ArticlePlant physiology1999
Hydrogen peroxide from the oxidative burst is neither necessary nor sufficient for hypersensitive cell death induction, phenylalanine ammonia lyase stimulation, salicylic acid accumulation, or scopoletin consumption in cultured tobacco cells treated with elicitin.
Article in Plant physiology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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31 citing papers in PubMed, 147 citations in OpenAlex.
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- Naphthalic anhydride decreases persistence of alachlor and atrazine and elevates tolerance of maize.Heliyon · 2020Article
- Salicylic Acid Induces Resistance in Rubber Tree againstInternational journal of molecular sciences · 2018Article
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- A novel protein elicitor (SsCut) from Sclerotinia sclerotiorum induces multiple defense responses in plants.Plant molecular biology · 2014Article
- Pathogen-associated molecular pattern-triggered immunity and resistance to the root pathogen Phytophthora parasitica in Arabidopsis.Journal of experimental botany · 2013Article
- Interspecific somatic hybrids between Cyclamen persicum and C. coum, two sexually incompatible species.Plant cell reports · 2012Article
- Programmed cell death in the plant immune system.Cell death and differentiation · 2011Review
- Active suppression of early immune response in tobacco by the human pathogen Salmonella Typhimurium.PloS one · 2011Article
- The role of respiratory burst oxidase homologues in elicitor-induced stomatal closure and hypersensitive response in Nicotiana benthamiana.Journal of experimental botany · 2009Article
- The AtrbohD-mediated oxidative burst elicited by oligogalacturonides in Arabidopsis is dispensable for the activation of defense responses effective against Botrytis cinerea.Plant physiology · 2008Article
- Reactive oxygen species signaling in response to pathogens.Plant physiology · 2006Article
- Extracellular ATP induces the accumulation of superoxide via NADPH oxidases in Arabidopsis.Plant physiology · 2006Article
- The E3 ubiquitin ligase activity of arabidopsis PLANT U-BOX17 and its functional tobacco homolog ACRE276 are required for cell death and defense.The Plant cell · 2006Article
- Proteomics of Rac GTPase signaling reveals its predominant role in elicitor-induced defense response of cultured rice cells.Plant physiology · 2006Article
- Thaxtomin A induces programmed cell death in Arabidopsis thaliana suspension-cultured cells.Planta · 2005Article
- NpPDR1, a pleiotropic drug resistance-type ATP-binding cassette transporter from Nicotiana plumbaginifolia, plays a major role in plant pathogen defense.Plant physiology · 2005Article
- Activation of the oxidative burst by yeast elicitor in Catharanthus roseus cells occurs independently of the activation of genes involved in alkaloid biosynthesis.Plant molecular biology · 2004Article
- Cloning of soybean genes induced during hypersensitive cell death caused by syringolide elicitor.Planta · 2004Article
- Colonization of flax roots and early physiological responses of flax cells inoculated with pathogenic and nonpathogenic strains of Fusarium oxysporum.Applied and environmental microbiology · 2003Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
H(2)O(2) from the oxidative burst, cell death, and defense responses such as the production of phenylalanine ammonia lyase (PAL), salicylic acid (SA), and scopoletin were analyzed in cultured tobacco (Nicotiana tabacum) cells treated with three proteinaceous elicitors: two elicitins (alpha-megaspermin and beta-megaspermin) and one glycoprotein. These three proteins have been isolated from Phytophthora megasperma H20 and have been previously shown to be equally efficient in inducing a hypersensitive response (HR) upon infiltration into tobacco leaves. However, in cultured tobacco cells these elicitors exhibited strikingly different biological activities. beta-Megaspermin was the only elicitor that caused cell death and induced a strong, biphasic H(2)O(2) burst. Both elicitins stimulated PAL activity similarly and strongly, while the glycoprotein caused only a slight increase. Only elicitins induced SA accumulation and scopoletin consumption, and beta-megaspermin was more efficient. To assess the role of H(2)O(2) in HR cell death and defense response expression in elicitin-treated cells, a gain and loss of function strategy was used. Our results indicated that H(2)O(2) was neither necessary nor sufficient for HR cell death, PAL activation, or SA accumulation, and that extracellular H(2)O(2) was not a direct cause of intracellular scopoletin consumption.
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