Class
Article
College
College of Science
Faculty Mentor
Noelle Beckman
Presentation Type
Oral Presentation
Abstract
Understanding the coexistence of a large number of species has long been one of the most fundamental questions in ecology. Several general hypotheses have been advanced, including, for example, niche differentiation, complexity of habitat, and the role of specialized predators and pathogens. The Janzen-Connell hypothesis was initially proposed to explain the unusually high diversity of tree species in tropical forest systems. This effect cumulates in a conspecific “Dead Zone” surrounding a parent tree due to species-specific seed predation and pathogenic infection. A ring of successful seedling establishment away from the crown of the parent tree can be expected, bounded on the outside by the maximum distance of seed dispersal. The “Dead Zone” can easily be colonized by other species, however, which promotes local species diversity. Spatial patterns of distance- and density-dependent mortality predicted by the Janzen-Connell hypothesis have been found in plant communities world-wide. Host-specific soilborne pathogens, specifically oomycetes, have been shown to play an important role in seedling establishment patterns around individual trees. This project aims to develop our understanding of how these patterns can arise from soilborne pathogens by development of a continuous multi-scale spatial simulation model. The model will employ empirically-derived functions and parameters that describe life histories of plants and pathogens, including seed and pathogen dispersal and infection. The results of these interactions will determine spatial arrangements for mature trees, which will in turn drive the next generation of seed dispersal and therefore pathogen mortality. We expect plant-pathogen interactions will drive the development of over-dispersed spatial patterns of trees at the population level. Results which reflect field data would indicate that our initial conditions and the structure of our model reflect the processes which govern real host-pathogen systems.
Location
Room 101
Start Date
4-12-2018 9:00 AM
End Date
4-12-2018 10:15 AM
The Influence of Soilborne Pathogens on Seedling Mortality
Room 101
Understanding the coexistence of a large number of species has long been one of the most fundamental questions in ecology. Several general hypotheses have been advanced, including, for example, niche differentiation, complexity of habitat, and the role of specialized predators and pathogens. The Janzen-Connell hypothesis was initially proposed to explain the unusually high diversity of tree species in tropical forest systems. This effect cumulates in a conspecific “Dead Zone” surrounding a parent tree due to species-specific seed predation and pathogenic infection. A ring of successful seedling establishment away from the crown of the parent tree can be expected, bounded on the outside by the maximum distance of seed dispersal. The “Dead Zone” can easily be colonized by other species, however, which promotes local species diversity. Spatial patterns of distance- and density-dependent mortality predicted by the Janzen-Connell hypothesis have been found in plant communities world-wide. Host-specific soilborne pathogens, specifically oomycetes, have been shown to play an important role in seedling establishment patterns around individual trees. This project aims to develop our understanding of how these patterns can arise from soilborne pathogens by development of a continuous multi-scale spatial simulation model. The model will employ empirically-derived functions and parameters that describe life histories of plants and pathogens, including seed and pathogen dispersal and infection. The results of these interactions will determine spatial arrangements for mature trees, which will in turn drive the next generation of seed dispersal and therefore pathogen mortality. We expect plant-pathogen interactions will drive the development of over-dispersed spatial patterns of trees at the population level. Results which reflect field data would indicate that our initial conditions and the structure of our model reflect the processes which govern real host-pathogen systems.