Ozone-induced programmed cell death in the Arabidopsis radical-induced cell death1 mutant

Short, high-concentration peaks of the atmospheric pollutant ozone (O-3) cause the formation of cell death lesions on the leaves of sensitive plants. Numerous similarities between the plant responses to O-3 and pathogens suggest that O-3 triggers hypersensitive response-like programmed cell death (PCD). We examined O-3 and superoxide-induced cell death in the O-3-sensitive radical-induced cell death1 (rcd1) mutant. Dying cells in O-3-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 O-3.