Serveur d'exploration Phytophthora

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Ethylene is required for elicitin-induced oxidative burst but not for cell death induction in tobacco cell suspension cultures.

Identifieur interne : 001E82 ( Main/Exploration ); précédent : 001E81; suivant : 001E83

Ethylene is required for elicitin-induced oxidative burst but not for cell death induction in tobacco cell suspension cultures.

Auteurs : Julia Koehl [Allemagne] ; Alma Djulic ; Veronika Kirner ; Tach Thao Nguyen ; Ingrid Heiser

Source :

RBID : pubmed:17913292

Descripteurs français

English descriptors

Abstract

The signal compound ethylene and its relationships with oxidative burst and cell death were analyzed in cultured tobacco cells treated with the proteinaceous elicitor quercinin. Quercinin belongs to the protein family of elicitins and was isolated from the soil-born oak pathogen Phytophthora quercina. It was shown to induce a dose-dependent oxidative burst in tobacco cell culture in concentrations from 0.05 to 0.5 nM, and subsequently, cell death. The characteristics of quercinin-induced cell death included both membrane damage and DNA fragmentation in tobacco cell culture. At higher quercinin concentrations (2 nM), H(2)O(2) formation and ethylene biosynthesis were inhibited. Ethylene at low concentrations proved to be necessary for induction and maintenance of H(2)O(2) production in tobacco cells treated with quercinin. It was demonstrated that external addition of inhibitors of ethylene biosynthesis such as alpha-amino-oxy-acetic acid (AOA) and CoCl(2) also decreased or even inhibited the quercinin-induced oxidative burst, but did not influence cell death induction. These results demonstrate evidence for a requirement of the plant hormone ethylene for the onset of the quercinin-induced oxidative burst.

DOI: 10.1016/j.jplph.2007.05.012
PubMed: 17913292


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Le document en format XML

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<term>Aminooxyacetic Acid (pharmacology)</term>
<term>Cell Death (drug effects)</term>
<term>Cells, Cultured (MeSH)</term>
<term>Cobalt (pharmacology)</term>
<term>DNA Fragmentation (drug effects)</term>
<term>Dose-Response Relationship, Drug (MeSH)</term>
<term>Ethylenes (metabolism)</term>
<term>Hydrogen Peroxide (metabolism)</term>
<term>Phytophthora (MeSH)</term>
<term>Respiratory Burst (drug effects)</term>
<term>Time Factors (MeSH)</term>
<term>Tobacco (cytology)</term>
<term>Tobacco (drug effects)</term>
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<term>Acide aminooxy-acétique (pharmacologie)</term>
<term>Cellules cultivées (MeSH)</term>
<term>Cobalt (pharmacologie)</term>
<term>Facteurs temps (MeSH)</term>
<term>Fragmentation de l'ADN (effets des médicaments et des substances chimiques)</term>
<term>Mort cellulaire (effets des médicaments et des substances chimiques)</term>
<term>Peroxyde d'hydrogène (métabolisme)</term>
<term>Phytophthora (MeSH)</term>
<term>Protéines d'algue (pharmacologie)</term>
<term>Relation dose-effet des médicaments (MeSH)</term>
<term>Stimulation du métabolisme oxydatif (effets des médicaments et des substances chimiques)</term>
<term>Tabac (cytologie)</term>
<term>Tabac (effets des médicaments et des substances chimiques)</term>
<term>Éthylènes (métabolisme)</term>
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<term>Hydrogen Peroxide</term>
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<term>Aminooxyacetic Acid</term>
<term>Cobalt</term>
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<term>Tabac</term>
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<keywords scheme="MESH" qualifier="cytology" xml:lang="en">
<term>Tobacco</term>
</keywords>
<keywords scheme="MESH" qualifier="drug effects" xml:lang="en">
<term>Cell Death</term>
<term>DNA Fragmentation</term>
<term>Respiratory Burst</term>
<term>Tobacco</term>
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<term>Fragmentation de l'ADN</term>
<term>Mort cellulaire</term>
<term>Stimulation du métabolisme oxydatif</term>
<term>Tabac</term>
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<term>Peroxyde d'hydrogène</term>
<term>Éthylènes</term>
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<term>Protéines d'algue</term>
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<term>Dose-Response Relationship, Drug</term>
<term>Phytophthora</term>
<term>Time Factors</term>
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<term>Cellules cultivées</term>
<term>Facteurs temps</term>
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<div type="abstract" xml:lang="en">The signal compound ethylene and its relationships with oxidative burst and cell death were analyzed in cultured tobacco cells treated with the proteinaceous elicitor quercinin. Quercinin belongs to the protein family of elicitins and was isolated from the soil-born oak pathogen Phytophthora quercina. It was shown to induce a dose-dependent oxidative burst in tobacco cell culture in concentrations from 0.05 to 0.5 nM, and subsequently, cell death. The characteristics of quercinin-induced cell death included both membrane damage and DNA fragmentation in tobacco cell culture. At higher quercinin concentrations (2 nM), H(2)O(2) formation and ethylene biosynthesis were inhibited. Ethylene at low concentrations proved to be necessary for induction and maintenance of H(2)O(2) production in tobacco cells treated with quercinin. It was demonstrated that external addition of inhibitors of ethylene biosynthesis such as alpha-amino-oxy-acetic acid (AOA) and CoCl(2) also decreased or even inhibited the quercinin-induced oxidative burst, but did not influence cell death induction. These results demonstrate evidence for a requirement of the plant hormone ethylene for the onset of the quercinin-induced oxidative burst.</div>
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<AbstractText>The signal compound ethylene and its relationships with oxidative burst and cell death were analyzed in cultured tobacco cells treated with the proteinaceous elicitor quercinin. Quercinin belongs to the protein family of elicitins and was isolated from the soil-born oak pathogen Phytophthora quercina. It was shown to induce a dose-dependent oxidative burst in tobacco cell culture in concentrations from 0.05 to 0.5 nM, and subsequently, cell death. The characteristics of quercinin-induced cell death included both membrane damage and DNA fragmentation in tobacco cell culture. At higher quercinin concentrations (2 nM), H(2)O(2) formation and ethylene biosynthesis were inhibited. Ethylene at low concentrations proved to be necessary for induction and maintenance of H(2)O(2) production in tobacco cells treated with quercinin. It was demonstrated that external addition of inhibitors of ethylene biosynthesis such as alpha-amino-oxy-acetic acid (AOA) and CoCl(2) also decreased or even inhibited the quercinin-induced oxidative burst, but did not influence cell death induction. These results demonstrate evidence for a requirement of the plant hormone ethylene for the onset of the quercinin-induced oxidative burst.</AbstractText>
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