|Bocsanczy, Ana - Mid Florida Research & Education Center|
|Dardick, Christopher - Chris|
|Korban, Schuyler - University Of Illinois|
Submitted to: Acta Horticulturae
Publication Type: Proceedings
Publication Acceptance Date: 6/30/2010
Publication Date: N/A
Technical Abstract: Infiltration of Erwinia amylovora (Ea) into host leaves induces an oxidative burst similar to that observed during incompatible reactions associated with Hypersensitive Response (HR). However, the subsequent progressive development of necrosis in apple and other hosts is unlike an incompatible reaction. Type III secretion system (T3SS) hrp genes and effector DspA/E are necessary for disease and eliciting the HR-like response in apple. To understand the mechanism of disease establishment, we first compared apple’s response to challenges by Ea and the incompatible pathogen, Pseudomonas syringae pv. syringae strain B86-6 (Pss). In a second experiment, we compared apple’s response to Ea, a T3SS and a DspA/E mutant. To identify the transciptome, we used a two-channel, printed Malus microarray that contains 39,412 long-oligonucleotide (70-mer) probes designed to non-redundant Malus EST contigs (unigenes) obtained from different tissues, genotypes, developmental stages and stress conditions. Leaf tissues were harvested from shoots of fire blight susceptible ‘Malling 26’ apple rootstock 6 h post-inoculation with either phosphate buffer (Mock), virulent Ea strain Ea273, Pss, or Ea mutants. Several protocols were tested to optimize transcript labeling and microarray hybridization. Differentially expressed genes were identified using two interconnected mixed linear models for normalization of array data and determination of gene effects. A total of 430 apple genes responded similarly to both compatible and incompatible interactions. Approximately 24% 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 MAMP-trigger immunity, 39 genes associated with specific responses to T3 effectors of Ea, and 6 genes associated with DspA/E-specific responses which seem to be good candidates for further studies.