have predicted that spite can be favored in sufficiently small populations, even when the harming behavior is directed indiscriminately at others. However, it is not clear that truly spiteful behavior could be favored without the harm being directed at a subset of social partners with relatively low genetic similarity to the actor (kin discrimination, causing a negative relatedness between actor and harmed recipient). Using mathematical models, we show that (1) the evolution of spite requires kin discrimination; (2) previous models suggesting indiscriminate spite involve scenarios where the actor gains a direct feedback benefit from harming others, and so the harming is selfish rather than spiteful; (3) extreme selfishness can be favored in small populations (or, more generally, under local competition) because this is where the direct feedback benefit of harming is greatest. [ABSTRACT FROM AUTHOR]

Bacteria eliminate competitors via 'chemical warfare' with bacteriocins. Some species appear to adjust bacteriocin production conditionally in response to the social environment. We tested whether variation in the cost and benefit of producing bacteriocins could explain such conditional behaviour, in the bacteria Lactobacillus plantarum. We found that: (a) bacterial bacteriocin production could be upregulated by either the addition of a synthetic autoinducer peptide (PLNC8IF; signalling molecule), or by a plasmid which constitutively encodes for the production of this peptide; (b) bacteriocin production is costly, leading to reduced growth when grown in poor and, to a lesser extent, in rich media; (c) bacteriocin production provides a fitness advantage, when grown in competition with sensitive strains; and (d) the fitness benefits provided by bacteriocin production are greater at higher cell densities. These results show how the costs and benefits of upregulating bacteriocin production can depend upon abiotic and biotic conditions. [ABSTRACT FROM AUTHOR]

Fields such as behavioural and evolutionary ecology are built on the assumption that natural selection leads to organisms that behave as if they are trying to maximise their fitness. However, there is considerable evidence for selfish genetic elements that change the behaviour of individuals to increase their own transmission. How can we reconcile this contradiction? Here we show that: (1) when selfish genetic elements have a greater impact at the individual level, they are more likely to be suppressed, and suppression spreads more quickly; (2) selection on selfish genetic elements leads them towards a greater impact at the individual level, making them more likely to be suppressed; (3) the majority interest within the genome generally prevails over 'cabals' of a few genes, irrespective of genome size, mutation rate and the sophistication of trait distorters. Overall, our results suggest that even when there is the potential for considerable genetic conflict, this will often have negligible impact at the individual level. The 'parliament of genes' hypothesis suggests that selfish genetic elements will be counteracted by suppressors that maintain equal transmission of the rest of the genome. Here, the authors find support for this hypothesis using mathematical models to explore a range of different scenarios. [ABSTRACT FROM AUTHOR]

Cooperative interactions between species, termed mutualisms, play a key role in shaping natural ecosystems, economically important agricultural systems, and in influencing human health. Across different mutualisms, there is significant variation in the benefit that hosts receive from their symbionts. Empirical data suggest that transmission mode can help explain this variation: vertical transmission, where symbionts infect their host's offspring, leads to symbionts that provide greater benefits to their hosts than horizontal transmission, where symbionts leave their host and infect other hosts in the population. However, two different theoretical explanations have been given for this pattern: firstly, vertical transmission aligns the fitness interests of hosts and their symbionts; secondly, vertical transmission leads to increased relatedness between symbionts sharing a host, favouring cooperation between symbionts. We used a combination of analytical models and dynamic simulations to tease these factors apart, in order to compare their separate influences and see how they interact. We found that relatedness between symbionts sharing a host, rather than transmission mode per se, was the most important factor driving symbiont cooperation. Transmission mode mattered mainly because it determined relatedness. We also found evolutionary branching throughout much of our simulation, suggesting that a combination of transmission mode and multiplicity of infections could lead to the stable coexistence of different symbiont strategies. [ABSTRACT FROM AUTHOR]

Inclusive fitness requires a careful accounting of all the fitness effects of a particular behavior. Verbal arguments can potentially exaggerate the inclusive fitness consequences of a behavior by including the fitness of relatives that was not caused by that behavior, leading to error. We show how this "double‐counting" error can arise, with a recent example from the signaling literature. In particular, we examine the recent debate over whether parental divorce increases parent–offspring conflict, selecting for less honest signaling. We found that, when all the inclusive fitness consequences are accounted for, parental divorce increases conflict between siblings, in a way that they can select for less honest signaling. This prediction is consistent with the empirical data. More generally, our results illustrate how verbal arguments can be misleading, emphasizing the advantage of formal mathematical models. [ABSTRACT FROM AUTHOR]

The first step in the evolution of complex multicellular organisms involves single cells forming a cooperative group. Consequently, to understand multicellularity, we need to understand the costs and benefits associated with multicellular group formation. We found that in the facultatively multicellular algae Chlorella sorokiniana: (1) the presence of the flagellate Ochromonas danica or the crustacean Daphnia magna leads to the formation of multicellular groups; (2) the formation of multicellular groups reduces predation by O. danica, but not by the larger predator D. magna; (3) under conditions of relatively low light intensity, where competition for light is greater, multicellular groups grow slower than single cells; (4) in the absence of live predators, the proportion of cells in multicellular groups decreases at a rate that does not vary with light intensity. These results can explain why, in cases such as this algae species, multicellular group formation is facultative, in response to the presence of predators. [ABSTRACT FROM AUTHOR]

The growth and virulence of bacteria depends upon a number of factors that are secreted into the environment. These factors can diffuse away from the producing cells, to be either lost or used by cells that do not produce them (cheats). Mechanisms that act to reduce the loss of secreted factors through diffusion are expected to be favoured. One such mechanism may be the production of Fap fibrils, needle-like fibres on the cell surface observed in P. aeruginosa, which can transiently bind several secreted metabolites produced by cells. We test whether Fap fibrils help retain a secreted factor, the iron-scavenging molecule pyoverdine, and hence reduce the potential for exploitation by non-producing, cheating cells. We found that: (i) wild-type cells retain more iron-chelating metabolites than fibril non-producers; (ii) purified Fap fibrils can prevent the loss of the iron-chelators PQS (Pseudomonas quinolone signal) and pyoverdine; and (iii) pyoverdine non-producers have higher fitness in competition with fibril non-producers than with wild-type cells. Our results suggest that by limiting the loss of a costly public good, Fap fibrils may play an important role in stabilizing cooperative production of secreted factors. [ABSTRACT FROM AUTHOR]

The growth and virulence of the bacteria Bacillus thuringiensis depend on the production of Cry toxins, which are used to perforate the gut of its host. Successful invasion of the host relies on producing a threshold amount of toxin, after which there is no benefit from producing more toxin. Consequently, the production of Cry toxin appears to be a different type of social problem compared with the public goods scenarios that bacteria usually encounter. We show that selection for toxin production is a volunteer's dilemma. We make specific predictions that (a) selection for toxin production depends upon an interplay between the number of bacterial cells that each host ingests and the genetic relatedness between those cells; (b) cheats that do not produce toxin gain an advantage when at low frequencies, and at high bacterial density, allowing them to be maintained in a population alongside toxin‐producing cells. More generally, our results emphasize the diversity of the social games that bacteria play. [ABSTRACT FROM AUTHOR]

Most organisms are built from a single genome. In striking contrast, arbuscular mycorrhizal fungi appear to maintain genomic variation within an individual fungal network. Arbuscular mycorrhizal fungi dwell in the soil, form mutualistic networks with plants, and bear multiple, potentially genetically diverse nuclei within a network. We explore, from a theoretical perspective, why such genetic diversity might be maintained within individuals. We consider selection acting within and between individual fungal networks. We show that genetic diversity could provide a benefit at the level of the individual, by improving growth in variable environments, and that this can stabilize genetic diversity even in the presence of nuclear conflict. Arbuscular mycorrhizal fungi complicate our understanding of organismality, but our findings offer a way of understanding such biological anomalies. Most organisms are built from a single genome. In striking contrast, arbuscular mycorrhizal fungi appear to maintain genomic variation within an individual fungal network. We explore, from a theoretical perspective, why such genetic diversity might be maintained within individuals. [ABSTRACT FROM AUTHOR]

Pleiotropy has been suggested as a novel mechanism for stabilising cooperation in bacteria and other microbes. The hypothesis is that linking cooperation with a trait that provides a personal (private) benefit can outweigh the cost of cooperation in situations when cooperation would not be favoured by mechanisms such as kin selection. We analysed the theoretical plausibility of this hypothesis, with analytical models and individual-based simulations. We found that (1) pleiotropy does not stabilise cooperation, unless the cooperative and private traits are linked via a genetic architecture that cannot evolve (mutational constraint); (2) if the genetic architecture is constrained in this way, then pleiotropy favours any type of trait and not especially cooperation; (3) if the genetic architecture can evolve, then pleiotropy does not favour cooperation; and (4) there are several alternative explanations for why traits may be linked, and causality can even be predicted in the opposite direction, with cooperation favouring pleiotropy. Our results suggest that pleiotropy could only explain cooperation under restrictive conditions and instead show how social evolution can shape the genetic architecture. [ABSTRACT FROM AUTHOR]

Abstract: With any theoretical model, the modeler must decide what kinds of detail to include and which simplifying assumptions to make. It could be assumed that models that include more detail are better, or more correct. However, no model is a perfect description of reality and the relative advantage of different levels of detail depends on the model's empirical purpose. We consider the specific case of how relatedness is modeled in the field of social evolution. Different types of model either leave relatedness as an independent parameter (open models), or include detail for how demography and life cycle determine relatedness (closed models). We exploit the social evolution literature, especially work on the evolution of cooperation, to analyze how useful these different approaches have been in explaining the natural world. We find that each approach has been successful in different areas of research, and that more demographic detail is not always the most empirically useful strategy. [ABSTRACT FROM AUTHOR]

In many viral infections, a large number of different genetic variants can coexist within a host, leading to more virulent infections that are better able to evolve antiviral resistance and adapt to new hosts. But how is this diversity maintained? Why do faster-growing variants not outcompete slower-growing variants, and erode this diversity? One hypothesis is if there are mutually beneficial interactions between variants, with host cells infected by multiple different viral genomes producing more, or more effective, virions. We modelled this hypothesis with both mathematical models and simulations, and found that moderate levels of beneficial coinfection can maintain high levels of coexistence, even when coinfection is relatively rare, and when there are significant fitness differences between competing variants. Rare variants are more likely to be coinfecting with a different variant, and hence beneficial coinfection increases the relative fitness of rare variants through negative frequency dependence, and maintains diversity. We further find that coexisting variants sometimes reach unequal frequencies, depending on the extent to which different variants benefit from coinfection, and the ratio of variants which leads to the most productive infected cells. These factors could help drive the evolution of defective interfering particles, and help to explain why the different segments of multipartite viruses persist at different equilibriumfrequencies. [ABSTRACT FROM AUTHOR]

Cooperative behaviours in archaic hunter-gatherers could have been maintained partly due to the gains from cooperation being shared with kin. However, the question arises as to how cooperation was maintained after early humans transitioned to larger groups of unrelated individuals. We hypothesize that after cooperation had evolved via benefits to kin, the consecutive evolution of cognition increased the returns from cooperating, to the point where benefits to self were sufficient for cooperation to remain stable when group size increased and relatedness decreased. We investigate the theoretical plausibility of this hypothesis, with both analytical modelling and simulations. We examine situations where cognition either (i) increases the benefits of cooperation, (ii) leads to synergistic benefits between cognitively enhanced cooperators, (iii) allows the exploitation of less intelligent partners, and (iv) the combination of these effects. We find that cooperation and cognition can coevolve-cooperation initially evolves, favouring enhanced cognition, which favours enhanced cooperation, and stabilizes cooperation against a drop in relatedness. These results suggest that enhanced cognition could have transformed the nature of cooperative dilemmas faced by early humans, thereby explaining the maintenance of cooperation between unrelated partners. [ABSTRACT FROM AUTHOR]

Cooperative interactions among species, termed mutualisms, have played a crucial role in the evolution of life on Earth. However, despite key potential benefits to partners, there are many cases in which two species cease to cooperate and mutualisms break down. What factors drive the evolutionary breakdown of mutualism? We examined the pathways toward breakdowns of the mutualism between plants and arbuscular mycorrhizal fungi. By using a comparative approach, we identify ~25 independent cases of complete mutualism breakdown across global seed plants. We found that breakdown of cooperation was only stable when host plants (i) partner with other root symbionts or (ii) evolve alternative resource acquisition strategies. Our results suggest that key mutualistic services are only permanently lost if hosts evolve alternative symbioses or adaptations. [ABSTRACT FROM AUTHOR]

1. Fig wasps have proved extremely useful study organisms for testing how reproductive decisions evolve in response to population structure. In particular, they provide textbook examples of how natural selection can favour female-biased offspring sex ratios, lethal combat for mates and dimorphic mating strategies. 2. However, previous work has been challenged, because supposedly single species have been discovered to be a number of cryptic species. Consequently, new studies are required to determine population structure and reproductive decisions of individuals unambiguously assigned to species. 3. Microsatellites were used to determine species identity and reproductive patterns in three non-pollinating Sycoscapter species associated with the same fig species. Foundress number was typically one to five and most figs contained more than one Sycoscapter species. Foundresses produced very small clutches of about one to four offspring, but one foundress may lay eggs in several figs. 4. Overall, the data were a poor match to theoretical predictions of solitary male clutches and gregarious clutches with n − 1 females. However, sex ratios were male-biased in solitary clutches and female-biased in gregarious ones. 5. At the brood level (all wasps in a fig), a decrease in sex ratio with increasing brood size was only significant in one species, and sex ratio was unrelated to foundress number. In addition, figs with more foundresses contain more wasp offspring. 6. Finally, 10-22% of females developed in patches without males. As males are wingless, these females disperse unmated and are constrained to produce only sons from unfertilised eggs. [ABSTRACT FROM AUTHOR]

Various steps in the RNA world required cooperation. Why did life's first inhabitants, from polymerases to synthetases, cooperate? We develop kin selection models of the RNA world to answer these questions. We develop a very simple model of RNA cooperation and then elaborate it to model three relevant issues in RNA biology: (1) whether cooperative RNAs receive the benefits of cooperation; (2) the scale of competition in RNA populations; and (3) explicit replicator diffusion and survival. We show: (1) that RNAs are likely to express partial cooperation; (2) that RNAs will need mechanisms for overcoming local competition; and (3) in a specific example of RNA cooperation, persistence after replication and offspring diffusion allow for cooperation to overcome competition. More generally, we show how kin selection can unify previously disparate answers to the question of RNA world cooperation. [ABSTRACT FROM AUTHOR]

In order for the first genomes to evolve, independent replicators had to act cooperatively, with some reducing their own replication rate to help copy others. It has been argued that limited diffusion explains this early cooperation. However, social evolution models have shown that limited diffusion on its own often does not favour cooperation. Here we model early replicators using social evolution tools. We show that: (i) replicators can be considered to be cooperating as a result of kin selection; (ii) limited diffusion on its own does not favour cooperation; and (iii) the addition of overlapping generations, probably a general trait of molecular replicators, promotes cooperation. These results suggest key life-history features in the evolution of the genome and that the same factors can favour cooperation across the entire tree of life. [ABSTRACT FROM AUTHOR]

Bacteria perform cooperative behaviors that are exploitable by noncooperative cheats, and cheats frequently arise and coexist with cooperators in laboratory microcosms. However, evidence of competitive dynamics between cooperators and cheats in nature remains limited. Using the production of pyoverdine, an iron-scavenging molecule, and natural soil populations of Pseudomonas fluorescens, we found that (1) nonproducers are present in the population; (2) they co-occur (<1cm3) with pyoverdine producers; (3) they retain functional pyoverdine receptors; and (4) they can use the pyoverdine of on average 52% of producers. This suggests nonproducers can potentially act as social cheats in soil: utilizing the pyoverdine of others while producing little or none themselves. However, we found considerable variation in the extent to which nonproducers can exploit producers, as some isolates appear to produce exclusive forms of pyoverdine or kill nonproducers with toxins. We examined the consequences of this variation using theoretical modeling. We found variance in exploitability leads to some cheats gaining increased fitness benefits and others decreased benefits. However, the absolute gain in fitness from high exploitation is lower than the drop in fitness from low exploitation, decreasing the mean fitness of cheats and subsequently lowering the proportion of cheats maintained in the population. Our results suggest that although cooperator-cheat dynamics can occur in soil, a range of mechanisms can prevent nonproducers from exploiting producers. [ABSTRACT FROM AUTHOR]

hypothesis, we experimentally manipulated the extent an individual's behaviour is known to others, and hence whether or not strategic cooperation is possible. In contrast with many previous studies, we avoided confounding factors by preventing individuals from learning during the game about either pay-offs or about how other individuals behave. We found clear evidence for strategic cooperators--just telling some individuals that their groupmates would be informed about their behaviour led to them tripling their initial level of cooperation, from 17 to 50%. We also found that many individuals play as if they do not understand the game, and their presence obscures the detection of strategic cooperation. Identifying such players allowed us to detect and study strategic motives for cooperation in novel, more powerful, ways. [ABSTRACT FROM AUTHOR]

It is becoming increasingly clear that the evolution of infectious disease is influenced by host population structure. Theory predicts that parasites should be more ‘prudent’—less transmissible—in spatially structured host populations. However, here we (i) highlight how low transmission, the phenotype being selected for in this in context, may also be achieved by rapacious host exploitation, if fast host exploitation confers a local, within-host competitive advantage and (ii) test this novel concept in a bacteria–virus system. We found that limited host availability and, to a lesser extent, low relatedness favour faster-killing parasites with reduced transmission. By contrast, high host availability and high relatedness favour slower-killing, more transmissible parasites. Our results suggest high, rather than low, virulence may be selected in spatially structured host–parasite communities where local competition and hence selection for a within-host fitness advantage is high. [ABSTRACT FROM AUTHOR]

The harm that pathogens cause to hosts during infection, termed virulence, varies across species from negligible to a high likelihood of rapid death. Classic theory for the evolution of virulence is based on a trade-off between pathogen growth, transmission and host survival, which predicts that higher within-host growth causes increased transmission and higher virulence. However, using data from 61 human pathogens, we found the opposite correlation to the expected positive correlation between pathogen growth rate and virulence. We found that (i) slower growing pathogens are significantly more virulent than faster growing pathogens, (ii) inhaled pathogens and pathogens that infect via skin wounds are significantly more virulent than pathogens that are ingested, but (iii) there is no correlation between symptoms of infection that aid transmission (such as diarrhoea and coughing) and virulence. Overall, our results emphasize how virulence can be influenced by mechanistic life-history details, especially transmission mode, that determine how parasites infect and exploit their hosts. [ABSTRACT FROM AUTHOR]

Humans have a sophisticated ability to learn from others, termed social learning, which has allowed us to spread over the planet, construct complex societies, and travel to the moon. It has been hypothesized that social learning has played a pivotal role in making human societies cooperative, by favouring cooperation even when it is not favoured by genetical selection. However, this hypothesis lacks direct experimental testing, and the opposite prediction has also been made, that social learning disfavours cooperation. We experimentally tested how different aspects of social learning affect the level of cooperation in public-goods games. We found that: (i) social information never increased cooperation and usually led to decreased cooperation; (ii) cooperation was lowest when individuals could observe how successful individuals behaved; and (iii) cooperation declined because individuals preferred to copy successful individuals, who cooperated less, rather than copy common behaviours. Overall, these results suggest that individuals use social information to try and improve their own success, and that this can lead to lower levels of cooperation. [ABSTRACT FROM AUTHOR]

Offspring survival can often depend on successful communication with parents about their state of need. Theory suggests that offspring will be less likely to honestly signal their need when they experience greater competition from either a greater number of nestmates or less-related nestmates. We found support for this hypothesis with a comparative analysis, examining data from across 60 species of birds. We found that offspring are less honest about their level of need when (i) they face competition from current siblings; (ii) their parents are likely to breed again, and so they are in competition with future siblings; and (iii) parental divorce or death means that they are likely to be less related to future siblings. More generally, these patterns highlight the sensitivity of communication systems to conflict between signaler and receiver while also suggesting that when there is little conflict, natural selection favors the honest. [ABSTRACT FROM AUTHOR]