Pathogens play an important part in shaping the structure and dynamics of natural communities, because species are not affected by them equally 1,2 . A shared goal of ecology and epidemiology is to predict when a species is most vulnerable to disease. A leading hypothesis asserts that the impact of disease should increase with host abundance, producing a 'rare-species advantage' 3-5 . However, the impact of a pathogen may be decoupled from host abundance, because most pathogens infect more than one species, leading to pathogen spillover onto closely related species 6,7 . Here we show that the phylogenetic and ecological structure of the surrounding community can be important predictors of disease pressure. We found that the amount of tissue lost to disease increased with the relative abundance of a species across a grassland plant community, and that this rare-species advantage had an additional phylogenetic component: disease pressure was stronger on species with many close relatives. We used a global model of pathogen sharing as a function of relatedness between hosts, which provided a robust predictor of relative disease pressure at the local scale. In our grassland, the total amount of disease was most accurately explained not by the abundance of the focal host alone, but by the abundance of all species in the community weighted by their phylogenetic distance to the host. Furthermore, the model strongly predicted observed disease pressure for 44 novel host species we introduced experimentally to our study site, providing evidence for a mechanism to explain why phylogenetically rare species are more likely to become invasive when introduced 8,9 . Our results demonstrate how the phylogenetic and ecological structure of communities can have a key role in disease dynamics, with implications for the maintenance of biodiversity, biotic resistance against introduced weeds, and the success of managed plants in agriculture and forestry.Plant pathogens can be important drivers of community diversity, structure and dynamics 1,2,10,11 . A basic premise of epidemiology is that pathogen transmission often increases with host density 12,13 . Densitydependent disease provides a mechanism for the maintenance of plant diversity in natural communities, in which locally uncommon species enjoy a rare-species advantage-based on lower enemy pressure-that mitigates the competitive impacts of dominant species 3-5 . Reports of density-dependent disease dynamics generally infer the potential effects on communities from studies of one or a few species 2 , while community-level studies 1 are scarce but essential to evaluate whether such a rarespecies advantage predicts patterns of disease across a community.An ongoing debate concerns how community context influences disease, and particularly whether biodiversity suppresses infection and emerging diseases 14,15 . If increasing the number of species in a community reduces the density of competent hosts or the frequency of infected vectors, then biodiversity shows a suppressive 'dilution e...

Global change has made it important to understand the factors that shape species' distributions. Central to this area of research is the question of whether species' range limits primarily reflect the distribution of suitable habitat (i.e. niche limits) or arise as a result of dispersal limitation. Over-the-edge transplant experiments and ecological niche models are commonly used to address this question, yet few studies have taken advantage of a combined approach for inferring the causes of range limits. Here, we synthesise results from existing transplant experiments with new information on the predicted suitability of sites based on niche models. We found that individual performance and habitat suitability independently decline beyond range limits across multiple species. Furthermore, inferences from transplant experiments and niche models were generally concordant within species, with 31 out of 40 cases fully supporting the hypothesis that range limits are niche limits. These results suggest that range limits are often niche limits and that the factors constraining species' ranges operate at scales detectable by both transplant experiments and niche models. In light of these findings, we outline an integrative framework for addressing the causes of range limits in individual species.

Recent theory and empirical evidence have provided new insights regarding how evolutionary forces interact to shape adaptation at stable and transient range margins. Predictions regarding trait divergence at leading edges are frequently supported. However, declines in fitness at and beyond edges show that trait divergence has sometimes been insufficient to maintain high fitness, so identifying constraints to adaptation at range edges remains a key challenge. Indirect evidence suggests that range expansion may be limited by adaptive genetic variation, but direct estimates of genetic constraints at and beyond range edges are still scarce. Sequence data suggest increased genetic load in edge populations in several systems, but its causes and fitness consequences are usually poorly understood. The balance between maladaptive and positive effects of gene flow on fitness at range edges deserves further study. It is becoming increasingly clear that characterizations about degree of adaptation based solely on geographical peripherality are unsupported.

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