Constitutive expression of mammalian nitric oxide synthase in tobacco plants triggers disease resistance to pathogens
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-typ...
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Published in | Molecules and cells Vol. 34; no. 5; pp. 463 - 471 |
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Main Authors | , , , , , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
Springer
Korean Society for Molecular and Cellular Biology
01.11.2012
Korea Society for Molecular and Cellular Biology 한국분자세포생물학회 |
Subjects | |
Online Access | Get full text |
ISSN | 1016-8478 0219-1032 |
DOI | 10.1007/s10059-012-0213-0 |
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Summary: | 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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Bibliography: | A50 2013001799 ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-1 content type line 14 These authors contributed equally to this work. G704-000079.2012.34.5.004 |
ISSN: | 1016-8478 0219-1032 |
DOI: | 10.1007/s10059-012-0213-0 |