Our Research

How do species intensely competing for the same resources coexist in diverse communities?

Disease carries negative connotations. In agriculture, disease can mean the loss of food and revenue. However, in species-rich forests, pathogens can promote the overall health of the forest by preventing any single tree species from monopolizing limited resources and becoming overly abundant, leading to the loss of other tree species with key ecosystem roles. Importantly, in this self-reinforcing system, the spread of disease is limited, and epidemics are avoided by the very plant diversity pathogens are maintaining. Currently, we have an incomplete understanding of fungal pathogens in tropical forests and their interactions with plants, despite their ubiquity and ecological and economical importance. This hinders our ability to detect and predict the impacts of exotic fungi, reductions in tree diversity in human-modified landscapes, and plant-microbe responses to a changing climate.

What happens when a rainforest tree dies? A lot: precious resources are released for other plants and new resources are created for wildlife, the act of falling crushes other nearby trees, and biomass turns to necromass. Stem breakage and uprooting account for almost half of tree deaths and these chronic sources of mortality often occur when a tree has extensive internal decay (heart rot) caused by fungi. In collaboration with STRI Research Associates (E. Gora, Cary Institute; G. Gilbert, UC Santa Cruz), we will use sonic and electric resistance tomography to look inside trees to quantify decay. We will connect the internal and external health of the tree with historic damage (e.g., lightning strikes), tree growth and mortality, and ultimately forest dynamics and carbon sequestration.

Plants evolve to defend themselves against the phytopathogens evolving to infect them. Yet there is a mismatch between the generation times, population sizes, and modes of genetic exchange for pathogenic fungi and oomycetes versus long-lived trees. Additionally, under some conditions, defenses against phytopathogens have costs that may exceed the benefit for plants. To explore the complex and nuanced nature of the co-evolutionary arms race between plants and phytopathogens, this project is focused on the charismatic tropical tree Virola nobilis ( = surinamensis). It explores the genotypic basis for variation in susceptibility to infection and pathogen transmission rates and whether root microbiomes are shaped by allelic diversity (collaborators: J. Wright & H. Capador, STRI; J. Marden, Pennsylvania State Univ; K. Broders, USDA).

What is the role of multi-host pathogens in the maintenance of tropical forest diversity?

Pathogens exhibit a continuum of specificities. Some infect across host families and orders (generalists), others are limited to specific host species or genotypes (specialists). For free-living, dispersal-limited pathogens inhabiting species-rich host communities, selection should favor an ability to infect a variety of unrelated hosts. Indeed, many seedling pathogens in Panama’s diverse lowland forests exhibit host generalism. Yet, on local scales, analyses of spatial and temporal patterns suggest host-specific pathogens are limiting the abundance of a given species. How do we reconcile these findings?  We are exploring non-mutually exclusive mechanisms by which multi-host pathogens could produce the patterns attributed to host-specific pathogens. Our lab is also interested in the factors dictating the host range of plant-associated pathogens in hyperdiverse tropical forests.

This project, led by Postdoctoral Researcher Dale Forrister, explores the role of plant chemistry in the host range and host-specific impacts of multi-host pathogens. This project includes the characterization of phytochemicals and bioassays measuring the anti-fungal activity (growth inhibition) of seedling crude extracts on confirmed seedling pathogens.

What factors exclude certain species from otherwise suitable habitats?

Disease varies across environmental gradients that impact pathogen and plant fitness. Tree species adapted to environments with elevated disease pressure are under selection to invest in disease-resistance and tolerance traits, despite the costs of those traits. Conversely, the fitness costs of defenses outweigh the benefits for tree species adapted to environments with reduced disease pressure. Consequently, poorly defended, disease-sensitive tree species can be excluded from disease-prone areas while well-defended, disease-tolerant species can persist. We are exploring disease gradients and interspecific variability in disease susceptibility to evaluate the role of microorganisms in the spatial turnover of tree species and, thereby, the maintenance of local and regional forest diversity.

How are microorganisms distributed across space and time, and what are the constraints?

We are testing five interlinked hypotheses: (1) fungal pathogen communities are diverse and differences in diversity across geographic space are driven by abiotic factors, and are largely independent of plant community diversity. The majority of pathogens are: (2) host generalized and (3) relatively geographically widespread, but (4) their relative abundances are spatially and temporally variable. (5) A given pathogen’s spatial distribution and abundance are decoupled from the presence of a single host species. To do this, we use a combination of culturing, metabarcoding, and other molecular diagnostic techniques to identify plant-associated fungi, particularly pathogens, and to describe their spatial and temporal distributions, and host associations.

Utilizing STRI’s Parque Natural Metropolitano canopy access crane, this multifaceted project (a) assesses whether and which adult trees are reservoirs of disease for understory juveniles; (b) identifies key dispersal mechanisms of micro-fungi; (c) explores the spatial turnover of microbial communities across vertical abiotic gradients that exist from forest floor to canopy; and (d) determines whether a disease gradient is correlated with vertical abiotic gradients. There is a marked temperature gradient from the forest floor to the canopy, with leaves in the canopy sometimes reaching 48°C (118.4°F). That vertical temperature gradient is a proxy for global warming and shifts in plant-pathogen interactions across this gradient will provide important insight for disease dynamics in the warming world. Furthermore, the fungi inhabiting leaves in the forest canopy can survive temperatures well above human body temperatures (37°C, 98.6°F) and they may be a window into future human health crises. Globally, fungal infections kill more people annually than malaria and human fungal infections are on the rise. Yet, most fungi currently cannot survive and cause disease in humans in part because of our high body temperature. By comparing understory and canopy fungi, we will gain insight into fungal evolution for thermal tolerance and increased disease-causing potential.

Seedling survival is a determinant of tropical forest biodiversity and community composition. Individuals that survive germination and the first year of life are most likely to persist. Fungal pathogens and wet-season dry spells are leading drivers of seedling mortality, sometimes acting synergistically. As the wet season shortens and/or is punctuated by more frequent and longer dry spells due to climate change, finer-scale data on shorter-term changes in seedling populations are increasingly informative for long-term recruitment studies. Similarly, intra- and inter-seasonal turnover of pathogen communities are understudied. In this project (led by intern Blaine Martin on Barro Colorado Island), we are tracking Anacardium excelsum seedling density and culturing foliar fungal pathogens over the course of a year and across the wet and dry seasons.

What makes a pathogen a pathogen?

Symbiotic relationships are omnipresent. Yet, we are just beginning to understand and characterize the nuanced nature of these relationships, particularly in tropical forests. Symbioses represent a continuum, from beneficial to detrimental for the host. Moreover, these relationships are not fixed in time and space, they are highly context dependent. A commensal microbe can become pathogenic when a plant’s health or nutritional status changes and plant-microbe mutualisms can fracture when a partner cheats. Moreover, a pathogen can actually benefit a host plant if the pathogen does more harm to the host plant’s neighbors who are competing for the same resources (sensu the enemy of my enemy is my friend).