First published online March 23, 2007; 10.1104/pp.107.095596
Plant Physiology 144:367-379 (2007)
© 2007 American Society of Plant Biologists
PLANTS INTERACTING WITH OTHER ORGANISMS
Resistance to Botrytis cinerea Induced in Arabidopsis by Elicitors Is Independent of Salicylic Acid, Ethylene, or Jasmonate Signaling But Requires PHYTOALEXIN DEFICIENT31,[W]
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, 23–35020 Legnaro, Italy (S.F.); Department of Genetics, Harvard Medical School, and Department of Molecular Biology, Massachusetts General Hospital, Boston, Massachusetts 02114 (C.D., F.M.A., J.D.); and Dipartimento di Biologia Vegetale, Università di Roma La Sapienza, 00185 Rome, Italy (R.G., G.D.L.)
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.
1 This work was supported by the Giovanni Armenise-Harvard Foundation, the Institute Pasteur-Fondazione Cenci Bolognetti, by Ministero dell'Università e della Ricerca Fondo per gli Investimenti della Ricerca di Base 2001 and Cofinanziamento 2002 grants awarded to G.D.L., by the European Union (grant no. 23044 "Nutra-Snacks" to S.F.), and by the National Science Foundation (grant no. DBI–0114783 to F.M.A.) and the National Institutes of Health (grant no. GM48707 to F.M.A.).
The author responsible for distribution of materials integral to the findings presented in this article in accordance with the policy described in the Instructions for Authors (www.plantphysiol.org) is: Simone Ferrari (simone.ferrari{at}unipd.it).
[W] The online version of this article contains Web-only data.
www.plantphysiol.org/cgi/doi/10.1104/pp.107.095596
* Corresponding author; e-mail simone.ferrari{at}unipd.it; fax 39–049–8272890.
Received January 8, 2007;
accepted March 20, 2007;
published March 23, 2007.
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