Transgenic tobacco plants with reduced capability to detoxify reactive oxygen intermediates are hyperresponsive to pathogen infection

Reactive oxygen intermediates (ROI) play a critical role in the defense of plants against invading pathogens. Produced during the "oxidative burst," they are thought to activate programmed cell death (PCD) and induce antimicrobial defenses such as pathogenesis-related proteins. It was show...

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Published in:Proceedings of the National Academy of Sciences - PNAS Vol. 96; no. 24; pp. 14165 - 14170
Main Authors: Mittler, R, Herr, E.H, Orvar, B.L, Camp, W. van, Willekens, H, Inze, D, Ellis, B.E
Format: Journal Article
Language:English
Published: United States National Academy of Sciences of the United States of America 23-11-1999
National Acad Sciences
National Academy of Sciences
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Abstract Reactive oxygen intermediates (ROI) play a critical role in the defense of plants against invading pathogens. Produced during the "oxidative burst," they are thought to activate programmed cell death (PCD) and induce antimicrobial defenses such as pathogenesis-related proteins. It was shown recently that during the interaction of plants with pathogens, the expression of ROI-detoxifying enzymes such as ascorbate peroxidase (APX) and catalase (CAT) is suppressed. It was suggested that this suppression, occurring upon pathogen recognition and coinciding with an enhanced rate of ROI production, plays a key role in elevating cellular ROI levels, thereby potentiating the induction of PCD and other defenses. To examine the relationship between the suppression of antioxidative mechanisms and the induction of PCD and other defenses during pathogen attack, we studied the interaction between transgenic antisense tobacco plants with reduced APX or CAT and a bacterial pathogen that triggers the hypersensitive response. Transgenic plants with reduced capability to detoxify ROI (i.e., antisense APX or CAT) were found to be hyperresponsive to pathogen attack. They activated PCD in response to low amounts of pathogens that did not trigger the activation of PCD in control plants. Our findings support the hypothesis that suppression of ROI-scavenging enzymes during the hypersensitive response plays an important role in enhancing pathogen-induced PCD.
AbstractList Reactive oxygen intermediates (ROI) play a critical role in the defense of plants against invading pathogens. Produced during the "oxidative burst," they are thought to activate programmed cell death (PCD) and induce antimicrobial defenses such as pathogenesis-related proteins. It was shown recently that during the interaction of plants with pathogens, the expression of ROI-detoxifying enzymes such as ascorbate peroxidase (APX) and catalase (CAT) is suppressed. It was suggested that this suppression, occurring upon pathogen recognition and coinciding with an enhanced rate of ROI production, plays a key role in elevating cellular ROI levels, thereby potentiating the induction of PCD and other defenses. To examine the relationship between the suppression of antioxidative mechanisms and the induction of PCD and other defenses during pathogen attack, we studied the interaction between transgenic antisense tobacco plants with reduced APX or CAT and a bacterial pathogen that triggers the hypersensitive response. Transgenic plants with reduced capability to detoxify ROI (i.e., antisense APX or CAT) were found to be hyperresponsive to pathogen attack. They activated PCD in response to low amounts of pathogens that did not trigger the activation of PCD in control plants. Our findings support the hypothesis that suppression of ROI-scavenging enzymes during the hypersensitive response plays an important role in enhancing pathogen-induced PCD.
Reactive oxygen intermediates (ROI) play a critical role in the defense of plants against invading pathogens. Produced during the "oxidative burst," they are thought to activate programmed cell death (PCD) and induce antimicrobial defenses such as pathogenesis-related proteins.
Reactive oxygen intermediates (ROI) play a critical role in the defense of plants against invading pathogens. Produced during the “oxidative burst,” they are thought to activate programmed cell death (PCD) and induce antimicrobial defenses such as pathogenesis-related proteins. It was shown recently that during the interaction of plants with pathogens, the expression of ROI-detoxifying enzymes such as ascorbate peroxidase (APX) and catalase (CAT) is suppressed. It was suggested that this suppression, occurring upon pathogen recognition and coinciding with an enhanced rate of ROI production, plays a key role in elevating cellular ROI levels, thereby potentiating the induction of PCD and other defenses. To examine the relationship between the suppression of antioxidative mechanisms and the induction of PCD and other defenses during pathogen attack, we studied the interaction between transgenic antisense tobacco plants with reduced APX or CAT and a bacterial pathogen that triggers the hypersensitive response. Transgenic plants with reduced capability to detoxify ROI (i.e., antisense APX or CAT) were found to be hyperresponsive to pathogen attack. They activated PCD in response to low amounts of pathogens that did not trigger the activation of PCD in control plants. Our findings support the hypothesis that suppression of ROI-scavenging enzymes during the hypersensitive response plays an important role in enhancing pathogen-induced PCD.
Author Inze, D
Mittler, R
Orvar, B.L
Ellis, B.E
Willekens, H
Camp, W. van
Herr, E.H
AuthorAffiliation Department of Plant Sciences, The Hebrew University of Jerusalem, Jerusalem 91904, Israel; ‡ Department of Plant Science, University of British Columbia, 2357 Main Mall, Vancouver, BC Canada V6T 1Z4; and § Department of Genetics, University of Gent, K. L. Ledeganckstraat 35, B-9000 Ghent, Belgium
AuthorAffiliation_xml – name: Department of Plant Sciences, The Hebrew University of Jerusalem, Jerusalem 91904, Israel; ‡ Department of Plant Science, University of British Columbia, 2357 Main Mall, Vancouver, BC Canada V6T 1Z4; and § Department of Genetics, University of Gent, K. L. Ledeganckstraat 35, B-9000 Ghent, Belgium
Author_xml – sequence: 1
  fullname: Mittler, R
– sequence: 2
  fullname: Herr, E.H
– sequence: 3
  fullname: Orvar, B.L
– sequence: 4
  fullname: Camp, W. van
– sequence: 5
  fullname: Willekens, H
– sequence: 6
  fullname: Inze, D
– sequence: 7
  fullname: Ellis, B.E
BackLink https://www.ncbi.nlm.nih.gov/pubmed/10570216$$D View this record in MEDLINE/PubMed
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Copyright Copyright 1993-1999 National Academy of Sciences of the United States of America
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To whom reprint requests should be addressed. E-mail: ron@vms.huji.ac.il.
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Snippet Reactive oxygen intermediates (ROI) play a critical role in the defense of plants against invading pathogens. Produced during the "oxidative burst," they are...
Reactive oxygen intermediates (ROI) play a critical role in the defense of plants against invading pathogens. Produced during the “oxidative burst,” they are...
Reactive oxygen intermediates (ROI) play a critical role in the defense of plants against invading pathogens. Produced during the “oxidative burst,” they are...
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StartPage 14165
SubjectTerms antisense RNA
Apoptosis
ascorbate peroxidase
Ascorbate Peroxidases
Bacteria
biological resistance
Biological Sciences
Botany
catalase
Catalase - genetics
Catalase - metabolism
Cell death
defense mechanisms
DNA
Enzymes
experimental infections
gene expression
hypersensitive response
Infections
inhibition
Leaves
messenger RNA
metabolic detoxification
Nicotiana - metabolism
Nicotiana - microbiology
Nicotiana tabacum
Oxygen
pathogenesis-related proteins
Pathogens
peroxidases
Peroxidases - genetics
Peroxidases - metabolism
plant diseases and disorders
Plants
Plants, Genetically Modified
Plants, Toxic
Pseudomonas - physiology
Pseudomonas syringae pv. phaseolicola
Pseudomonas syringae pv. tabaci
reactive oxygen intermediates
Reactive Oxygen Species - metabolism
RNA, Antisense
Tobacco
Transgenic plants
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Title Transgenic tobacco plants with reduced capability to detoxify reactive oxygen intermediates are hyperresponsive to pathogen infection
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