1997
DOI: 10.1146/annurev.arplant.48.1.251
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The Oxidative Burst in Plant Disease Resistance

Abstract: Rapid generation of superoxide and accumulation of H2O2 is a characteristic early feature of the hypersensitive response following perception of pathogen avirulence signals. Emerging data indicate that the oxidative burst reflects activation of a membrane-bound NADPH oxidase closely resembling that operating in activated neutrophils. The oxidants are not only direct protective agents, but H2O2 also functions as a substrate for oxidative cross-linking in the cell wall, as a threshold trigger for hypersensitive … Show more

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Cited by 2,831 publications
(2,081 citation statements)
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References 149 publications
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“…An RNA blot was prepared with 32 Arabidopsis, in CaM-mediated cell death. We demonstrate that (i) oxidative stress, involved in plant PCD processes, [40][41][42][43] induces the transient expression of AtBAG6, (ii) AtBAG6 physically interacts with AtCaMs, (iii) the IQ motif in the AtBAG6 is required for Ca 2 þ -independent CaM complex formation, and (iv) the CaM-binding IQ motif and BAG domain are required for AtBAG6-mediated cell death in both yeast and plant. In animals, Ca 2 þ released into the cytoplasm can induce mitochondrial permeability transition (PT) pore opening, which induces release of apoptotic activators to the cytoplasm and consequently activates caspase-mediated PCD.…”
Section: Discussionmentioning
confidence: 86%
See 1 more Smart Citation
“…An RNA blot was prepared with 32 Arabidopsis, in CaM-mediated cell death. We demonstrate that (i) oxidative stress, involved in plant PCD processes, [40][41][42][43] induces the transient expression of AtBAG6, (ii) AtBAG6 physically interacts with AtCaMs, (iii) the IQ motif in the AtBAG6 is required for Ca 2 þ -independent CaM complex formation, and (iv) the CaM-binding IQ motif and BAG domain are required for AtBAG6-mediated cell death in both yeast and plant. In animals, Ca 2 þ released into the cytoplasm can induce mitochondrial permeability transition (PT) pore opening, which induces release of apoptotic activators to the cytoplasm and consequently activates caspase-mediated PCD.…”
Section: Discussionmentioning
confidence: 86%
“…Transcription of AtBAG6 was specifically induced by SA, H 2 O 2 , and high temperature, all of which are known to be involved in plant PCD processes. [40][41][42][43] To further determine the biological roles of AtBAG6 in plants, we constructed each plasmid containing CDD or CDD I575S under the control of the constitutive cauliflower mosaic virus 35S promoter using the pCAMBIA1302 binary vector and used these plasmids to transform Arabidopsis. Transgenic CDD plants showed midget (dwarfism) phenotypes and formed disease-like necrotic lesions on their leaves (Figure 9b and c).…”
Section: Induction Of Cell Death By Atbag6 In Arabidopsis Plantmentioning
confidence: 99%
“…Induced defense enzymes like, PPO and PO participate in a vital role in activation of hypersensitive response. Both of them not only help in the strengthening of cell wall but also act as a transducer of signals to the neighboring unaffected cells (Lamb and Dixon 1997;Acharya et al 2011a;Chandra et al 2014a). Another defense enzyme, PAL, being one of the key enzymes of the phenylpropanoid pathway, involved in the biosynthesis of phytoalexins, lignins and related phenolic compounds (Pellegrini et al 1994).…”
Section: Discussionmentioning
confidence: 99%
“…Production of reactive oxygen species (ROS) at the cell surface is one of the earliest events detected in the plant defence response (Hammond-Kosack and Jones, 1996;Lamb and Dixon, 1997). The generation of superoxide anion (O 2 -) was first reported in incompatible interactions between potato and Phytophthora infestans (Doke et al, 1983).…”
Section: Introductionmentioning
confidence: 99%
“…However, in most studies the product of its rapid dismutation, hydrogen peroxide (H 2 O 2 ), is detected. Several roles for ROS have been proposed in plant defence, such as direct killing of the attacking pathogen, strengthening cell walls via oxidative crosslinking of cellwall glycoproteins, signalling, or as a cause of cell death (Dangl et al, 1996;Hammond-Kosack and Jones, 1996;Lamb and Dixon, 1997).…”
Section: Introductionmentioning
confidence: 99%