|Abstract or Summary
- Phytophthora ramorum, an oomycete plant pathogen, is the causal agent of sudden oak death, a serious disease of Fagaceous trees in California and Oregon over the last decade. Tanoak (Notholithocarpus densiflorus) is one of the most susceptible host species, but the cause of host mortality is poorly understood. Previous research has implicated disruption in stem water transport, phloem girdling, and activity of a class of secreted proteins known as elicitins as possible mechanisms of pathogenesis.
In this study I investigated certain physiological impacts of P. ramorum infection on tanoak saplings and tanoak seedlings. In growth chamber experiments, stems of plants were inoculated with isolates that differed in the amount of elicitin secreted in vitro. Stem-wounded, non-inoculated plants served as controls. Parameters measured included net photosynthetic rate, stomatal conductance, whole plant water usage, stem specific hydraulic conductivity, tylosis production, starch partitioning, and mortality.
Inoculated saplings exhibited a reduction in whole plant water usage, followed by a reduction in stem specific hydraulic conductivity implicating an interruption in stem water transport as the primary symptom. A reduction in net photosynthetic rate and stomatal conductance occurred one week later. Experiments conducted on inoculated tanoak seedlings supported the hypothesis that a reduction in stem water transport is the primary disease symptom. Stem specific hydraulic conductivity was the only parameter that appeared to be significantly impacted when treatments were compared during each measurement period. There was, however, a significant difference between treatments over the course of the entire experiment. Due to differences in isolate growth rates and similar levels of elicitin secretion, symptom expression could not be tied to elicitin production. To determine where elicitins are produced in planta, an immunolabeling technique was tested utilizing an elicitin-specific fluorescent antibody. The elicitin protein was most apparent in paratracheal parenchyma cells, although nonspecific staining in control samples confounded interpretation.