ArticleProceedings of the National Academy of Sciences of the United States of America2001
Signal interactions between nitric oxide and reactive oxygen intermediates in the plant hypersensitive disease resistance response.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 267 papers.
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267 citing papers in PubMed, 1,068 citations in OpenAlex.
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- Redox Regulation of Plant-Root-Knot Nematode Interactions: From ROS-Mediated Immunity to Sustainable Resistance.Antioxidants (Basel, Switzerland) · 2026Review
- GSNOR is essential for nitric oxide homeostasis and involved in aflatoxin biosynthesis and pathogenicity inApplied and environmental microbiology · 2026Article
- Antioxidant Defense Strategies AgainstBiology · 2025Article
- Proteomic analysis of differential responses to norflurazon herbicide in the model green alga Chlamydomonas reinhardtii.Scientific reports · 2025Article
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- Genome-wide characterization of nitric oxide-induced NBS-LRR genes from Arabidopsis thaliana and their association in monocots and dicots.BMC plant biology · 2024Article
- HScience (New York, N.Y.) · 2024Article
- Antimicrobial Effects of Nitric Oxide against Plant Pathogens.ACS omega · 2024Article
- Antioxidant Systems of Plant Pathogenic Fungi: Functions in Oxidative Stress Response and Their Regulatory Mechanisms.The plant pathology journal · 2024Review
- Transcriptional Profiling of Early Defense Response to White Pine Blister Rust Infection inGenes · 2024Article
- CaSTH2 disables CaWRKY40 from activating pepper thermotolerance and immunity againstHorticulture research · 2024Article
- Involvement of oxidative stress in localization of bacterial spot infection in pepper plants.Journal of biosciences · 2024Article
- Plant cathepsin B, a versatile protease.Frontiers in plant science · 2024Review
- Identification of nitric oxide mediated defense signaling and its microRNA mediated regulation duringPhysiology and molecular biology of plants : an international journal of functional plant biology · 2024Article
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- Cytological and transcriptomic analysis to unveil the mechanism of web blotch resistance in Peanut.BMC plant biology · 2023Article
207 more citing papers are in PubMed but not listed here.
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Nitric oxide (NO) and reactive oxygen intermediates (ROIs) play key roles in the activation of disease resistance mechanisms both in animals and plants. In animals NO cooperates with ROIs to kill tumor cells and for macrophage killing of bacteria. Such cytotoxic events occur because unregulated NO levels drive a diffusion-limited reaction with O(2)(-) to generate peroxynitrite (ONOO(-)), a mediator of cellular injury in many biological systems. Here we show that in soybean cells unregulated NO production at the onset of a pathogen-induced hypersensitive response (HR) is not sufficient to activate hypersensitive cell death. The HR is triggered only by balanced production of NO and ROIs. Moreover, hypersensitive cell death is activated after interaction of NO not with O(2)- but with H(2)O(2) generated from O(2)(-) by superoxide dismutase. Increasing the level of O(2)(-) reduces NO-mediated toxicity, and ONOO(-) is not a mediator of hypersensitive cell death. During the HR, superoxide dismutase accelerates O(2)(-) dismutation to H(2)O(2) to minimize the loss of NO by reaction with O(2)(-) and to trigger hypersensitive cell death through NO/H(2)O(2) cooperation. However, O(2)(-) rather than H(2)O(2) is the primary ROI signal for pathogen induction of glutathione S-transferase, and the rates of production and dismutation of O(2)(-) generated during the oxidative burst play a crucial role in the modulation and integration of NO/H(2)O(2) signaling in the HR. Thus although plants and animals use a similar repertoire of signals in disease resistance, ROIs and NO are deployed in strikingly different ways to trigger host cell death.
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