Plant Physiology Preview
Published on March 23, 2007; 10.1104/pp.107.095596
Received January 8, 2007
Accepted March 20, 2007
Resistance to Botrytis Cinerea Induced in Arabidopsis by Elicitors Is Independent of Salicylic Acid, Ethylene or Jasmonate Signaling but Requires PAD3
Simone Ferrari *, Roberta Galletti , Carine Denoux , Giulia De Lorenzo , Frederick M. Ausubel , and Julia Dewdney
Dipartimento Territorio e Sistemi Agro-Forestali, Università degli Studi di Padova, c/o Agripolis, Viale dell'Università, 23 - 35020 Legnaro (PD), Italy; Department of Genetics, Harvard Medical School, and Department of Molecular Biology, Massachusetts General Hospital, Boston, MA 02114 USA; Dipartimento di Biologia Vegetale, Università di Roma "La Sapienza", Piazzale Aldo Moro 5, 00185 Rome, Italy
* Corresponding author; email: simone.ferrari{at}unipd.it.
Oligogalacturonides (OGs) released from plant cell walls by pathogen polygalacturonases induce a variety of host defense responses. Here we show that in 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 Deficient 3 (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, nor in ups1, 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.
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