First author: United States Department of Agriculture (USDA) Agricultural Research Service, Ft. Collins, CO, 80526; second author: USDA Forest Service, Pacific Northwest Research Station, Corvallis, OR 97331; and third author: Oregon State University, Wood Science and Engineering Department, Corvallis 97331.
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Accepted for publication 26 January 2007.
Phytophthora ramorum, causal agent of sudden oak death, is responsible for widespread oak mortality in California and Oregon, and has the potential to infect 100 or more species. Symptoms range from stem girdling and shoot blight to leaf spotting. In this study, we examined the physiological impacts of P. ramorum infection on Rhododendron macrophyllum. In stem-inoculated plants, photosynthetic capacity (Vcmax) significantly declined by ≈21% 3 weeks after inoculation in visibly asymptomatic leaves. By 4 weeks, after the development of significant stem lesions and loss in water transport capacity, water stress led to stomatal closure and additional declines in photosynthetic capacity. We also report the isolation, characterization, and biological activity of two P. ramorum elicitins. Both elicitins were capable of inducing a hypersensitive-like response in one incompatible (Nicotiana tabacum SR1) and three compatible hosts (R. macrophyllum, Lithocarpus densiflorus, and Umbellularia californica). Infiltration of leaves from all three compatible hosts with both P. ramorum elicitins caused significant declines in chlorophyll fluorescence (Fv /Fm). For all four species, the loss of photosynthetic capacity was directly proportional to H+ uptake and ethylene production, two common components of the hypersensitive response. This is the first report of elicitins causing photosynthetic declines in compatible hosts independent of plant water stress.
The American Phytopathological Society, 2007