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Published on February 22, 2005; 10.1104/pp.104.055681


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Received October 27, 2004
Returned for revision December 20, 2004
Accepted December 27, 2004

Ozone-Induced Programmed Cell Death in the Arabidopsis radical-induced cell death1 Mutant

Kirk Overmyer , Mikael Brosché , Riikka Pellinen , Tero Kuittinen , Hannele Tuominen , Reetta Ahlfors , Markku Keinänen , Mart Saarma , Dierk Scheel , and Jaakko Kangasjärvi *

Department of Biological and Environmental Sciences, University of Helsinki, FIN-00014 Helsinki, Finland; Institute of Biotechnology, University of Helsinki, FIN-00014 Helsinki, Finland
Department of Biological and Environmental Sciences, University of Helsinki, FIN-00014 Helsinki, Finland
Institute of Biotechnology, University of Helsinki, FIN-00014 Helsinki, Finland
Department of Stress and Developmental Biology, Leibniz Institute of Plant Biochemistry, D-06120 Halle/Saale, Germany

* Corresponding author; email: jaakko.kangasjarvi{at}helsinki.fi.

Short, high-concentration peaks of the atmospheric pollutant ozone (O3) cause the formation of cell death lesions on the leaves of sensitive plants. Numerous similarities between the plant responses to O3 and pathogens suggest that O3 triggers hypersensitive response-like programmed cell death (PCD). We examined O3 and superoxide-induced cell death in the O3-sensitive radical-induced cell death1 (rcd1) mutant. Dying cells in O3-exposed rcd1 exhibited several of the typical morphological characteristics of the hypersensitive response and PCD. Double-mutant analyses indicated a requirement for salicylic acid and the function of the cyclic nucleotide-gated ion channel AtCNGC2 in cell death. Furthermore, a requirement for ATPases, kinases, transcription, Ca2+ flux, caspase-like proteolytic activity, and also one or more phenylmethylsulfonyl fluoride-sensitive protease activities was shown for the development of cell death lesions in rcd1. Furthermore, mitogen-activated protein kinases showed differential activation patterns in rcd1 and Columbia. Taken together, these results directly demonstrate the induction of PCD by O3.




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