Constitutive expression of mammalian nitric oxide synthase in tobacco plants triggers disease resistance to pathogens

被引:43
作者
Chun, Hyun Jin [1 ]
Park, Hyeong Cheol [1 ]
Koo, Sung Cheol [2 ]
Lee, Ju Huck [1 ]
Park, Chan Young [1 ]
Choi, Man Soo [2 ]
Kang, Chang Ho [1 ]
Baek, Dongwon [1 ]
Cheong, Yong Hwa [3 ]
Yun, Dae-Jin [1 ]
Chung, Woo Sik [1 ]
Cho, Moo Je [1 ]
Kim, Min Chul [1 ]
机构
[1] Gyeongsang Natl Univ, Div Appl Life Sci, Brain Korea Program 21, Plant Mol Biol & Biotechnol Res Ctr, Jinju 660701, South Korea
[2] Rural Dev Adm, Natl Inst Crop Sci, Suwon 441857, South Korea
[3] Sunchon Natl Univ, Dept Bioenvironm Sci, Sunchon 550742, South Korea
基金
新加坡国家研究基金会;
关键词
nitric oxide (NO); nitric oxide synthase (NOS); plant defense signaling; reactive oxygen species; salicylic acid; SALICYLIC-ACID; CELL-DEATH; ARABIDOPSIS; NO; SIGNAL; H2O2; IDENTIFICATION; LOCALIZATION; ACCUMULATION; INHIBITION;
D O I
10.1007/s10059-012-0213-0
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Nitric oxide (NO) is known for its role in the activation of plant defense responses. To examine the involvement and mode of action of NO in plant defense responses, we introduced calmodulin-dependent mammalian neuronal nitric oxide synthase (nNOS), which controls the CaMV35S promoter, into wild-type and NahG tobacco plants. Constitutive expression of nNOS led to NO production and triggered spontaneous induction of leaf lesions. Transgenic plants accumulated high amounts of H2O2, with catalase activity lower than that in the wild type. nNOS transgenic plants contained high levels of salicylic acid (SA), and they induced an array of SA-, jasmonic acid (JA)-, and/or ethylene (ET)-related genes. Consequently, NahG co-expression blocked the induction of systemic acquired resistance (SAR)-associated genes in transgenic plants, implying SA is involved in NO-mediated induction of SAR genes. The transgenic plants exhibited enhanced resistance to a spectrum of pathogens, including bacteria, fungi, and viruses. Our results suggest a highly ranked regulatory role for NO in SA-, JA-, and/or ET-dependent pathways that lead to disease resistance.
引用
收藏
页码:463 / 471
页数:9
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