Characterization of the early response of the orchid, Phalaenopsis amabilis, to Erwinia chrysanthemi infection using expression profiling
2012
Fu, Shih‐Feng | Tsai, Tsung‐Mu | Chen, Ying‐Ru | Liu, Ching‐Pei | Haiso, Lin‐June | Syue, Li‐Hsin | Yeh, Hsin‐Hung | Huang, Hao‐Jen
Erwinia chrysanthemi is a devastating bacterial pathogen in Phalaenopsis amabilis and causes soft‐rotting disease by secretion of cell wall‐degrading enzymes. However, the molecular mechanisms underlying the interaction of P. amabilis with E. chrysanthemi remain elusive. In this study, early molecular events of the plant in response to the pathogen attack were investigated. The alteration in reactive oxygen species accumulation and peroxidase activity occurred at the site of infection. Subsequently, a systematic sequencing of expressed sequence tags (ESTs) using suppression subtractive hybridization (SSH) was performed to obtain the first global picture of the assembly of genes involved in the pathogenesis. The majority of the SSH clones showed a high identity with genes coding for proteins that have known roles in redox homeostasis, responses to pathogens and metabolism. A notable number of the SSH clones were those encoding WRKY, MYB and basic leucine zipper transcription factors, indicating the stimulation of intracellular signal transduction. An orchid gene encoding trans‐2‐enoyl‐CoA reductase (ECR) was the most abundant transcripts in the EST library. ECR is an enzyme catalyzing the very long chain fatty acids (VLCFAs) biosynthesis, and the full‐length cDNA of the ECR gene (PaECR1) was obtained. Functional analysis of PaECR1 was conducted by virus‐induced gene silencing to knock down the gene expression in P. amabilis. The PaECR1‐silenced plants were more susceptible to E. chrysanthemi infection, implying potential roles for VLCFAs in the pathogenesis. In summary, the pathogen‐responsive gene expression profiles facilitated a more comprehensive view of the molecular events that underlie this economically important plant–pathogen interaction.
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