Minisymposium 26: Plant Pathogen Interactions

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Abs # M2601: Genetic and Genomic Approaches to Dissect Plant Defense Responses Mediated by Elicitors.

Presenter:	Ferrari, Simone       Contact Presenter
Authors	Ferrari, Simone  (A)   Denoux, Carine  (B)   Galletti, Roberta  (C)   Dewdney, Julia  (B)   Ausubel, Frederick M (B)   De Lorenzo, Giulia  (C)
Affiliations:	(A): Dipartimento Territorio e Sistemi Agroforestali, University of Padova, Legnaro, Italy (B): Department of Molecular Biology, Massachusetts General Hospital and Department of Genetics, Harvard Medical School, Boston, MA, USA (C): Dipartimento di Biologia Vegetale, University of Rome La Sapienza, Rome, Italy

Fungal pathogens secrete enzymes that selectively degrade structural polysaccharides of the plant cell wall. Among the first secreted enzymes are polygalacturonases (PGs), which hydrolyze the homogalacturonan component of pectin. The action of PGs releases oligogalacturonide fragments (OGs) in the apoplast of attacked plant cells. OGs with a degree of polymerization between 10 and 15 induce defense responses, including the accumulation of reactive oxygen species (ROS), phytoalexins and pathogenesis-related proteins, in several plant species. We have previously demonstrated that OGs can induce the expression of the Arabidopsis thaliana Polygalacturonase-Inhibiting Protein gene AtPGIP1 independently of the signaling molecules salicylic acid (SA), jasmonic acid (JA) or ethylene. In order to characterize the role of OGs in the plant innate immune response, we have undertaken a full-scale expression analysis of Arabidopsis genes that respond to OG treatments and found an extensive overlap with the expression profile of plants inoculated with the fungal pathogen Botrytis cinerea. Both treatments induce the expression of genes encoding enzymes potentially involved in the accumulation of antimicrobial compounds, including PAD3, which is required for the biosynthesis of the antifungal compound camalexin. We have previously shown that camalexin is an effective inhibitor of B. cinerea germination and growth, and that the pad3 mutant has enhanced susceptibility to this pathogen. Pre-treatments of Arabidopsis plants with OGs induce expression of PAD3 and resistance against B. cinerea infection independently of SA, JA or ethylene. In contrast, mutants affected in camalexin accumulation are not protected by OGs. We have also compared defense responses activated by OGs and by the bacterial elicitor flagellin and their ability to protect against B. cinerea. Our results suggest that endogenous elicitors released during fungal infection contribute to restrict pathogen growth independently of SA, JA or ethylene signaling.