Explore the vast range of titles available.

The human brain is unusually large. It has tripled in size from Australopithecines to modern humans 1 and has become almost six times larger than expected for a placental mammal of human size 2 . Brains incur high metabolic costs 3 and accordingly a long-standing question is why the large human brain has evolved 4 . The leading hypotheses propose benefits of improved cognition for overcoming ecological 5 – 7 , social 8 – 10 or cultural 11 – 14 challenges. However, these hypotheses are typically assessed using correlative analyses, and establishing causes for brain-size evolution remains difficult 15 , 16 . Here we introduce a metabolic approach that enables causal assessment of social hypotheses for brain-size evolution. Our approach yields quantitative predictions for brain and body size from formalized social hypotheses given empirical estimates of the metabolic costs of the brain. Our model predicts the evolution of adult Homo sapiens -sized brains and bodies when individuals face a combination of 60% ecological, 30% cooperative and 10% between-group competitive challenges, and suggests that between-individual competition has been unimportant for driving human brain-size evolution. Moreover, our model indicates that brain expansion in Homo was driven by ecological rather than social challenges, and was perhaps strongly promoted by culture. Our metabolic approach thus enables causal assessments that refine, refute and unify hypotheses of brain-size evolution. Using estimates of metabolic costs of the brain and body, mathematical predictions suggest that the evolution of adult Homo sapiens -sized brains and bodies is driven by ecological rather than social challenges and is perhaps strongly promoted by culture.

The evolution of life on earth has been driven by a small number of major evolutionary transitions. These transitions have been characterized by individuals that could previously replicate independently, cooperating to form a new, more complex life form. For example, archaea and eubacteria formed eukaryotic cells, and cells formed multicellular organisms. However, not all cooperative groups are en route to major transitions. How can we explain why major evolutionary transitions have or haven’t taken place on different branches of the tree of life? We break down major transitions into two steps: the formation of a cooperative group and the transformation of that group into an integrated entity. We show how these steps require cooperation, division of labor, communication, mutual dependence, and negligible within-group conflict. We find that certain ecological conditions and the ways in which groups form have played recurrent roles in driving multiple transitions. In contrast, we find that other factors have played relatively minor roles at many key points, such as within-group kin discrimination and mechanisms to actively repress competition. More generally, by identifying the small number of factors that have driven major transitions, we provide a simpler and more unified description of how life on earth has evolved.

Hamilton's theory of inclusive fitness showed how natural selection could lead to behaviors that decrease the relative fitness of the actor and also either benefit (altruism) or harm (spite) other individuals. However, several fundamental issues in the evolution of altruism and spite have remained contentious. Here, we show how recent work has resolved three key debates, helping clarify how Hamilton's theoretical overview links to real-world examples, in organisms ranging from bacteria to humans: Is the evolution of extreme altruism, represented by the sterile workers of social insects, driven by genetics or ecology? Does spite really exist in nature? And, can altruism be favored between individuals who are not close kin but share a \"greenbeard\" gene for altruism?

Metamorphosis, the discrete morphological change between postembryonic life stages, is widespread across the animal kingdom. The suggested advantages of metamorphosis have usually been framed in terms of population benefits, i.e., ecological explanations. In contrast, evolutionary explanations concern whether and how metamorphosis spreads through a population owing to individual‐fitness benefits. However, how kin selection modulates evolution of metamorphosis remains to be investigated formally. Here we develop a mathematical model to investigate how kin selection shapes the optimal timing of metamorphosis from foraging, non‐reproductive larva to reproductive adult, when larvae tend to cluster with their genetic relatives. We consider the full range of larval competition intensities—from no competition to full competition—and the full range of relatedness coefficients—from unrelated to clonality. We provide testable predictions as to how kin selection modulates the timing of metamorphosis, as well as a conceptual framework within which empirical observations may be understood. We develop a mathematical model to investigate how kin selection shapes the optimal timing of metamorphosis. We consider the full range of larval competition intensities and the full range of relatedness coefficients. This yields testable predictions as to how kin selection modulates the timing of metamorphosis.

Price's equation provides a very simple—and very general—encapsulation of evolutionary change. It forms the mathematical foundations of several topics in evolutionary biology, and has also been applied outwith evolutionary biology to a wide range of other scientific disciplines. However, the equation's combination of simplicity and generality has led to a number of misapprehensions as to what it is saying and how it is supposed to be used. Here, I give a simple account of what Price's equation is, how it is derived, what it is saying and why this is useful. In particular, I suggest that Price's equation is useful not primarily as a predictor of evolutionary change but because it provides a general theory of selection. As an illustration, I discuss some of the insights Price's equation has brought to the study of social evolution. This article is part of the theme issue ‘Fifty years of the Price equation’.

Our understanding of the social lives of microbes has been revolutionized over the past 20 years. It used to be assumed that bacteria and other microorganisms lived relatively independent unicellular lives, without the cooperative behaviors that have provoked so much interest in mammals, birds, and insects. However, a rapidly expanding body of research has completely overturned this idea, showing that microbes indulge in a variety of social behaviors involving complex systems of cooperation, communication, and synchronization. Work in this area has already provided some elegant experimental tests of social evolutionary theory, demonstrating the importance of factors such as relatedness, kin discrimination, competition between relatives, and enforcement of cooperation. Our aim here is to review these social behaviors, emphasizing the unique opportunities they offer for testing existing evolutionary theory as well as highlighting the novel theoretical problems that they pose.

Differences in transmission and ploidy between sex chromosomes and autosomes drive divergent evolutionary trajectories, with sex chromosomes generally evolving faster. Because sex-linked genes are transmitted less frequently, they are under less efficient selection. Conversely, exposure of recessive mutations on haploid sex chromosomes creates more efficient selection. In most systems, these effects occur simultaneously and are confounded. The fly families Sciaridae (fungus gnats) and Cecidomyiidae (gall midges) have X0 sex determination, but males transmit only maternally inherited chromosomes. This phenomenon results in equal transmission of the X and autosomes, allowing the effect of haploid selection to be studied in isolation. We discover that, unlike well-studied systems, X chromosomes diverge more slowly than autosomes in these flies. Using population genomic and expression data, we show that despite the X evolving more adaptively, stronger purifying selection explains slower divergence. Our findings demonstrate the utility of non-Mendelian inheritance systems for understanding fundamental evolutionary processes. X chromosomes evolve faster than autosomes, but confounding factors make this a difficult phenomenon to study. Utilising the unusual sex determination system of Sciaridae flies, this study finds a slower evolution of the X chromosomes which appears to be driven by strong purifying selection.

A gene mediating interactions between mouse mothers and their pups has recently been claimed to support coadaptation rather than the kinship theory of genomic imprinting. This Formal Comment argues that this claim is unfounded.

They are all individuals The conventional view of adaptation is that it operates at the level of the individual organism, but recent observations of the evolution of virulence in viruses infecting moths and bacteria in spatially structured populations (where dispersal is limited) have been interpreted as examples of group selection. Wild et al . here extend previous models mathematically to show that the effect of dispersal on parasite virulence can be understood as an individual-level adaptation by the parasite entirely within the context of kin selection theory. The evolution of lowered virulence in spatially structured populations with limited dispersal has been suggested to be an example of adaptation at the group level. The extension of previous models now shows that the effect of dispersal can be understood within the framework of inclusive fitness theory, demonstrating that reduced virulence could be due to individual-level adaptation by the parasite. Adaptation is conventionally regarded as occurring at the level of the individual organism, where it functions to maximize the individual’s inclusive fitness 1 , 2 , 3 . However, it has recently been argued that empirical studies on the evolution of parasite virulence in spatial populations show otherwise 4 , 5 , 6 , 7 . In particular, it has been claimed that the evolution of lower virulence in response to limited parasite dispersal 8 , 9 provides proof of Wynne-Edwards’s 10 idea of adaptation at the group level. Although previous theoretical work has shown that limited dispersal can favour lower virulence, it has not clarified why, with five different suggestions having been given 6 , 8 , 11 , 12 , 13 , 14 , 15 . Here we show that the effect of dispersal on parasite virulence can be understood entirely within the framework of inclusive fitness theory. Limited parasite dispersal favours lower parasite growth rates and, hence, reduced virulence because it (1) decreases the direct benefit of producing offspring (dispersers are worth more than non-dispersers, because they can go to patches with no or fewer parasites), and (2) increases the competition for hosts experienced by both the focal individual (‘self-shading’) and their relatives (‘kin shading’). This demonstrates that reduced virulence can be understood as an individual-level adaptation by the parasite to maximize its inclusive fitness, and clarifies the links with virulence theory more generally 16 .

Malaria parasites and related Apicomplexans are the causative agents of the some of the most serious infectious diseases of humans, companion animals, livestock and wildlife. These parasites must undergo sexual reproduction to transmit from vertebrate hosts to vectors, and their sex ratios are consistently female-biased. Sex allocation theory, a cornerstone of evolutionary biology, is remarkably successful at explaining female-biased sex ratios in multicellular taxa, but has proved controversial when applied to malaria parasites. Here we show that, as predicted by theory, sex ratio is an important fitness-determining trait and Plasmodium chabaudi parasites adjust their sex allocation in response to the presence of unrelated conspecifics. This suggests that P. chabaudi parasites use kin discrimination to evaluate the genetic diversity of their infections, and they adjust their behaviour in response to environmental cues. Malaria parasites provide a novel way to test evolutionary theory, and support the generality and power of a darwinian approach. Sex and the malaria parasite Malaria parasites need to reproduce sexually before they can transmit to vectors, but despite extensive research on ways of blocking transmission, little is known about their reproductive strategies. Reece et al . use novel experiments to show that the assumptions of sex-allocation theory, previously controversial when used to explain sex ratios in malaria parasites, are in fact valid. As predicted by this plank of evolutionary theory, Plasmodium chabaudi parasites adjust their sex-allocation in response to the presence of unrelated conspecifics. By means of this kin discrimination they evaluate the genetic diversity of their infections, and adjust their behaviour in response to environmental cues. Malaria parasites must reproduce sexually to transmit to vectors, but very little is understood about their reproductive strategies. This paper details that malaria parasites adjust their sex ratios in response to unrelated conspecifics, as predicted by evolutionary theory.