237 Apple (Malus  domestica) Transcriptome in Response to the Compatible Pathogen Erwinia amylovora and the Incompatible Pathogen Pseudomonas syringae A.M. Bocsanczy a USDA-Agricultural Research Service (ARS) Kearneysville, WV USA J.G. Phillips USDA-ARS Wyndmoor, PA USA S.S. Korban Department of Natural Resources & Environmental Sciences University of Illinois at Urbana-Champaign Urbana, IL USA C.D. Dardick, C.L. Bassett, M.E. Wisniewski and J.L. Norelli USDA-ARS Kearneysville, WV USA Keywords: mRNA, microarray, expression profiles, defense responses, MAMPs, T3SS, MAMP-triggered immunity, effector triggered immunity 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 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 transcriptome, we used a two-channel, printed Malus microarray. 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. A total of 2430 differentially expressed genes were identified for the first experiment. Of those, 430 apple genes responded similarly to both compatible and incompatible interactions. In the second experiment 1332 differentially expressed genes were identified. Interesting subsets of genes potentially associated with MAMP-trigger immunity, and with responses to T3 effectors of Ea, including DspA/E-specific responses were further analyzed. INTRODUCTION Fire blight is a devastating disease of rosaceous plants. The disease has a severe impact on agricultural productivity worldwide, especially on apple (Malus  domestica) and pear (Pyrus communis) production. Fire blight is caused by the bacterial pathogen Erwinia amylovora (Ea), which enters the host plant through wounds or natural openings, preferentially blossoms, but also through other tissues, including rootstock crowns. The bacteria migrates through the plant via vascular tissues; and either cause cell necrosis and wilting, or can reside in symptomless tissue (Vanneste and Eden-Green, 2000). Pathogenesis by Ea is directly dependent on effector proteins which are thought to function as elicitors and suppressors of host defense (Chisholm et al., 2006), and by enzymes involved in synthesis of extracellular polysaccharides (Bernhard et al., 1993; Geider, 2000), however virulence also depends indirectly on factors that contribute to the pathogen fitness inside the host (Oh and Beer, 2005). Effectors are delivered by the Type a Current address: MREC/IFAS, University of Florida, Apopka, FL, USA Proc. 12 th Int. Workshop on Fire Blight Eds.: P. Sobiczewski et al. Acta Hort. 896, ISHS 2011