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

机译:拟南芥自由基诱导的细胞死亡1突变体中臭氧诱导的程序性细胞死亡

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摘要

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.
机译:大气污染物臭氧(O-3)的短而高浓度的峰会在敏感植物的叶子上形成细胞死亡损伤。植物对O-3和病原体的反应之间的许多相似之处表明,O-3会触发超敏反应样程序性细胞死亡(PCD)。我们检查了O-3敏感自由基诱导的细胞死亡1(rcd1)突变体中的O-3和超氧化物诱导的细胞死亡。 O-3-暴露的rcd1中的垂死细胞表现出一些超敏反应和PCD的典型形态特征。双突变分析表明需要水杨酸和环状核苷酸门控离子通道AtCNGC2在细胞死亡中的功能。此外,对于rcd1中细胞死亡病变的发展,显示出需要ATPase,激酶,转录,Ca2 +通量,类似caspase的蛋白水解活性以及一种或多种对苯甲基磺酰氟敏感的蛋白酶活性。此外,有丝分裂原激活的蛋白激酶在rcd1和Columbia中显示出不同的激活模式。综上所述,这些结果直接证明了O-3对PCD的诱导。

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