Ozone sensitivity in hybrid poplar correlates with insensitivity to both salicylic acid and jasmonic acid. The role of programmed cell death in lesion formation.
Identifieur interne : 004784 ( Main/Exploration ); précédent : 004783; suivant : 004785Ozone sensitivity in hybrid poplar correlates with insensitivity to both salicylic acid and jasmonic acid. The role of programmed cell death in lesion formation.
Auteurs : J R Koch [États-Unis] ; R A Creelman ; S M Eshita ; M. Seskar ; J E Mullet ; K R DavisSource :
- Plant physiology [ 0032-0889 ] ; 2000.
Descripteurs français
- KwdFr :
- Acide salicylique (métabolisme), Apoptose (effets des médicaments et des substances chimiques), Arbres (cytologie), Arbres (effets des médicaments et des substances chimiques), Arbres (métabolisme), Cyclopentanes (métabolisme), Facteur de croissance végétal (métabolisme), Hybridation génétique (MeSH), Méthode TUNEL (MeSH), Oxylipines (MeSH), Ozone (pharmacologie).
- MESH :
- cytologie : Arbres.
- effets des médicaments et des substances chimiques : Apoptose, Arbres.
- métabolisme : Acide salicylique, Arbres, Cyclopentanes, Facteur de croissance végétal.
- pharmacologie : Ozone.
- Hybridation génétique, Méthode TUNEL, Oxylipines.
English descriptors
- KwdEn :
- MESH :
- chemical , metabolism : Cyclopentanes, Plant Growth Regulators, Salicylic Acid.
- cytology : Trees.
- drug effects : Apoptosis, Trees.
- metabolism : Trees.
- chemical , pharmacology : Ozone.
- Hybridization, Genetic, In Situ Nick-End Labeling, Oxylipins.
Abstract
Our earlier studies demonstrated that the ozone-sensitive hybrid poplar clone NE-388 displays an attenuated level of ozone-, wound-, and phytopathogen-induced defense gene expression. To determine if this reduced gene activation involves signal transduction pathways dependent on salicylic acid (SA) and/or jasmonic acid (JA), we compared the responses of NE-388 and an ozone-tolerant clone, NE-245, to these signal molecules. JA levels increased in both clones in response to ozone, but only minimal increases in SA levels were measured for either clone. Treatment with SA and methyl jasmonate induced defense gene expression only in NE-245, indicating that NE-388 is insensitive to these signal molecules. DNA fragmentation, an indicator of programmed cell death (PCD), was detected in NE-245 treated with either ozone or an avirulent phytopathogen, but was not detected in NE-388. We conclude that these clones undergo two distinct mechanisms of ozone-induced lesion formation. In NE-388, lesions appear to be due to toxic cell death resulting from a limited ability to perceive and subsequently activate SA- and/or JA-mediated antioxidant defense responses. In NE-245, SA-dependent PCD precedes lesion formation via a process related to the PCD pathway activated by phytopathogenic bacteria. These results support the hypothesis that ozone triggers a hypersensitive response.
DOI: 10.1104/pp.123.2.487
PubMed: 10859179
PubMed Central: PMC59017
Affiliations:
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The role of programmed cell death in lesion formation.</title><author><name sortKey="Koch, J R" sort="Koch, J R" uniqKey="Koch J" first="J R" last="Koch">J R Koch</name><affiliation wicri:level="1"><nlm:affiliation>Department of Molecular Genetics, The Ohio State University, Columbus 43210-1002, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Molecular Genetics, The Ohio State University, Columbus 43210-1002</wicri:regionArea><wicri:noRegion>Columbus 43210-1002</wicri:noRegion></affiliation></author><author><name sortKey="Creelman, R A" sort="Creelman, R A" uniqKey="Creelman R" first="R A" last="Creelman">R A Creelman</name></author><author><name sortKey="Eshita, S M" sort="Eshita, S M" uniqKey="Eshita S" first="S M" last="Eshita">S M Eshita</name></author><author><name sortKey="Seskar, M" sort="Seskar, M" uniqKey="Seskar M" first="M" last="Seskar">M. Seskar</name></author><author><name sortKey="Mullet, J E" sort="Mullet, J E" uniqKey="Mullet J" first="J E" last="Mullet">J E Mullet</name></author><author><name sortKey="Davis, K R" sort="Davis, K R" uniqKey="Davis K" first="K R" last="Davis">K R Davis</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2000">2000</date><idno type="RBID">pubmed:10859179</idno><idno type="pmid">10859179</idno><idno type="pmc">PMC59017</idno><idno type="doi">10.1104/pp.123.2.487</idno><idno type="wicri:Area/Main/Corpus">004855</idno><idno type="wicri:explorRef" wicri:stream="Main" wicri:step="Corpus" wicri:corpus="PubMed">004855</idno><idno type="wicri:Area/Main/Curation">004855</idno><idno type="wicri:explorRef" wicri:stream="Main" wicri:step="Curation">004855</idno><idno type="wicri:Area/Main/Exploration">004855</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Ozone sensitivity in hybrid poplar correlates with insensitivity to both salicylic acid and jasmonic acid. The role of programmed cell death in lesion formation.</title><author><name sortKey="Koch, J R" sort="Koch, J R" uniqKey="Koch J" first="J R" last="Koch">J R Koch</name><affiliation wicri:level="1"><nlm:affiliation>Department of Molecular Genetics, The Ohio State University, Columbus 43210-1002, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Molecular Genetics, The Ohio State University, Columbus 43210-1002</wicri:regionArea><wicri:noRegion>Columbus 43210-1002</wicri:noRegion></affiliation></author><author><name sortKey="Creelman, R A" sort="Creelman, R A" uniqKey="Creelman R" first="R A" last="Creelman">R A Creelman</name></author><author><name sortKey="Eshita, S M" sort="Eshita, S M" uniqKey="Eshita S" first="S M" last="Eshita">S M Eshita</name></author><author><name sortKey="Seskar, M" sort="Seskar, M" uniqKey="Seskar M" first="M" last="Seskar">M. Seskar</name></author><author><name sortKey="Mullet, J E" sort="Mullet, J E" uniqKey="Mullet J" first="J E" last="Mullet">J E Mullet</name></author><author><name sortKey="Davis, K R" sort="Davis, K R" uniqKey="Davis K" first="K R" last="Davis">K R Davis</name></author></analytic><series><title level="j">Plant physiology</title><idno type="ISSN">0032-0889</idno><imprint><date when="2000" type="published">2000</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Apoptosis (drug effects)</term><term>Cyclopentanes (metabolism)</term><term>Hybridization, Genetic (MeSH)</term><term>In Situ Nick-End Labeling (MeSH)</term><term>Oxylipins (MeSH)</term><term>Ozone (pharmacology)</term><term>Plant Growth Regulators (metabolism)</term><term>Salicylic Acid (metabolism)</term><term>Trees (cytology)</term><term>Trees (drug effects)</term><term>Trees (metabolism)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Acide salicylique (métabolisme)</term><term>Apoptose (effets des médicaments et des substances chimiques)</term><term>Arbres (cytologie)</term><term>Arbres (effets des médicaments et des substances chimiques)</term><term>Arbres (métabolisme)</term><term>Cyclopentanes (métabolisme)</term><term>Facteur de croissance végétal (métabolisme)</term><term>Hybridation génétique (MeSH)</term><term>Méthode TUNEL (MeSH)</term><term>Oxylipines (MeSH)</term><term>Ozone (pharmacologie)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Cyclopentanes</term><term>Plant Growth Regulators</term><term>Salicylic Acid</term></keywords><keywords scheme="MESH" qualifier="cytologie" xml:lang="fr"><term>Arbres</term></keywords><keywords scheme="MESH" qualifier="cytology" xml:lang="en"><term>Trees</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Apoptosis</term><term>Trees</term></keywords><keywords scheme="MESH" qualifier="effets des médicaments et des substances chimiques" xml:lang="fr"><term>Apoptose</term><term>Arbres</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Trees</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Acide salicylique</term><term>Arbres</term><term>Cyclopentanes</term><term>Facteur de croissance végétal</term></keywords><keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Ozone</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Ozone</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Hybridization, Genetic</term><term>In Situ Nick-End Labeling</term><term>Oxylipins</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Hybridation génétique</term><term>Méthode TUNEL</term><term>Oxylipines</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Our earlier studies demonstrated that the ozone-sensitive hybrid poplar clone NE-388 displays an attenuated level of ozone-, wound-, and phytopathogen-induced defense gene expression. To determine if this reduced gene activation involves signal transduction pathways dependent on salicylic acid (SA) and/or jasmonic acid (JA), we compared the responses of NE-388 and an ozone-tolerant clone, NE-245, to these signal molecules. JA levels increased in both clones in response to ozone, but only minimal increases in SA levels were measured for either clone. Treatment with SA and methyl jasmonate induced defense gene expression only in NE-245, indicating that NE-388 is insensitive to these signal molecules. DNA fragmentation, an indicator of programmed cell death (PCD), was detected in NE-245 treated with either ozone or an avirulent phytopathogen, but was not detected in NE-388. We conclude that these clones undergo two distinct mechanisms of ozone-induced lesion formation. In NE-388, lesions appear to be due to toxic cell death resulting from a limited ability to perceive and subsequently activate SA- and/or JA-mediated antioxidant defense responses. In NE-245, SA-dependent PCD precedes lesion formation via a process related to the PCD pathway activated by phytopathogenic bacteria. These results support the hypothesis that ozone triggers a hypersensitive response.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">10859179</PMID><DateCompleted><Year>2000</Year><Month>09</Month><Day>07</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>123</Volume><Issue>2</Issue><PubDate><Year>2000</Year><Month>Jun</Month></PubDate></JournalIssue><Title>Plant physiology</Title><ISOAbbreviation>Plant Physiol</ISOAbbreviation></Journal><ArticleTitle>Ozone sensitivity in hybrid poplar correlates with insensitivity to both salicylic acid and jasmonic acid. The role of programmed cell death in lesion formation.</ArticleTitle><Pagination><MedlinePgn>487-96</MedlinePgn></Pagination><Abstract><AbstractText>Our earlier studies demonstrated that the ozone-sensitive hybrid poplar clone NE-388 displays an attenuated level of ozone-, wound-, and phytopathogen-induced defense gene expression. To determine if this reduced gene activation involves signal transduction pathways dependent on salicylic acid (SA) and/or jasmonic acid (JA), we compared the responses of NE-388 and an ozone-tolerant clone, NE-245, to these signal molecules. JA levels increased in both clones in response to ozone, but only minimal increases in SA levels were measured for either clone. Treatment with SA and methyl jasmonate induced defense gene expression only in NE-245, indicating that NE-388 is insensitive to these signal molecules. DNA fragmentation, an indicator of programmed cell death (PCD), was detected in NE-245 treated with either ozone or an avirulent phytopathogen, but was not detected in NE-388. We conclude that these clones undergo two distinct mechanisms of ozone-induced lesion formation. In NE-388, lesions appear to be due to toxic cell death resulting from a limited ability to perceive and subsequently activate SA- and/or JA-mediated antioxidant defense responses. In NE-245, SA-dependent PCD precedes lesion formation via a process related to the PCD pathway activated by phytopathogenic bacteria. These results support the hypothesis that ozone triggers a hypersensitive response.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Koch</LastName><ForeName>J R</ForeName><Initials>JR</Initials><AffiliationInfo><Affiliation>Department of Molecular Genetics, The Ohio State University, Columbus 43210-1002, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Creelman</LastName><ForeName>R A</ForeName><Initials>RA</Initials></Author><Author ValidYN="Y"><LastName>Eshita</LastName><ForeName>S M</ForeName><Initials>SM</Initials></Author><Author ValidYN="Y"><LastName>Seskar</LastName><ForeName>M</ForeName><Initials>M</Initials></Author><Author ValidYN="Y"><LastName>Mullet</LastName><ForeName>J E</ForeName><Initials>JE</Initials></Author><Author ValidYN="Y"><LastName>Davis</LastName><ForeName>K R</ForeName><Initials>KR</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType><PublicationType UI="D013486">Research Support, U.S. Gov't, Non-P.H.S.</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="D003517">Cyclopentanes</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D054883">Oxylipins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D010937">Plant Growth Regulators</NameOfSubstance></Chemical><Chemical><RegistryNumber>66H7ZZK23N</RegistryNumber><NameOfSubstance UI="D010126">Ozone</NameOfSubstance></Chemical><Chemical><RegistryNumber>6RI5N05OWW</RegistryNumber><NameOfSubstance UI="C011006">jasmonic acid</NameOfSubstance></Chemical><Chemical><RegistryNumber>O414PZ4LPZ</RegistryNumber><NameOfSubstance UI="D020156">Salicylic Acid</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D017209" MajorTopicYN="N">Apoptosis</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="Y">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003517" MajorTopicYN="N">Cyclopentanes</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006824" MajorTopicYN="N">Hybridization, Genetic</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D020287" MajorTopicYN="N">In Situ Nick-End Labeling</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D054883" MajorTopicYN="N">Oxylipins</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D010126" MajorTopicYN="N">Ozone</DescriptorName><QualifierName 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sortKey="Seskar, M" sort="Seskar, M" uniqKey="Seskar M" first="M" last="Seskar">M. Seskar</name></noCountry><country name="États-Unis"><noRegion><name sortKey="Koch, J R" sort="Koch, J R" uniqKey="Koch J" first="J R" last="Koch">J R Koch</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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