Deficiencies in Jasmonate-Mediated Plant Defense Reveal Quantitative Variation in Botrytis cinerea Pathogenesis

• DOI: 10.1371/journal.ppat.1000861
• Publication Date: 2010-04-15T19:50:41Z
• Authors: Heather C. Rowe; Justin W. Walley; Jason Corwin; Eva K.-F. Chan; Katayoon Dehesh; Daniel J. Klieben...
• Keywords: 570; Indoles; QH301-705.5; Immunology; Arabidopsis; Plant Biology; Gene Expression; Cyclopentanes; Microbiology; Host-Parasite Interactions; 03 medical and health sciences; Gene Expression Regulation, Plant; Virology; 2.1 Biological and endogenous factors; Oxylipins; Aetiology; Biology (General); Plant Diseases; 2. Zero hunger; 0303 health sciences; Biomedical and Clinical Sciences; Arabidopsis Proteins; Reverse Transcriptase Polymerase Chain Reaction; Gene Expression Profiling; Plant; Biological Sciences; Medical microbiology; RC581-607; Thiazoles; Infectious Diseases; Phenotype; Gene Expression Regulation; Mycoses; Medical Microbiology; Botrytis; Immunologic diseases. Allergy; Infection; Research Article; Signal Transduction

Despite the described central role of jasmonate signaling in plant defense against necrotrophic pathogens, the existence of intraspecific variation in pathogen capacity to activate or evade plant jasmonate-mediated defenses is rarely considered. Experimental infection of jasmonate-deficient and jasmonate-insensitive Arabidopsis thaliana with diverse isolates of the necrotrophic fungal pathogen Botrytis cinerea revealed pathogen variation for virulence inhibition by jasmonate-mediated plant defenses and induction of plant defense metabolites. Comparison of the transcriptional effects of infection by two distinct B. cinerea isolates showed only minor differences in transcriptional responses of wild-type plants, but notable isolate-specific transcript differences in jasmonate-insensitive plants. These transcriptional differences suggest B. cinerea activation of plant defenses that require plant jasmonate signaling for activity in response to only one of the two B. cinerea isolates tested. Thus, similar infection phenotypes observed in wild-type plants result from different signaling interactions with the plant that are likely integrated by jasmonate signaling.