4.5 Article

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

期刊

MOLECULES AND CELLS
卷 34, 期 5, 页码 463-471

出版社

KOREAN SOC MOLECULAR & CELLULAR BIOLOGY
DOI: 10.1007/s10059-012-0213-0

关键词

nitric oxide (NO); nitric oxide synthase (NOS); plant defense signaling; reactive oxygen species; salicylic acid

资金

  1. Next-Generation BioGreen21 Program of the Rural Development Administration [PJ008025]
  2. World Class University Program [R32-10148]
  3. Ministry of Education, Science and Technology
  4. National Research Foundation of Korea (NRF)
  5. Ministry of Education, Science and Technology, Republic of Korea [2010-0009092]
  6. National Research Foundation of Korea [2010-0009092] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)

向作者/读者索取更多资源

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.

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