Control of emerging infectious diseases often hinges on identifying a pathogen reservoir, the source of disease transmission. The potential to function as a pathogen reservoir can be influenced by host lifespan, geographic provenance and phylogeny. Yet, no study has identified factors that causally determine the reservoir potential of diverse host species. We propose the host physiological phenotype hypothesis, which predicts that hosts with short-lived, poorly defended, nutrient rich and high metabolism tissue have greater values for three epidemiological parameters that determine reservoir potential: host susceptibility to infection, competence to infect vectors and ability to support vector populations. We experimentally tested these predictions using a generalist vectored virus and six wild grass species. Host physiological phenotype explained why hosts differed in all three epidemiological parameters while host lifespan, provenance and phylogeny could not explain host competence. Thus, a single, general axis describing variation in host physiological phenotype may explain reservoir potential.

Identifying and clearly communicating the drivers of ecosystem function is a crucially important goal for both basic and applied ecology. This has proven difficult because the putative causes (e.g., environment, species identity, biodiversity, and functional traits) are numerous and correlated. The problem is exacerbated by a lack of a formal framework for unambiguously relating theoretical language to precise, quantitative expressions of that language. Using a formal framework for the graphical expression of complex causal hypotheses, we developed a causal diagram of the concepts required to comprehensively test whether hypothesized sets of functional traits mediate the relationship between community structure and ecosystem function. We then used causal analysis, simulations, and field data to develop and test analytical strategies for understanding how community structure influences ecosystem functions via functional traits. Formal causal analysis showed that biodiversity-ecosystem function correlations are noncausal associations. Using simulations, we showed how biodiversity correlations and species identity effects can arise from misspecification or incomplete mediation by functional trait composites. We also found that different types of model misspecification result in different patterns of residuals, which may be used to diagnose gaps in functional trait hypotheses. Treating the model misspecifications eliminated associations between species identity or biodiversity and ecosystem function. Finally, we provide an example of the analysis of field data to demonstrate how to use these insights to conduct a research program that has the goal of understanding the mechanistic trait relationships that link community structure to ecosystem function.

In spite of increasing awareness that interactions between herbivory and the supply rates of multiple nutrients control biodiversity, ecosystem functions and ecosystem services in ecological communities, few experimental studies have concurrently examined the independent and joint effects of multiple nutrients and mammalian consumers on these responses in natural systems. Here we quantify the independent and interactive effects of multiple concurrent changes to resources and consumers in an invaded annual grassland community in California. In a two‐year study using thirty‐seven 400‐m2 plots, we examine interactions among four nutrient treatments (N, P, K and micronutrients) and a keystone herbivore (pocket gopher Thomomys bottae) on four plant community outcomes: 1) plant diversity, 2) functional group composition, 3) net biomass production, an important ecosystem function, and 4) infection risk by a group of viral pathogens shared by crop and non‐crop grasses (barley and cereal yellow dwarf viruses), an important regulating ecosystem service. We found that grassland biodiversity and infection risk were controlled by nutrient identity and supply ratio whereas nutrients interacted strongly with consumers to control grassland composition and net primary productivity. The most important insights arising from this multi‐factor experiment are that net biomass production increased with phosphorus or nitrogen supply; however, when gophers were present, nitrogen caused no net effect on biomass production. In addition, infection risk was driven by phosphorus, nitrogen and micronutrient supply. Infection in a sentinel host increased strongly with the addition of micronutrients or phosphorus; however, infection declined with increasing N/P supply ratio, indicating stoichiometric control of infection risk. Finally, in spite of manipulating multiple factors, plant species richness declined with nitrogen, alone. The importance of higher‐order interactions demonstrates that a multi‐factor approach is critical for effective predictions in a world in which anthropogenic activities are simultaneously changing herbivore abundance and the relative supply of many nutrients.

Online enhancement: appendixes. Dryad data: http://dx.doi.org/10.5061/dryad.8mq2q.abstract: Primary axes of host developmental tempo (HDT; e.g., slow-quick return continuum) represent latent biological processes and are increasingly used to a priori identify hosts that contribute disproportionately more to pathogen transmission. The influence of HDT on host contributions to transmission depends on how HDT influences both resistance and tolerance of disease. Here, we use structural equation modeling to address known limitations of conventional measures of resistance and tolerance. We first provide a general resistance-tolerance metamodel from which system-specific models can be derived. We then develop a model specific to a group of vector-transmitted viruses that infect hundreds of grass species worldwide. We tested the model using experimental inoculations of six phylogenetically paired grass species. We found that (1) host traits covaried according to a prominent HDT axis, the slow-quick continuum; (2) infection caused a greater reduction in the performance of quick returns, with 180% of that greater impact explained by lesser resistance; (3) resistance-tolerance trade-off did not occur; and (4) phylogenetic control was necessary to measure the slow-quick continuum, resistance, and tolerance. These results support the conclusion that HDT's main influence on host contributions to transmission is via resistance. More broadly, this study provides a framework for quantifying HDT's influence on host contributions to transmission.

We sought to determine the contribution of scaffold topography to the migration and morphology of neural stem cells by mimicking anatomical features of scaffolds found in vivo. We mimicked two types of central nervous system scaffolds encountered by neural stem cells during development in vitro by constructing different diameter electrospun polycaprolactone (PCL) fiber mats, a substrate that we have shown to be topographically similar to brain scaffolds. We compared the effects of large fibers (made to mimic blood vessel topography) with those of small-diameter fibers (made to mimic radial glial process topography) on the migration and differentiation of neural stem cells. Neural stem cells showed differential migratory and morphological reactions with laminin in different topographical contexts. We demonstrate, for the first time, that neural stem cell biological responses to laminin are dependent on topographical context. Large-fiber topography without laminin prevented cell migration, which was partially reversed by treatment with rock inhibitor. Cell morphology complexity assayed by fractal dimension was inhibited in nocodazole- and cytochalasin-D-treated neural precursor cells in large-fiber topography, but was not changed in small-fiber topography with these inhibitors. These data indicate that cell morphology has different requirements on cytoskeletal proteins dependent on the topographical environment encountered by the cell. We propose that the physical structure of distinct scaffolds induces unique signaling cascades that regulate migration and morphology in embryonic neural precursor cells. J. Comp. Neurol. 524:3485-3502, 2016. © 2016 Wiley Periodicals, Inc.