Pre-activating wounding response in tobacco prior to high-level ozone exposure prevents necrotic injury.
Pre-activating wounding response in tobacco prior to high-level ozone exposure prevents necrotic injury.
复制标题
在暴露于高水平臭氧之前预先激活烟草的损伤反应可以防止坏死性损伤。
DOI：
--
复制
发表时间：
1997
期刊：
影响因子：
--
通讯作者：
Brian E. Ellis
中科院分区：
文献类型：
--
作者：
B. L. Örvar;Joan Mcpherson;Brian E. Ellis
在烟草中，在组织暴露于高浓度臭氧（250至500 p.p.b.）之前，大大减少了对臭氧层的伤害。一个系统的模式，增加臭氧耐受性开发后3-6小时内受伤，也局部应用茉莉酸酯。臭氧处理转基因（NahG）烟草植物表明，这些植物不能积累水杨酸也伴随着增加臭氧耐受性。编码抗氧化酶抗坏血酸过氧化物酶的mRNA的表达上调臭氧的挑战，创伤和茉莉酸甲酯曝光在3-4小时内，而碳酸酐酶mRNA的水平同时抑制臭氧曝光和茉莉酸甲酯治疗。这些结果的模式表明，烟草对臭氧挑战的反应涉及类似于在植物中由其他产生活性氧的环境胁迫诱导的信号传导机制。
In tobacco, both wounding and treatment with jasmonates prior to exposure of the tissue to high concentrations of ozone (250 to 500 p.p.b.) produce a dramatic decrease in ozone injury. A systemic pattern of increased ozone tolerance developed within 3-6 h after wounding and also after local application of jasmonates. Ozone treatment of transgenic (NahG) tobacco plants showed that the inability of these plants to accumulate salicylic acid is also accompanied by increased ozone tolerance. Expression of mRNA encoding the anti-oxidant enzyme ascorbate peroxidase is upregulated by ozone challenge, wounding and by methyl jasmonate exposure within 3-4 h, while levels of carbonic anhydrase mRNA are simultaneously depressed following ozone exposure and methyl jasmonate treatment. The pattern of these results shows that the response to ozone challenge in tobacco involves signalling mechanisms similar to those induced in plants by other environmental stresses that generate reactive oxygen species.