Function of a mitogen-activated protein kinase pathway in N gene-mediated resistance in tobacco.
Identifieur interne : 000840 ( Main/Corpus ); précédent : 000839; suivant : 000841Function of a mitogen-activated protein kinase pathway in N gene-mediated resistance in tobacco.
Auteurs : Hailing Jin ; Yidong Liu ; Kwang-Yeol Yang ; Cha Young Kim ; Barbara Baker ; Shuqun ZhangSource :
- The Plant journal : for cell and molecular biology [ 0960-7412 ] ; 2003.
English descriptors
- KwdEn :
- Amino Acid Sequence (MeSH), Apoptosis (genetics), Apoptosis (physiology), Gene Expression Regulation, Enzymologic (MeSH), Gene Expression Regulation, Plant (MeSH), Gene Silencing (MeSH), Genetic Complementation Test (MeSH), Immunity, Innate (genetics), MAP Kinase Kinase 2 (MeSH), Mitogen-Activated Protein Kinase Kinases (genetics), Mitogen-Activated Protein Kinase Kinases (metabolism), Mitogen-Activated Protein Kinases (genetics), Mitogen-Activated Protein Kinases (metabolism), Molecular Sequence Data (MeSH), Mutation (MeSH), Nucleocapsid Proteins (genetics), Nucleocapsid Proteins (metabolism), Plant Diseases (genetics), Plant Diseases (virology), Plant Proteins (genetics), Plant Proteins (metabolism), Plants, Genetically Modified (MeSH), Potexvirus (growth & development), Protein Interaction Mapping (MeSH), Protein-Tyrosine Kinases (genetics), Protein-Tyrosine Kinases (metabolism), Tobacco (enzymology), Tobacco (genetics), Tobacco (virology), Tobacco Mosaic Virus (growth & development).
- MESH :
- chemical , genetics : Mitogen-Activated Protein Kinase Kinases, Mitogen-Activated Protein Kinases, Nucleocapsid Proteins, Plant Proteins, Protein-Tyrosine Kinases.
- chemical , metabolism : Mitogen-Activated Protein Kinase Kinases, Mitogen-Activated Protein Kinases, Nucleocapsid Proteins, Plant Proteins, Protein-Tyrosine Kinases.
- chemical : MAP Kinase Kinase 2.
- enzymology : Tobacco.
- genetics : Apoptosis, Immunity, Innate, Plant Diseases, Tobacco.
- growth & development : Potexvirus, Tobacco Mosaic Virus.
- physiology : Apoptosis.
- virology : Plant Diseases, Tobacco.
- Amino Acid Sequence, Gene Expression Regulation, Enzymologic, Gene Expression Regulation, Plant, Gene Silencing, Genetic Complementation Test, Molecular Sequence Data, Mutation, Plants, Genetically Modified, Protein Interaction Mapping.
Abstract
The active defense of plants against pathogens often includes rapid and localized cell death known as hypersensitive response (HR). Protein phosphorylation and dephosphorylation are implicated in this event based on studies using protein kinase and phosphatase inhibitors. Recent transient gain-of-function studies demonstrated that the activation of salicylic acid-induced protein kinase (SIPK) and wounding-induced protein kinase (WIPK), two tobacco mitogen-activated protein kinases (MAPKs) by their upstream MAPK kinase (MAPKK), NtMEK2 leads to HR-like cell death. Here, we report that the conserved kinase interaction motif (KIM) in MAPKKs is required for NtMEK2 function. Mutation of the conserved basic amino acids in this motif, or the deletion of N-terminal 64 amino acids containing this motif significantly compromised or abolished the ability of NtMEK2DD to activate SIPK/WIPK in vivo. These mutants were also defective in interacting with SIPK and WIPK, suggesting protein-protein interaction is required for the functional integrity of this MAPK cascade. To eliminate Agrobacterium that is known to activate a number of defense responses in transient transformation experiments, we generated permanent transgenic plants. Induction of NtMEK2DD expression by dexamethasone induced HR-like cell death in both T1 and T2 plants. In addition, by using PVX-induced gene silencing, we demonstrated that the suppression of all three known components in the NtMEK2-SIPK/WIPK pathway attenuated N gene-mediated TMV resistance. Together with previous report that SIPK and WIPK are activated by TMV in a gene-for-gene-dependent manner, we conclude that NtMEK2-SIPK/WIPK pathway plays a positive role in N gene-mediated resistance, possibly through regulating HR cell death.
DOI: 10.1046/j.1365-313x.2003.01664.x
PubMed: 12609044
Links to Exploration step
pubmed:12609044Le document en format XML
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first="Barbara" last="Baker">Barbara Baker</name></author><author><name sortKey="Zhang, Shuqun" sort="Zhang, Shuqun" uniqKey="Zhang S" first="Shuqun" last="Zhang">Shuqun Zhang</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2003">2003</date><idno type="RBID">pubmed:12609044</idno><idno type="pmid">12609044</idno><idno type="doi">10.1046/j.1365-313x.2003.01664.x</idno><idno type="wicri:Area/Main/Corpus">000840</idno><idno type="wicri:explorRef" wicri:stream="Main" wicri:step="Corpus" wicri:corpus="PubMed">000840</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Function of a mitogen-activated protein kinase pathway in N gene-mediated resistance in tobacco.</title><author><name sortKey="Jin, Hailing" sort="Jin, Hailing" uniqKey="Jin H" first="Hailing" last="Jin">Hailing Jin</name><affiliation><nlm:affiliation>Department of Plant and Microbial Biology, University of California, Berkeley & Plant Gene Expression Center, USDA-ARS, 800 Buchanan St., Albany, CA 94710, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Liu, Yidong" sort="Liu, Yidong" uniqKey="Liu Y" first="Yidong" last="Liu">Yidong Liu</name></author><author><name sortKey="Yang, Kwang Yeol" sort="Yang, Kwang Yeol" uniqKey="Yang K" first="Kwang-Yeol" last="Yang">Kwang-Yeol Yang</name></author><author><name sortKey="Kim, Cha Young" sort="Kim, Cha Young" uniqKey="Kim C" first="Cha Young" last="Kim">Cha Young Kim</name></author><author><name sortKey="Baker, Barbara" sort="Baker, Barbara" uniqKey="Baker B" first="Barbara" last="Baker">Barbara Baker</name></author><author><name sortKey="Zhang, Shuqun" sort="Zhang, Shuqun" uniqKey="Zhang S" first="Shuqun" last="Zhang">Shuqun Zhang</name></author></analytic><series><title level="j">The Plant journal : for cell and molecular biology</title><idno type="ISSN">0960-7412</idno><imprint><date when="2003" type="published">2003</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Amino Acid Sequence (MeSH)</term><term>Apoptosis (genetics)</term><term>Apoptosis (physiology)</term><term>Gene Expression Regulation, Enzymologic (MeSH)</term><term>Gene Expression Regulation, Plant (MeSH)</term><term>Gene Silencing (MeSH)</term><term>Genetic Complementation Test (MeSH)</term><term>Immunity, Innate (genetics)</term><term>MAP Kinase Kinase 2 (MeSH)</term><term>Mitogen-Activated Protein Kinase Kinases (genetics)</term><term>Mitogen-Activated Protein Kinase Kinases (metabolism)</term><term>Mitogen-Activated Protein Kinases (genetics)</term><term>Mitogen-Activated Protein Kinases (metabolism)</term><term>Molecular Sequence Data (MeSH)</term><term>Mutation (MeSH)</term><term>Nucleocapsid Proteins (genetics)</term><term>Nucleocapsid Proteins (metabolism)</term><term>Plant Diseases (genetics)</term><term>Plant Diseases (virology)</term><term>Plant Proteins (genetics)</term><term>Plant Proteins (metabolism)</term><term>Plants, Genetically Modified (MeSH)</term><term>Potexvirus (growth & development)</term><term>Protein Interaction Mapping (MeSH)</term><term>Protein-Tyrosine Kinases (genetics)</term><term>Protein-Tyrosine Kinases (metabolism)</term><term>Tobacco (enzymology)</term><term>Tobacco (genetics)</term><term>Tobacco (virology)</term><term>Tobacco Mosaic Virus (growth & development)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Mitogen-Activated Protein Kinase Kinases</term><term>Mitogen-Activated Protein Kinases</term><term>Nucleocapsid Proteins</term><term>Plant Proteins</term><term>Protein-Tyrosine Kinases</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Mitogen-Activated Protein Kinase Kinases</term><term>Mitogen-Activated Protein Kinases</term><term>Nucleocapsid Proteins</term><term>Plant Proteins</term><term>Protein-Tyrosine Kinases</term></keywords><keywords scheme="MESH" type="chemical" xml:lang="en"><term>MAP Kinase Kinase 2</term></keywords><keywords scheme="MESH" qualifier="enzymology" xml:lang="en"><term>Tobacco</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Apoptosis</term><term>Immunity, Innate</term><term>Plant Diseases</term><term>Tobacco</term></keywords><keywords scheme="MESH" qualifier="growth & development" xml:lang="en"><term>Potexvirus</term><term>Tobacco Mosaic Virus</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Apoptosis</term></keywords><keywords scheme="MESH" qualifier="virology" xml:lang="en"><term>Plant Diseases</term><term>Tobacco</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Amino Acid Sequence</term><term>Gene Expression Regulation, Enzymologic</term><term>Gene Expression Regulation, Plant</term><term>Gene Silencing</term><term>Genetic Complementation Test</term><term>Molecular Sequence Data</term><term>Mutation</term><term>Plants, Genetically Modified</term><term>Protein Interaction Mapping</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The active defense of plants against pathogens often includes rapid and localized cell death known as hypersensitive response (HR). Protein phosphorylation and dephosphorylation are implicated in this event based on studies using protein kinase and phosphatase inhibitors. Recent transient gain-of-function studies demonstrated that the activation of salicylic acid-induced protein kinase (SIPK) and wounding-induced protein kinase (WIPK), two tobacco mitogen-activated protein kinases (MAPKs) by their upstream MAPK kinase (MAPKK), NtMEK2 leads to HR-like cell death. Here, we report that the conserved kinase interaction motif (KIM) in MAPKKs is required for NtMEK2 function. Mutation of the conserved basic amino acids in this motif, or the deletion of N-terminal 64 amino acids containing this motif significantly compromised or abolished the ability of NtMEK2DD to activate SIPK/WIPK in vivo. These mutants were also defective in interacting with SIPK and WIPK, suggesting protein-protein interaction is required for the functional integrity of this MAPK cascade. To eliminate Agrobacterium that is known to activate a number of defense responses in transient transformation experiments, we generated permanent transgenic plants. Induction of NtMEK2DD expression by dexamethasone induced HR-like cell death in both T1 and T2 plants. In addition, by using PVX-induced gene silencing, we demonstrated that the suppression of all three known components in the NtMEK2-SIPK/WIPK pathway attenuated N gene-mediated TMV resistance. Together with previous report that SIPK and WIPK are activated by TMV in a gene-for-gene-dependent manner, we conclude that NtMEK2-SIPK/WIPK pathway plays a positive role in N gene-mediated resistance, possibly through regulating HR cell death.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">12609044</PMID><DateCompleted><Year>2003</Year><Month>05</Month><Day>15</Day></DateCompleted><DateRevised><Year>2019</Year><Month>09</Month><Day>06</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0960-7412</ISSN><JournalIssue CitedMedium="Print"><Volume>33</Volume><Issue>4</Issue><PubDate><Year>2003</Year><Month>Feb</Month></PubDate></JournalIssue><Title>The Plant journal : for cell and molecular biology</Title><ISOAbbreviation>Plant J</ISOAbbreviation></Journal><ArticleTitle>Function of a mitogen-activated protein kinase pathway in N gene-mediated resistance in tobacco.</ArticleTitle><Pagination><MedlinePgn>719-31</MedlinePgn></Pagination><Abstract><AbstractText>The active defense of plants against pathogens often includes rapid and localized cell death known as hypersensitive response (HR). Protein phosphorylation and dephosphorylation are implicated in this event based on studies using protein kinase and phosphatase inhibitors. Recent transient gain-of-function studies demonstrated that the activation of salicylic acid-induced protein kinase (SIPK) and wounding-induced protein kinase (WIPK), two tobacco mitogen-activated protein kinases (MAPKs) by their upstream MAPK kinase (MAPKK), NtMEK2 leads to HR-like cell death. Here, we report that the conserved kinase interaction motif (KIM) in MAPKKs is required for NtMEK2 function. Mutation of the conserved basic amino acids in this motif, or the deletion of N-terminal 64 amino acids containing this motif significantly compromised or abolished the ability of NtMEK2DD to activate SIPK/WIPK in vivo. These mutants were also defective in interacting with SIPK and WIPK, suggesting protein-protein interaction is required for the functional integrity of this MAPK cascade. To eliminate Agrobacterium that is known to activate a number of defense responses in transient transformation experiments, we generated permanent transgenic plants. Induction of NtMEK2DD expression by dexamethasone induced HR-like cell death in both T1 and T2 plants. In addition, by using PVX-induced gene silencing, we demonstrated that the suppression of all three known components in the NtMEK2-SIPK/WIPK pathway attenuated N gene-mediated TMV resistance. Together with previous report that SIPK and WIPK are activated by TMV in a gene-for-gene-dependent manner, we conclude that NtMEK2-SIPK/WIPK pathway plays a positive role in N gene-mediated resistance, possibly through regulating HR cell death.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Jin</LastName><ForeName>Hailing</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>Department of Plant and Microbial Biology, University of California, Berkeley & Plant Gene Expression Center, USDA-ARS, 800 Buchanan St., Albany, CA 94710, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Liu</LastName><ForeName>Yidong</ForeName><Initials>Y</Initials></Author><Author ValidYN="Y"><LastName>Yang</LastName><ForeName>Kwang-Yeol</ForeName><Initials>KY</Initials></Author><Author ValidYN="Y"><LastName>Kim</LastName><ForeName>Cha Young</ForeName><Initials>CY</Initials></Author><Author ValidYN="Y"><LastName>Baker</LastName><ForeName>Barbara</ForeName><Initials>B</Initials></Author><Author ValidYN="Y"><LastName>Zhang</LastName><ForeName>Shuqun</ForeName><Initials>S</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>England</Country><MedlineTA>Plant J</MedlineTA><NlmUniqueID>9207397</NlmUniqueID><ISSNLinking>0960-7412</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D019590">Nucleocapsid Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D010940">Plant Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.10.1</RegistryNumber><NameOfSubstance UI="D011505">Protein-Tyrosine Kinases</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.11.24</RegistryNumber><NameOfSubstance UI="D020928">Mitogen-Activated Protein Kinases</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.11.24</RegistryNumber><NameOfSubstance UI="C106405">SA-induced protein kinase</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.11.24</RegistryNumber><NameOfSubstance UI="C113423">WIPK protein, Nicotiana tabacum</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.12.2</RegistryNumber><NameOfSubstance UI="D048370">MAP Kinase Kinase 2</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.12.2</RegistryNumber><NameOfSubstance UI="D020929">Mitogen-Activated Protein Kinase Kinases</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000595" MajorTopicYN="N">Amino Acid Sequence</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D017209" MajorTopicYN="N">Apoptosis</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015971" MajorTopicYN="N">Gene Expression Regulation, Enzymologic</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018506" MajorTopicYN="N">Gene Expression Regulation, Plant</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D020868" MajorTopicYN="N">Gene Silencing</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005816" MajorTopicYN="N">Genetic Complementation Test</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007113" MajorTopicYN="N">Immunity, Innate</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D048370" MajorTopicYN="N">MAP Kinase Kinase 2</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D020929" MajorTopicYN="N">Mitogen-Activated Protein Kinase Kinases</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D020928" MajorTopicYN="N">Mitogen-Activated Protein Kinases</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008969" MajorTopicYN="N">Molecular Sequence Data</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009154" MajorTopicYN="N">Mutation</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D019590" MajorTopicYN="N">Nucleocapsid Proteins</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010935" MajorTopicYN="N">Plant Diseases</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000821" MajorTopicYN="N">virology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010940" MajorTopicYN="N">Plant Proteins</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D030821" MajorTopicYN="N">Plants, Genetically Modified</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D017863" MajorTopicYN="N">Potexvirus</DescriptorName><QualifierName UI="Q000254" MajorTopicYN="N">growth & development</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D025941" MajorTopicYN="N">Protein Interaction Mapping</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D011505" MajorTopicYN="N">Protein-Tyrosine Kinases</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D014026" MajorTopicYN="N">Tobacco</DescriptorName><QualifierName UI="Q000201" MajorTopicYN="N">enzymology</QualifierName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName><QualifierName UI="Q000821" MajorTopicYN="N">virology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D014027" MajorTopicYN="N">Tobacco Mosaic Virus</DescriptorName><QualifierName UI="Q000254" MajorTopicYN="N">growth & development</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2003</Year><Month>3</Month><Day>1</Day><Hour>4</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate 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