SEED BANK PATHOGEN COMMUNITY ECOLOGY
Meyer, S.E.1, Allen, P.S.2 and Beckstead, J.3
1US Forest Service Rocky Mountain Research Station Shrub Sciences Laboratory, Provo, Utah, USA
2Department of Plant and Wildlife Sciences, Brigham Young University, Provo, Utah, USA
3Department of Biology, Gonzaga University, Spokane, Washington, USA
Contact: Susan E. Meyer, firstname.lastname@example.org
Wildland seed pathogens are a remarkably understudied group of organisms, with most studies using a ‘black box’ approach. We have used seeds of the winter annual grass Bromus tectorum (cheatgrass) as a model system to understand the community of fungal seedbank pathogens associated with cheatgrass seeds and their interactions with host seeds, environmental conditions, and each other, focusing specifically on how they share this common resource through niche partitioning. In this presentation we examine niche differentiation in two ascomycete pathogens common on cheatgrass seeds, Pyrenophora semeniperda and Fusarium cf. reticulatum. SEM studies have shown that the infection hyphae of P. semeniperda, which most often attacks dormant seeds, penetrate directly through the caryopsis wall and first grow into the endosperm. Fusarium responds to chemical stimuli released early in germination to initiate hyphal growth toward the point of radicle emergence, where it forms an infection cushion and penetrates the embryo of the germinating seed. It thus restricts its attack to nondormant seeds. Because these fungi can actively function at reduced water potentials that prevent radicle emergence, they are at an advantage under conditions of fluctuating water availability, increasing their ability to kill nondormant seeds. We successfully modeled P. semeniperda spore germination and mycelial growth using hydrothermal time to determine base temperatures and water potentials for these developmental processes. We also explored whether the wide variation in mycelial growth rate we observed in P. semeniperda might be related to strain specialization onto different subsets of the host seed population, a form of intraspecific niche partitioning. We found that slow-growing strains were better able to kill nondormant seeds at high inoculum loads and related this to their increased production of a seed-crippling phyotoxin, cytochalasin B. Fast-growing strains were better able to kill dormant seeds at low inoculum loads. We concluded that mycelial growth rate polymorphism was maintained through temporally varying selection, with slow-growing strains best adapted to attack nondormant seeds in the fall and more common fast-growing strains most successful on dormant seeds in the carry-over seed bank. This somewhat counter-intuitive result highlights the importance of mechanistic studies in a model system for understanding seed-pathogen interactions.