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The AtrbohD-Mediated Oxidative Burst Elicited by Oligogalacturonides in Arabidopsis Is Dispensable for
 

Summary: The AtrbohD-Mediated Oxidative Burst Elicited by
Oligogalacturonides in Arabidopsis Is Dispensable for
the Activation of Defense Responses Effective against
Botrytis cinerea1[W][OA]
Roberta Galletti, Carine Denoux, Stefano Gambetta, Julia Dewdney, Frederick M. Ausubel,
Giulia De Lorenzo, and Simone Ferrari*
Dipartimento di Biologia Vegetale, Universita` di Roma "La Sapienza," 500185 Rome, Italy (R.G., G.D.L., S.F.);
Dipartimento Territorio e Sistemi Agro-Forestali, Universita` degli Studi di Padova, 35020 Legnaro, Italy
(S.G.); and Department of Genetics, Harvard Medical School, and Department of Molecular Biology,
Massachusetts General Hospital, Boston, Massachusetts 02114 (C.D., J.D., F.M.A.)
Oligogalacturonides (OGs) are endogenous elicitors of defense responses released after partial degradation of pectin in the
plant cell wall. We have previously shown that, in Arabidopsis (Arabidopsis thaliana), OGs induce the expression of
PHYTOALEXIN DEFICIENT3 (PAD3) and increase resistance to the necrotrophic fungal pathogen Botrytis cinerea indepen-
dently of signaling pathways mediated by jasmonate, salicylic acid, and ethylene. Here, we illustrate that the rapid induction
of the expression of a variety of genes by OGs is also independent of salicylic acid, ethylene, and jasmonate. OGs elicit a robust
extracellular oxidative burst that is generated by the NADPH oxidase AtrbohD. This burst is not required for the expression of
OG-responsive genes or for OG-induced resistance to B. cinerea, whereas callose accumulation requires a functional AtrbohD.
OG-induced resistance to B. cinerea is also unaffected in powdery mildew resistant4, despite the fact that callose accumulation was
almost abolished in this mutant. These results indicate that the OG-induced oxidative burst is not required for the activation of
defense responses effective against B. cinerea, leaving open the question of the role of reactive oxygen species in elicitor-

  

Source: Ausubel, Frederick M. - Department of Genetics, Harvard University

 

Collections: Biology and Medicine