Resistance to Botrytis cinerea Induced in Arabidopsis by Elicitors Is Independent of Salicylic Acid, Ethylene, or Jasmonate Signaling But Requires PHYTOALEXIN DEFICIENT3

• Published in: Plant physiology (Bethesda) Vol. 144; no. 1; pp. 367 - 379
• Main Authors: Ferrari, Simone, Galletti, Roberta, Denoux, Carine, De Lorenzo, Giulia, Ausubel, Frederick M, Dewdney, Julia
• Format: Journal Article
• Language: English
• Published: United States American Society of Plant Biologists 01.05.2007
• Subjects: Arabidopsis - metabolism; Arabidopsis - microbiology; Arabidopsis Proteins - genetics; Arabidopsis Proteins - metabolism; Arabidopsis Proteins - physiology; Arabidopsis thaliana; Biosynthesis; Botrytis; Botrytis - physiology; Botrytis cinerea; Cyclopentanes - metabolism; Cytochrome P-450 Enzyme System - genetics; Cytochrome P-450 Enzyme System - metabolism; Cytochrome P-450 Enzyme System - physiology; Ethylenes - metabolism; Fungal infections; Gene Expression Regulation, Plant; Immunity, Innate - genetics; Infections; Inoculation; Leaves; Lesions; Mixed Function Oxygenases - genetics; Mixed Function Oxygenases - metabolism; Mixed Function Oxygenases - physiology; Mutation; Oxylipins; Pathogens; Plant Diseases - genetics; Plant Growth Regulators - metabolism; Plants; Plants Interacting with Other Organisms; Salicylates - metabolism; Seedlings; Signal Transduction
• ISSN: 0032-0889; 1532-2548; 1532-2548
• DOI: 10.1104/pp.107.095596

Oligogalacturonides (OGs) released from plant cell walls by pathogen polygalacturonases induce a variety of host defense responses. Here we show that in Arabidopsis (Arabidopsis thaliana), OGs increase resistance to the necrotrophic fungal pathogen Botrytis cinerea independently of jasmonate (JA)-, salicylic acid (SA)-, and ethylene (ET)-mediated signaling. Microarray analysis showed that about 50% of the genes regulated by OGs, including genes encoding enzymes involved in secondary metabolism, show a similar change of expression during B. cinerea infection. In particular, expression of PHYTOALEXIN DEFICIENT3 (PAD3) is strongly up-regulated by both OGs and infection independently of SA, JA, and ET. OG treatments do not enhance resistance to B. cinerea in the pad3 mutant or in underinducer after pathogen and stress1, a mutant with severely impaired PAD3 expression in response to OGs. Similarly to OGs, the bacterial flagellin peptide elicitor flg22 also enhanced resistance to B. cinerea in a PAD3-dependent manner, independently of SA, JA, and ET. This work suggests, therefore, that elicitors released from the cell wall during pathogen infection contribute to basal resistance against fungal pathogens through a signaling pathway also activated by pathogen-associated molecular pattern molecules.