This Article Full Text Full Text (PDF) Supplemental Data All Versions of this Article: 151/3/1459    most recent pp.109.141994v1 Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via CrossRef Google Scholar Articles by Pogány, M. Articles by Durner, J. PubMed PubMed Citation Articles by Pogány, M. Articles by Durner, J. Agricola Articles by Pogány, M. Articles by Durner, J.

PLANTS INTERACTING WITH OTHER ORGANISMS

Dual Roles of Reactive Oxygen Species and NADPH Oxidase RBOHD in an Arabidopsis-Alternaria Pathosystem^1,[W]

Institute of Biochemical Plant Pathology, Helmholtz Zentrum München, German Research Center for Environmental Health, 85764 Munich/Neuherberg, Germany (M.P., U.v.R., S.G., G.B., J.D.); Plant Protection Institute, Hungarian Academy of Sciences, 1022 Budapest, Hungary (M.P., A.P., L.K., B.B.); and IFR 149 QUASAV, UMR PaVé A77, F–49045 Angers cedex, France (A.D., P.S.)

Arabidopsis (Arabidopsis thaliana) NADPH oxidases have been reported to suppress the spread of pathogen- and salicylic acid-induced cell death. Here, we present dual roles of RBOHD (for respiratory burst oxidase homolog D) in an Arabidopsis-Alternaria pathosystem, suggesting either initiation or prevention of cell death dependent on the distance from pathogen attack. Our data demonstrate that a rbohD knockout mutant exhibits increased spread of cell death at the macroscopic level upon inoculation with the fungus Alternaria brassicicola. However, the cellular patterns of reactive oxygen species accumulation and cell death are fundamentally different in the AtrbohD mutant compared with the wild type. Functional RBOHD causes marked extracellular hydrogen peroxide accumulation as well as cell death in distinct, single cells of A. brassicicola-infected wild-type plants. This single cell response is missing in the AtrbohD mutant, where infection triggers spreading-type necrosis preceded by less distinct chloroplastic hydrogen peroxide accumulation in large clusters of cells. While the salicylic acid analog benzothiadiazole induces the action of RBOHD and the development of cell death in infected tissues, the ethylene inhibitor aminoethoxyvinylglycine inhibits cell death, indicating that both salicylic acid and ethylene positively regulate RBOHD and cell death. Moreover, A. brassicicola-infected AtrbohD plants hyperaccumulate ethylene and free salicylic acid compared with the wild type, suggesting negative feedback regulation of salicylic acid and ethylene by RBOHD. We propose that functional RBOHD triggers death in cells that are damaged by fungal infection but simultaneously inhibits death in neighboring cells through the suppression of free salicylic acid and ethylene levels.

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: Jörg Durner (durner{at}helmholtz-muenchen.de).

^[W] The online version of this article contains Web-only data.

www.plantphysiol.org/cgi/doi/10.1104/pp.109.141994

^* Corresponding author; e-mail durner{at}helmholtz-muenchen.de.

Received May 24, 2009; accepted August 28, 2009; published September 2, 2009.