Overmyer Kirk, Brosché Mikael, Pellinen Riikka, Kuittinen Tero, Tuominen Hannele, Ahlfors Reetta, Keinänen Markku, Saarma Mart, Scheel Dierk, Kangasjärvi Jaakko
Department of Biological and Environmental Sciences , University of Helsinki, FIN-00014 Helsinki, Finland.
Plant Physiol. 2005 Mar;137(3):1092-104. doi: 10.1104/pp.104.055681. Epub 2005 Feb 22.
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, Ca(2+) 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).
大气污染物臭氧（O₃）短时间、高浓度的峰值会导致敏感植物叶片上出现细胞死亡损伤。植物对O₃和病原体的反应存在许多相似之处，这表明O₃会引发类似过敏反应的程序性细胞死亡（PCD）。我们研究了O₃敏感的自由基诱导细胞死亡1（rcd1）突变体中O₃和超氧化物诱导的细胞死亡。暴露于O₃的rcd1中的垂死细胞表现出过敏反应和PCD的一些典型形态特征。双突变分析表明，细胞死亡需要水杨酸和环核苷酸门控离子通道AtCNGC2的功能。此外，还表明rcd1中细胞死亡损伤的发展需要ATP酶、激酶、转录、Ca²⁺通量、类半胱天冬酶蛋白水解活性，以及一种或多种苯甲基磺酰氟敏感的蛋白酶活性。此外，丝裂原活化蛋白激酶在rcd1和哥伦比亚品种中表现出不同的激活模式。综上所述，这些结果直接证明了O₃可诱导PCD。
