Classical ecological theory suggests that the coexistence of consumer species is fostered by resource-use differences, leading to greater resource use in communities with more species. However, explicit empirical support for this idea is lacking, because resource use by species is generally confounded with other species-specific attributes. We overcame this obstacle by co-opting behavioral plasticity in food choice among a group of animal consumers, allowing us to manipulate patterns of resource use while controlling for the effects of species identity and diversity. Within an aphid-parasitoid-radish community, we created a fully factorial manipulation of consumer resource-use breadth (specialist versus generalist) and species diversity (one versus three species) and found that resource exploitation improved with greater specialist, but not generalist, diversity. Therefore, resource partitioning, and not diversity per se, fostered greater overall resource consumption in our multispecies consumer communities.

Predicting disease dynamics requires a community perspective, incorporating multi‐species interactions involving hosts, pathogens, vectors, and consumers. In systems where pathogens are dependent on a vector for transmission from one host to another, predators can indirectly influence disease risk through direct effects on vectors. These effects may be consumptive if predators reduce vector abundance by capturing and killing vectors, or non‐consumptive if predators induce anti‐predator behavioral responses by vectors. Studies are accumulating that document cascading effects of predators on vector‐borne disease risk, but the mechanisms underlying these effects are often uncertain. Using a previously developed epidemiological model as a framework, I outline several mechanistic pathways by which predators can have consumptive and non‐consumptive effects on vectors, and present theoretical predictions about the cascading influence of these pathways on pathogen prevalence. I then review selected examples from the literature of vector‐borne plant pathogen systems where particular mechanistic pathways have been implicated. Together, the model predictions and the literature review reveal that, depending on the particular mechanisms at work, predators may reduce, leave unaffected, or even increase pathogen prevalence. In general, the consumptive effects of predators on vectors result in consistent reductions in pathogen prevalence. However, the non‐consumptive effects of predators that arise as a result of changes in pathogen transmission rates, vector birth rates, and non‐predation vector mortality rates are more variable, with the potential for context‐dependency and counter‐intuitive outcomes. Interactions among pathways are also possible, such that the magnitude of consumptive effects can depend upon the strength of non‐consumptive effects and vice versa. I conclude by highlighting the importance of teasing apart the various mechanistic pathways by which predators may indirectly influence pathogen prevalence, and clarifying the relationships among them, to accurately predict the consequences of predation for disease risk and the usefulness of biological control of vectors for suppression of plant pathogens.

Evolution of resistance to transgenic crops producing toxins from Bacillus thuringiensis (Bt) threatens the sustainability of the technology. Examination of resistance mechanisms has largely focused on characterization of mutations in proteins serving as Bt toxin binding sites. However, insect microbial communities have the potential to provide host resistance to pesticides in a myriad of ways. Previous findings suggest the killing mechanism of Bt relies on enteric bacteria becoming pathogenic in the disrupted gut environment of the insect following Bt intoxication. Thus, here we hypothesized that resistance to Bt would alter the microbiome composition of the insect. Previous studies have manipulated the microbiome of susceptible insects and monitored their response to Bt. In our study, we characterized the associated bacterial communities of Bt‐resistant and ‐susceptible western corn rootworms, a widespread pest of maize in the United States. We found resistant insects harbor a bacterial community that is less rich and distinct from susceptible insects. After feeding on Bt‐expressing maize, susceptible insects exhibited dysbiosis of the associated bacterial community, whereas the community within resistant insects remained relatively unchanged. These results suggest resistance to Bt produces alterations in the microbiome of the western corn rootworm that may contribute to resistance. We further demonstrated that by itself, feeding on Bt toxin‐expressing seedlings caused a shift in the microbiota. This work provides a broader picture of the effect stressors have on microbiome composition, and the potential heritable changes induced as a result of intense selection.

The effects of drought‐induced changes in plant quality on aphid performance and population growth is well‐studied. The response of aphid behaviour to plant water limitation has received less attention. Water limitation may affect host‐plant colonization by altering the attractiveness of plants. Additionally, plant water limitation may inhibit feeding site establishment and phloem ingestion. Our goal was to examine bird cherry‐oat aphid ( Rhopalosiphum padi L.) host selection and feeding behaviour under water limitation. We assessed aphid response to well‐watered, mildly‐stressed, and highly‐stressed wheat ( Triticum aestivum L.) by evaluating (i) host‐plant selection through two‐choice assays, (ii) feeding behaviour using the electrical penetration graph technique, and (iii) phloem ingestion by quantifying honeydew production. Aphids were less likely to select highly stressed plants than a mildly stressed or well‐watered alternative. Aphids did not distinguish between mildly stressed and well‐watered plants. Aphid feeding behaviours, including duration of phloem ingestion, were not affected by water availability. However, honeydew production was reduced under both levels of water limitation. These results suggest that the volume of phloem ingested by aphids per unit time declined on stressed plants. The combination of lower colonization and diminished access to food on stressed plants may lead to a reduction in aphid abundance, independent of the direct effects of nutrition on individual aphid performance. This study highlights the potential contribution of herbivore behaviour to documented changes in aphid abundance on stressed plants and underscores the important role of plant water stress intensity in mediating plant‐herbivore interactions.