OXI1 kinase is necessary for oxidative burst-mediated signalling in Arabidopsis

Maike C. Rentel (), David Lecourieux, Fatma Ouaked, Sarah L. Usher, Lindsay Petersen, Haruko Okamoto, Heather Knight, Scott C. Peck, Claire S. Grierson, Heribert Hirt () and Marc R. Knight
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Maike C. Rentel: University of Oxford
David Lecourieux: Austrian Academy of Sciences, Vienna Biocenter
Fatma Ouaked: Austrian Academy of Sciences, Vienna Biocenter
Sarah L. Usher: University of Bristol
Lindsay Petersen: University of Oxford
Haruko Okamoto: University of Oxford
Heather Knight: University of Oxford
Scott C. Peck: Sainsbury Laboratory
Claire S. Grierson: University of Bristol
Heribert Hirt: Austrian Academy of Sciences, Vienna Biocenter
Marc R. Knight: University of Oxford

Nature, 2004, vol. 427, issue 6977, 858-861

Abstract: Abstract Active oxygen species (AOS) generated in response to stimuli and during development can function as signalling molecules in eukaryotes, leading to specific downstream responses1,2. In plants these include such diverse processes as coping with stress (for example pathogen attack3, wounding4 and oxygen deprivation5), abscisic-acid-induced guard-cell closure6, and cellular development (for example root hair growth7). Despite the importance of signalling via AOS in eukaryotes, little is known about the protein components operating downstream of AOS that mediate any of these processes. Here we show that expression of an Arabidopsis thaliana gene (OXI1) encoding a serine/threonine kinase is induced in response to a wide range of H2O2-generating stimuli. OXI1 kinase activity is itself also induced by H2O2 in vivo. OXI1 is required for full activation of the mitogen-activated protein kinases (MAPKs) MPK3 and MPK6 after treatment with AOS or elicitor and is necessary for at least two very different AOS-mediated processes: basal resistance to Peronospora parasitica infection, and root hair growth. Thus, OXI1 is an essential part of the signal transduction pathway linking oxidative burst signals to diverse downstream responses.

Date: 2004
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DOI: 10.1038/nature02353

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