Broadly, my research asks the following questions, with specific projects nested within these central themes:

• How do species intensely competing for the same resources coexist in diverse communities?
  • 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. Host-specific pathogens are credited with the maintenance of local diversity under the commonly invoked Janzen-Connell Hypothesis (JCH). The JCH assumes that (1) host-specific natural enemies, such as pathogens, promote coexistence by responding to host density and preventing the host from becoming overly abundant, and (2) that host-specific natural enemies accumulate near reproductive adults and reduce the survival of conspecific seeds and seedlings in close proximity, facilitating the establishment of heterospecifics. Empirical support for the assumptions of JCH is primarily based on spatial and temporal patterns of plant communities. We have an incomplete understanding of fungal pathogens in natural systems (e.g., richness, taxonomy, and distributions) and their interactions with plants (e.g. host ranges and host-specific impacts). To influence forest structure and dynamics, pathogens must differentially impact the survival and/or reproductive output of their host(s).
• What is the role of multi-host pathogens in the maintenance of tropical forest diversity?
  • Pathogens exhibit a continuum of specificities. For free-living, dispersal-limited pathogens inhabiting species-rich host communities, selection should favor the ability to infect a variety of unrelated hosts. Indeed, many phytopathogens in Panama’s diverse lowland forests exhibit host generalism. Yet, the widely cited Janzen-Connell Hypothesis (JCH) and plant community spatial and temporal patterns suggest host-specific pathogens are limiting the abundance of a given plant species. How do we reconcile these findings and theory?  My research explores non-mutually exclusive mechanisms by which multi-host pathogens could produce the patterns attributed to host-specific pathogens and maintain plant community diversity. I am also interested in the factors dictating the host range of plant-associated pathogens in hyperdiverse tropical forests.
• What factors exclude certain plant 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. I explore 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. My previous, ongoing, and planned research provide a fine-scale estimation of the taxonomy, diversity, host ranges and affinities, and spatial structure of tropical fungal pathogens of tropical trees at community-wide and trans-isthmian scales, addressing gaps in our knowledge of fungi in the understudied tropics.

Dr. Erin Spear has conducted research in the forests of Panama for the past 15 years and has been a permanent Staff Scientist at the Smithsonian Tropical Research Institute (STRI) in Panama since 2022. Her research intersects disease ecology (who gets sick from what, where, and why), mycology (the study of fungi), and community ecology (how different species and the environment interact and how those interactions shape a community).

Her lab, aptly called the DEATH Lab for its focus on tree disease and mortality, addresses two key questions in ecology: (1) How do multiple, competing species coexist in diverse communities (why doesn’t the best competitor win and the losers disappear?); and (2) What factors exclude certain species from otherwise suitable habitats? As STRI’s Forest Microbial Ecologist generously funded by the Simons Foundation, Dr. Spear is developing novel approaches for understanding the distributions of microorganisms across host plants, geographic space, and time to transform microbial research in tropical forests. She is also a passionate advocate for diversity, equity, and inclusion in ecology, reflected in her mentorship of a large, energetic team of early career scientists from around the world.

Previously, she received a Ph.D. in Biology from the University of Utah, served as a postdoctoral researcher at Stanford University, and was an assistant professor at Regis University in Denver, Colorado.

Article

• Spear, Erin R. and Broders, Kirk D. 2021. "Host-generalist fungal pathogens of seedlings may maintain forest diversity via host-specific impacts and differential susceptibility among tree species." New Phytologist, 231, (1) 460–474. https://doi.org/10.1111/nph.17379. 2021
• Farner, Johannah E., Spear, Erin R., and Mordecai, Erin A. 2020. "Habitat type and interannual variation shape unique fungal pathogen communities on a California native bunchgrass." Fungal Ecology, 48 100983–100983. https://doi.org/10.1016/j.funeco.2020.100983. 2020
• Kendig, Amy E., Spear, Erin R., Daws, S. Caroline, Flory, S. Luke, and Mordecai, Erin A. 2020. "Native perennial and non-native annual grasses shape pathogen community composition and disease severity in a California grassland." Journal of Ecology, https://doi.org/10.1111/1365-2745.13515. 2020
• Uricchio, Lawrence H., Daws, S. C., Spear, Erin R., and Mordecai, Erin A. 2019. "Priority Effects and Nonhierarchical Competition Shape Species Composition in a Complex Grassland Community." The American Naturalist, 193, (2) 213–226. https://doi.org/10.1086/701434. 2019
• Spear, Erin R. and Mordecai, Erin A. 2018. "Foliar pathogens are unlikely to stabilize coexistence of competing species in a California grassland." Ecology, 99, (10) 2250–2259. https://doi.org/10.1002/ecy.2427. 2018
• Spear, Erin R. 2017. "Phylogenetic relationships and spatial distributions of putative fungal pathogens of seedlings across a rainfall gradient in Panama." Fungal Ecology, 26 65–73. https://doi.org/10.1016/j.funeco.2016.12.004. 2017
• Spear, Erin R., Coley, Phyllis D., and Kursar, Thomas A. 2015. "Do pathogens limit the distributions of tropical trees across a rainfall gradient?" Journal of Ecology, 103, (1) 165–174. https://doi.org/10.1111/1365-2745.12339. 2015