USING FUNCTIONAL AND APPLIED GENOMICS TO IMPROVE STRESS AND DISEASE RESISTANCE IN FRUIT TREES
Location: Appalachian Fruit Research Laboratory: Innovative Fruit Production, Improvement and Protection
Title: Analysis of apple (Malus) responses to bacterial pathogens using an oligo microarray
Submitted to: American Phytopathological Society Annual Meeting
Publication Type: Abstract Only
Publication Acceptance Date: May 1, 2009
Publication Date: June 1, 2009
Citation: Bocsanczy, A.M., Phillips, J.G., Dardick, C.D., Korban, S.S., Bassett, C.L., Wisniewski, M.E., Norelli, J.L. 2009. Analysis of apple (Malus) responses to bacterial pathogens using an oligo microarray. American Phytopathological Society Annual Meeting. Phytopathology 99:514.
Fire blight is a devastating disease of apple (Malus x domestica) caused by the bacterial pathogen Erwinia amylovora (Ea). When infiltrated into host leaves, Ea induces reactions similar to a hypersensitive response (HR). Type III (T3SS) associated effectors, especially DspA/E, are suspected to have a major role in eliciting the HR-type response in apple. To understand the mechanism of disease establishment, we first compared apple responses to challenges by Ea and the incompatible pathogen Pseudomonas syringae pv. syringae strain B86-6 (Pss). In a second experiment, we compared the responses to Ea, a T3SS and a DspA/E mutant. Gene expression profiles were accessed using a 39,412 long-oligo (70-mer) Malus microarray. Leaf tissue was harvested at 6 h.p.i. from apple shoots of susceptible 'Malling 26' rootstock inoculated with the different treatments. Several protocols were tested to optimize transcript labeling and microarray hybridization. A total of 430 apple genes responded similarly to both compatible and incompatible interactions. Approximately 24 percent of those genes coded for defense or stress related proteins, including Mal d 1, LRR-rich proteins, and dehydrins. In the second experiment, we identified a core of 80 genes associated with general responses (MAMP) to Ea, 320 genes associated with responses to T3 effectors of Ea, and 24 genes associated with DspA/E-specific responses. A detailed annotation of the genes identified in our study is in progress.