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United States Department of Agriculture

Agricultural Research Service

Research Project: IMPROVING SOIL AND NUTRIENT MANAGEMENT SYSTEMS FOR SUSTAINED PRODUCTIVITY AND ENVIRONMENTAL QUALITY

Location: Soil Plant Nutrient Research (SPNR)

Title: Photosynthesis Declines in Phyrophthora ramorum-Infected Plants Develop Prior to Water Stree and in Response to Exogenous Application of Elicitins

Authors
item MANTER, DANIEL
item Kelsey, R - USDA FS, CORVALLIS, OR
item Karchesy, J - OSU, CORVALLIS, OR

Submitted to: Phytopathology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: January 26, 2007
Publication Date: June 25, 2007
Citation: Manter, D.K., Kelsey, R.G., Karchesy, J.J. 2007. Isolation, characterization and biological activity of phytophthora ramorum elicitins in compatible and incompatible hosts. Journal of Phytopathology. 97:850-856.

Interpretive Summary: Phytophthora ramorum the causal agent of sudden oak death (SOD) is responsible for the widespread death of oaks in California and Oregon, and has the potential to infect up to 70 different plant species. Depending upon the host species, symptoms of SOD range from stem girdling, shoot blight, and leaf spotting. The research presented here focuses on the identification, purification, and role that elicitin proteins play in the development of SOD. In this work we have shown that elicitins are important fungal-derived signals that contribute to the development of SOD. In some hosts, elicitins may trigger host defense responses that are sufficient to limit fungal colonization and growth; whereas, in others, responses may lead to physiological impairments, reducing growth, vigor and susceptibility to secondary pathogens. This is the first known report of elicitins contributing to the pathogenicity of a Phytophthora spp., resulting in a decline in photosynthesis distal to the infection site, and prior to the development of stem necrosis and plant water stress.

Technical Abstract: Phytophthora ramorum the causal agent of sudden oak death is responsible for the widespread death of oaks in California and Oregon, and has the potential to infect up to 70 different plant species, which exhibit varying forms of disease ranging from stem girdling, shoot blight, and leaf spotting. In this study, we first studied the physiological impacts of P. ramorum-infection on Rhododendron macrophyllum. In stem-inoculated plants, photosynthetic capacity (Vcmax) significantly declined by ca. 21% three weeks after inoculation in visibly asymptomatic leaves. By four weeks, after the development of significant stem lesions and a loss in water transport capacity, water stress led to stomatal closure and additional declines in photosynthetic capacity. Here we also report the isolation, characterization and biological activity of two P. ramorum elicitins. Both elicitins were capable of generating the hypersensitive response (HR) in the incompatible host (Nicotiana tabacum), and a more limited HR was observed in three compatible host species (R. macrophyllum, Lithocarpus densiflorus, and Umbellaria californica). Infiltration of leaves from all three compatible hosts with both P. ramorum elicitins caused significant declines in photosynthesis capacity (Fv/Fm, or efficiency of open PSII centers). For all four species, the loss of photosynthetic capacity was directly proportional to the HR, as determined by ethylene production. This is the first known report of elicitins contributing to the pathogenicity of a Phytophthora spp., resulting in a decline in photosynthesis distal to the infection site, and prior to the development of stem necrosis and plant water stress.

Last Modified: 7/25/2014
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