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.
Identifieur interne : 002912 ( Main/Exploration ); précédent : 002911; suivant : 002913Hydrogen 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.
Auteurs : S. Dorey [France] ; M. Kopp ; P. Geoffroy ; B. Fritig ; S. KauffmannSource :
- Plant physiology [ 0032-0889 ] ; 1999.
Descripteurs français
- KwdFr :
- Acide salicylique (métabolisme), Activation enzymatique (effets des médicaments et des substances chimiques), Cellules cultivées (MeSH), Facteur de croissance végétal (pharmacologie), Feuilles de plante (cytologie), Feuilles de plante (effets des médicaments et des substances chimiques), Feuilles de plante (enzymologie), Feuilles de plante (métabolisme), Glycoprotéines (pharmacologie), Maladies des plantes (induit chimiquement), Mort cellulaire (effets des médicaments et des substances chimiques), Peroxyde d'hydrogène (métabolisme), Phenylalanine ammonia-lyase (métabolisme), Phytophthora (MeSH), Protéines d'algue (pharmacologie), Scopolétine (métabolisme), Stimulation du métabolisme oxydatif (effets des médicaments et des substances chimiques), Tabac (cytologie), Tabac (effets des médicaments et des substances chimiques), Tabac (enzymologie), Tabac (métabolisme), Végétaux toxiques (MeSH).
- MESH :
- cytologie : Feuilles de plante, Tabac.
- effets des médicaments et des substances chimiques : Activation enzymatique, Feuilles de plante, Mort cellulaire, Stimulation du métabolisme oxydatif, Tabac.
- enzymologie : Feuilles de plante, Tabac.
- induit chimiquement : Maladies des plantes.
- métabolisme : Acide salicylique, Feuilles de plante, Peroxyde d'hydrogène, Phenylalanine ammonia-lyase, Scopolétine, Tabac.
- pharmacologie : Facteur de croissance végétal, Glycoprotéines, Protéines d'algue.
- Cellules cultivées, Phytophthora, Végétaux toxiques.
English descriptors
- KwdEn :
- Algal Proteins (pharmacology), Cell Death (drug effects), Cells, Cultured (MeSH), Enzyme Activation (drug effects), Glycoproteins (pharmacology), Hydrogen Peroxide (metabolism), Phenylalanine Ammonia-Lyase (metabolism), Phytophthora (MeSH), Plant Diseases (chemically induced), Plant Growth Regulators (pharmacology), Plant Leaves (cytology), Plant Leaves (drug effects), Plant Leaves (enzymology), Plant Leaves (metabolism), Plants, Toxic (MeSH), Respiratory Burst (drug effects), Salicylic Acid (metabolism), Scopoletin (metabolism), Tobacco (cytology), Tobacco (drug effects), Tobacco (enzymology), Tobacco (metabolism).
- MESH :
- chemical , metabolism : Hydrogen Peroxide, Phenylalanine Ammonia-Lyase, Salicylic Acid, Scopoletin.
- chemical , pharmacology : Algal Proteins, Glycoproteins, Plant Growth Regulators.
- chemically induced : Plant Diseases.
- cytology : Plant Leaves, Tobacco.
- drug effects : Cell Death, Enzyme Activation, Plant Leaves, Respiratory Burst, Tobacco.
- enzymology : Plant Leaves, Tobacco.
- metabolism : Plant Leaves, Tobacco.
- Cells, Cultured, Phytophthora, Plants, Toxic.
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.
DOI: 10.1104/pp.121.1.163
PubMed: 10482671
PubMed Central: PMC59364
Affiliations:
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Dorey</name><affiliation wicri:level="4"><nlm:affiliation>Institut de Biologie Moléculaire des Plantes du Centre National de la Recherche Scientifique, Université Louis Pasteur, 12 rue du Général Zimmer, 67084 Strasbourg cedex, France.</nlm:affiliation><country xml:lang="fr">France</country><wicri:regionArea>Institut de Biologie Moléculaire des Plantes du Centre National de la Recherche Scientifique, Université Louis Pasteur, 12 rue du Général Zimmer, 67084 Strasbourg cedex</wicri:regionArea><placeName><region type="region" nuts="2">Grand Est</region><region type="old region" nuts="2">Alsace (région administrative)</region><settlement type="city">Strasbourg</settlement></placeName><orgName type="university">Université Strasbourg 1</orgName></affiliation></author><author><name sortKey="Kopp, M" sort="Kopp, M" uniqKey="Kopp M" first="M" last="Kopp">M. Kopp</name></author><author><name sortKey="Geoffroy, P" sort="Geoffroy, P" uniqKey="Geoffroy P" first="P" last="Geoffroy">P. Geoffroy</name></author><author><name sortKey="Fritig, B" sort="Fritig, B" uniqKey="Fritig B" first="B" last="Fritig">B. Fritig</name></author><author><name sortKey="Kauffmann, S" sort="Kauffmann, S" uniqKey="Kauffmann S" first="S" last="Kauffmann">S. Kauffmann</name></author></analytic><series><title level="j">Plant physiology</title><idno type="ISSN">0032-0889</idno><imprint><date when="1999" type="published">1999</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Algal Proteins (pharmacology)</term><term>Cell Death (drug effects)</term><term>Cells, Cultured (MeSH)</term><term>Enzyme Activation (drug effects)</term><term>Glycoproteins (pharmacology)</term><term>Hydrogen Peroxide (metabolism)</term><term>Phenylalanine Ammonia-Lyase (metabolism)</term><term>Phytophthora (MeSH)</term><term>Plant Diseases (chemically induced)</term><term>Plant Growth Regulators (pharmacology)</term><term>Plant Leaves (cytology)</term><term>Plant Leaves (drug effects)</term><term>Plant Leaves (enzymology)</term><term>Plant Leaves (metabolism)</term><term>Plants, Toxic (MeSH)</term><term>Respiratory Burst (drug effects)</term><term>Salicylic Acid (metabolism)</term><term>Scopoletin (metabolism)</term><term>Tobacco (cytology)</term><term>Tobacco (drug effects)</term><term>Tobacco (enzymology)</term><term>Tobacco (metabolism)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Acide salicylique (métabolisme)</term><term>Activation enzymatique (effets des médicaments et des substances chimiques)</term><term>Cellules cultivées (MeSH)</term><term>Facteur de croissance végétal (pharmacologie)</term><term>Feuilles de plante (cytologie)</term><term>Feuilles de plante (effets des médicaments et des substances chimiques)</term><term>Feuilles de plante (enzymologie)</term><term>Feuilles de plante (métabolisme)</term><term>Glycoprotéines (pharmacologie)</term><term>Maladies des plantes (induit chimiquement)</term><term>Mort cellulaire (effets des médicaments et des substances chimiques)</term><term>Peroxyde d'hydrogène (métabolisme)</term><term>Phenylalanine ammonia-lyase (métabolisme)</term><term>Phytophthora (MeSH)</term><term>Protéines d'algue (pharmacologie)</term><term>Scopolétine (métabolisme)</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>Tabac (enzymologie)</term><term>Tabac (métabolisme)</term><term>Végétaux toxiques (MeSH)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Hydrogen Peroxide</term><term>Phenylalanine Ammonia-Lyase</term><term>Salicylic Acid</term><term>Scopoletin</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Algal Proteins</term><term>Glycoproteins</term><term>Plant Growth Regulators</term></keywords><keywords scheme="MESH" qualifier="chemically induced" xml:lang="en"><term>Plant Diseases</term></keywords><keywords scheme="MESH" qualifier="cytologie" xml:lang="fr"><term>Feuilles de plante</term><term>Tabac</term></keywords><keywords scheme="MESH" qualifier="cytology" xml:lang="en"><term>Plant Leaves</term><term>Tobacco</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Cell Death</term><term>Enzyme Activation</term><term>Plant Leaves</term><term>Respiratory Burst</term><term>Tobacco</term></keywords><keywords scheme="MESH" qualifier="effets des médicaments et des substances chimiques" xml:lang="fr"><term>Activation enzymatique</term><term>Feuilles de plante</term><term>Mort cellulaire</term><term>Stimulation du métabolisme oxydatif</term><term>Tabac</term></keywords><keywords scheme="MESH" qualifier="enzymologie" xml:lang="fr"><term>Feuilles de plante</term><term>Tabac</term></keywords><keywords scheme="MESH" qualifier="enzymology" xml:lang="en"><term>Plant Leaves</term><term>Tobacco</term></keywords><keywords scheme="MESH" qualifier="induit chimiquement" xml:lang="fr"><term>Maladies des plantes</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Plant Leaves</term><term>Tobacco</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Acide salicylique</term><term>Feuilles de plante</term><term>Peroxyde d'hydrogène</term><term>Phenylalanine ammonia-lyase</term><term>Scopolétine</term><term>Tabac</term></keywords><keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Facteur de croissance végétal</term><term>Glycoprotéines</term><term>Protéines d'algue</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Cells, Cultured</term><term>Phytophthora</term><term>Plants, Toxic</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Cellules cultivées</term><term>Phytophthora</term><term>Végétaux toxiques</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">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.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">10482671</PMID><DateCompleted><Year>1999</Year><Month>10</Month><Day>28</Day></DateCompleted><DateRevised><Year>2019</Year><Month>05</Month><Day>14</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0032-0889</ISSN><JournalIssue CitedMedium="Print"><Volume>121</Volume><Issue>1</Issue><PubDate><Year>1999</Year><Month>Sep</Month></PubDate></JournalIssue><Title>Plant physiology</Title><ISOAbbreviation>Plant Physiol</ISOAbbreviation></Journal><ArticleTitle>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.</ArticleTitle><Pagination><MedlinePgn>163-72</MedlinePgn></Pagination><Abstract><AbstractText>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.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Dorey</LastName><ForeName>S</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Institut de Biologie Moléculaire des Plantes du Centre National de la Recherche Scientifique, Université Louis Pasteur, 12 rue du Général Zimmer, 67084 Strasbourg cedex, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kopp</LastName><ForeName>M</ForeName><Initials>M</Initials></Author><Author ValidYN="Y"><LastName>Geoffroy</LastName><ForeName>P</ForeName><Initials>P</Initials></Author><Author ValidYN="Y"><LastName>Fritig</LastName><ForeName>B</ForeName><Initials>B</Initials></Author><Author ValidYN="Y"><LastName>Kauffmann</LastName><ForeName>S</ForeName><Initials>S</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D003160">Comparative Study</PublicationType><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Plant Physiol</MedlineTA><NlmUniqueID>0401224</NlmUniqueID><ISSNLinking>0032-0889</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D020418">Algal Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D006023">Glycoproteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D010937">Plant Growth Regulators</NameOfSubstance></Chemical><Chemical><RegistryNumber>BBX060AN9V</RegistryNumber><NameOfSubstance UI="D006861">Hydrogen Peroxide</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 4.3.1.24</RegistryNumber><NameOfSubstance UI="D010650">Phenylalanine Ammonia-Lyase</NameOfSubstance></Chemical><Chemical><RegistryNumber>KLF1HS0SXJ</RegistryNumber><NameOfSubstance UI="D012603">Scopoletin</NameOfSubstance></Chemical><Chemical><RegistryNumber>O414PZ4LPZ</RegistryNumber><NameOfSubstance UI="D020156">Salicylic Acid</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D020418" MajorTopicYN="N">Algal Proteins</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D016923" MajorTopicYN="N">Cell Death</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002478" MajorTopicYN="N">Cells, Cultured</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004789" MajorTopicYN="N">Enzyme Activation</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006023" MajorTopicYN="N">Glycoproteins</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006861" MajorTopicYN="N">Hydrogen Peroxide</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010650" MajorTopicYN="N">Phenylalanine Ammonia-Lyase</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010838" MajorTopicYN="N">Phytophthora</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D010935" MajorTopicYN="N">Plant Diseases</DescriptorName><QualifierName UI="Q000139" MajorTopicYN="N">chemically induced</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010937" MajorTopicYN="N">Plant Growth Regulators</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018515" MajorTopicYN="N">Plant Leaves</DescriptorName><QualifierName UI="Q000166" MajorTopicYN="N">cytology</QualifierName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000201" MajorTopicYN="N">enzymology</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010947" MajorTopicYN="Y">Plants, Toxic</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D016897" MajorTopicYN="N">Respiratory Burst</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D020156" MajorTopicYN="N">Salicylic Acid</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D012603" MajorTopicYN="N">Scopoletin</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D014026" MajorTopicYN="N">Tobacco</DescriptorName><QualifierName UI="Q000166" MajorTopicYN="Y">cytology</QualifierName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000201" MajorTopicYN="N">enzymology</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>1999</Year><Month>9</Month><Day>11</Day></PubMedPubDate><PubMedPubDate 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IdType="pubmed">9847105</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></pubmed><affiliations><list><country><li>France</li></country><region><li>Alsace (région administrative)</li><li>Grand Est</li></region><settlement><li>Strasbourg</li></settlement><orgName><li>Université Strasbourg 1</li></orgName></list><tree><noCountry><name sortKey="Fritig, B" sort="Fritig, B" uniqKey="Fritig B" first="B" last="Fritig">B. Fritig</name><name sortKey="Geoffroy, P" sort="Geoffroy, P" uniqKey="Geoffroy P" first="P" last="Geoffroy">P. Geoffroy</name><name sortKey="Kauffmann, S" sort="Kauffmann, S" uniqKey="Kauffmann S" first="S" last="Kauffmann">S. Kauffmann</name><name sortKey="Kopp, M" sort="Kopp, M" uniqKey="Kopp M" first="M" last="Kopp">M. Kopp</name></noCountry><country name="France"><region name="Grand Est"><name sortKey="Dorey, S" sort="Dorey, S" uniqKey="Dorey S" first="S" last="Dorey">S. Dorey</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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