Pathogen-induced expression of a cecropin A-melittin antimicrobial peptide gene confers antifungal resistance in transgenic tobacco.
Identifieur interne : 004069 ( Main/Corpus ); précédent : 004068; suivant : 004070Pathogen-induced expression of a cecropin A-melittin antimicrobial peptide gene confers antifungal resistance in transgenic tobacco.
Auteurs : Dmytro P. Yevtushenko ; Rafael Romero ; Benjamin S. Forward ; Robert E. Hancock ; William W. Kay ; Santosh MisraSource :
- Journal of experimental botany [ 0022-0957 ] ; 2005.
English descriptors
- KwdEn :
- Antimicrobial Cationic Peptides (biosynthesis), Antimicrobial Cationic Peptides (genetics), Fusarium (MeSH), Immunity, Innate (genetics), Immunity, Innate (physiology), Melitten (biosynthesis), Melitten (genetics), Plant Diseases (microbiology), Plants, Genetically Modified (MeSH), Promoter Regions, Genetic (MeSH), Recombinant Fusion Proteins (biosynthesis), Tobacco (genetics), Tobacco (metabolism), Tobacco (microbiology).
- MESH :
- chemical , biosynthesis : Antimicrobial Cationic Peptides, Melitten, Recombinant Fusion Proteins.
- chemical , genetics : Antimicrobial Cationic Peptides, Melitten.
- genetics : Immunity, Innate, Tobacco.
- metabolism : Tobacco.
- microbiology : Plant Diseases, Tobacco.
- physiology : Immunity, Innate.
- Fusarium, Plants, Genetically Modified, Promoter Regions, Genetic.
Abstract
Expression of defensive genes from a promoter that is specifically activated in response to pathogen invasion is highly desirable for engineering disease-resistant plants. A plant transformation vector was constructed with transcriptional fusion between the pathogen-responsive win3.12T promoter from poplar and the gene encoding the novel cecropin A-melittin hybrid peptide (CEMA) with strong antimicrobial activity. This promoter-transgene combination was evaluated in transgenic tobacco (Nicotiana tabacum L. cv. Xanthi) for enhanced plant resistance against a highly virulent pathogenic fungus Fusarium solani. Transgene expression in leaves was strongly increased after fungal infection or mechanical wounding, and the accumulation of CEMA transcripts was found to be systemic and positively correlated with the number of transgene insertions. A simple and efficient in vitro regeneration bioassay for preliminary screening of transgenic lines against pathogenic fungi was developed. CEMA had strong antifungal activity in vitro, inhibiting conidia germination at concentrations that were non-toxic to tobacco protoplasts. Most importantly, the expression level of the CEMA peptide in vivo, regulated by the win3.12T promoter, was sufficient to confer resistance against F. solani in transgenic tobacco. The antifungal resistance of plants with high CEMA expression was strong and reproducible. In addition, leaf tissue extracts from transgenic plants significantly reduced the number of fungal colonies arising from germinated conidia. Accumulation of CEMA peptide in transgenic tobacco had no deleterious effect on plant growth and development. This is the first report showing the application of a heterologous pathogen-inducible promoter to direct the expression of an antimicrobial peptide in plants, and the feasibility of this approach to provide disease resistance in tobacco and, possibly, other crops.
DOI: 10.1093/jxb/eri165
PubMed: 15863447
Links to Exploration step
pubmed:15863447Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Pathogen-induced expression of a cecropin A-melittin antimicrobial peptide gene confers antifungal resistance in transgenic tobacco.</title><author><name sortKey="Yevtushenko, Dmytro P" sort="Yevtushenko, Dmytro P" uniqKey="Yevtushenko D" first="Dmytro P" last="Yevtushenko">Dmytro P. Yevtushenko</name><affiliation><nlm:affiliation>Department of Biochemistry and Microbiology, University of Victoria, Victoria, British Columbia, V8W 3P6 Canada.</nlm:affiliation></affiliation></author><author><name sortKey="Romero, Rafael" sort="Romero, Rafael" uniqKey="Romero R" first="Rafael" last="Romero">Rafael Romero</name></author><author><name sortKey="Forward, Benjamin S" sort="Forward, Benjamin S" uniqKey="Forward B" first="Benjamin S" last="Forward">Benjamin S. Forward</name></author><author><name sortKey="Hancock, Robert E" sort="Hancock, Robert E" uniqKey="Hancock R" first="Robert E" last="Hancock">Robert E. Hancock</name></author><author><name sortKey="Kay, William W" sort="Kay, William W" uniqKey="Kay W" first="William W" last="Kay">William W. Kay</name></author><author><name sortKey="Misra, Santosh" sort="Misra, Santosh" uniqKey="Misra S" first="Santosh" last="Misra">Santosh Misra</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2005">2005</date><idno type="RBID">pubmed:15863447</idno><idno type="pmid">15863447</idno><idno type="doi">10.1093/jxb/eri165</idno><idno type="wicri:Area/Main/Corpus">004069</idno><idno type="wicri:explorRef" wicri:stream="Main" wicri:step="Corpus" wicri:corpus="PubMed">004069</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Pathogen-induced expression of a cecropin A-melittin antimicrobial peptide gene confers antifungal resistance in transgenic tobacco.</title><author><name sortKey="Yevtushenko, Dmytro P" sort="Yevtushenko, Dmytro P" uniqKey="Yevtushenko D" first="Dmytro P" last="Yevtushenko">Dmytro P. 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Kay</name></author><author><name sortKey="Misra, Santosh" sort="Misra, Santosh" uniqKey="Misra S" first="Santosh" last="Misra">Santosh Misra</name></author></analytic><series><title level="j">Journal of experimental botany</title><idno type="ISSN">0022-0957</idno><imprint><date when="2005" type="published">2005</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Antimicrobial Cationic Peptides (biosynthesis)</term><term>Antimicrobial Cationic Peptides (genetics)</term><term>Fusarium (MeSH)</term><term>Immunity, Innate (genetics)</term><term>Immunity, Innate (physiology)</term><term>Melitten (biosynthesis)</term><term>Melitten (genetics)</term><term>Plant Diseases (microbiology)</term><term>Plants, Genetically Modified (MeSH)</term><term>Promoter Regions, Genetic (MeSH)</term><term>Recombinant Fusion Proteins (biosynthesis)</term><term>Tobacco (genetics)</term><term>Tobacco (metabolism)</term><term>Tobacco (microbiology)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="biosynthesis" xml:lang="en"><term>Antimicrobial Cationic Peptides</term><term>Melitten</term><term>Recombinant Fusion Proteins</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Antimicrobial Cationic Peptides</term><term>Melitten</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Immunity, Innate</term><term>Tobacco</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Tobacco</term></keywords><keywords scheme="MESH" qualifier="microbiology" xml:lang="en"><term>Plant Diseases</term><term>Tobacco</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Immunity, Innate</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Fusarium</term><term>Plants, Genetically Modified</term><term>Promoter Regions, Genetic</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Expression of defensive genes from a promoter that is specifically activated in response to pathogen invasion is highly desirable for engineering disease-resistant plants. A plant transformation vector was constructed with transcriptional fusion between the pathogen-responsive win3.12T promoter from poplar and the gene encoding the novel cecropin A-melittin hybrid peptide (CEMA) with strong antimicrobial activity. This promoter-transgene combination was evaluated in transgenic tobacco (Nicotiana tabacum L. cv. Xanthi) for enhanced plant resistance against a highly virulent pathogenic fungus Fusarium solani. Transgene expression in leaves was strongly increased after fungal infection or mechanical wounding, and the accumulation of CEMA transcripts was found to be systemic and positively correlated with the number of transgene insertions. A simple and efficient in vitro regeneration bioassay for preliminary screening of transgenic lines against pathogenic fungi was developed. CEMA had strong antifungal activity in vitro, inhibiting conidia germination at concentrations that were non-toxic to tobacco protoplasts. Most importantly, the expression level of the CEMA peptide in vivo, regulated by the win3.12T promoter, was sufficient to confer resistance against F. solani in transgenic tobacco. The antifungal resistance of plants with high CEMA expression was strong and reproducible. In addition, leaf tissue extracts from transgenic plants significantly reduced the number of fungal colonies arising from germinated conidia. Accumulation of CEMA peptide in transgenic tobacco had no deleterious effect on plant growth and development. This is the first report showing the application of a heterologous pathogen-inducible promoter to direct the expression of an antimicrobial peptide in plants, and the feasibility of this approach to provide disease resistance in tobacco and, possibly, other crops.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">15863447</PMID><DateCompleted><Year>2005</Year><Month>07</Month><Day>07</Day></DateCompleted><DateRevised><Year>2008</Year><Month>11</Month><Day>21</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Print">0022-0957</ISSN><JournalIssue CitedMedium="Print"><Volume>56</Volume><Issue>416</Issue><PubDate><Year>2005</Year><Month>Jun</Month></PubDate></JournalIssue><Title>Journal of experimental botany</Title><ISOAbbreviation>J Exp Bot</ISOAbbreviation></Journal><ArticleTitle>Pathogen-induced expression of a cecropin A-melittin antimicrobial peptide gene confers antifungal resistance in transgenic tobacco.</ArticleTitle><Pagination><MedlinePgn>1685-95</MedlinePgn></Pagination><Abstract><AbstractText>Expression of defensive genes from a promoter that is specifically activated in response to pathogen invasion is highly desirable for engineering disease-resistant plants. A plant transformation vector was constructed with transcriptional fusion between the pathogen-responsive win3.12T promoter from poplar and the gene encoding the novel cecropin A-melittin hybrid peptide (CEMA) with strong antimicrobial activity. This promoter-transgene combination was evaluated in transgenic tobacco (Nicotiana tabacum L. cv. Xanthi) for enhanced plant resistance against a highly virulent pathogenic fungus Fusarium solani. Transgene expression in leaves was strongly increased after fungal infection or mechanical wounding, and the accumulation of CEMA transcripts was found to be systemic and positively correlated with the number of transgene insertions. A simple and efficient in vitro regeneration bioassay for preliminary screening of transgenic lines against pathogenic fungi was developed. CEMA had strong antifungal activity in vitro, inhibiting conidia germination at concentrations that were non-toxic to tobacco protoplasts. Most importantly, the expression level of the CEMA peptide in vivo, regulated by the win3.12T promoter, was sufficient to confer resistance against F. solani in transgenic tobacco. The antifungal resistance of plants with high CEMA expression was strong and reproducible. In addition, leaf tissue extracts from transgenic plants significantly reduced the number of fungal colonies arising from germinated conidia. Accumulation of CEMA peptide in transgenic tobacco had no deleterious effect on plant growth and development. This is the first report showing the application of a heterologous pathogen-inducible promoter to direct the expression of an antimicrobial peptide in plants, and the feasibility of this approach to provide disease resistance in tobacco and, possibly, other crops.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Yevtushenko</LastName><ForeName>Dmytro P</ForeName><Initials>DP</Initials><AffiliationInfo><Affiliation>Department of Biochemistry and Microbiology, University of Victoria, Victoria, British Columbia, V8W 3P6 Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Romero</LastName><ForeName>Rafael</ForeName><Initials>R</Initials></Author><Author ValidYN="Y"><LastName>Forward</LastName><ForeName>Benjamin S</ForeName><Initials>BS</Initials></Author><Author ValidYN="Y"><LastName>Hancock</LastName><ForeName>Robert E</ForeName><Initials>RE</Initials></Author><Author ValidYN="Y"><LastName>Kay</LastName><ForeName>William W</ForeName><Initials>WW</Initials></Author><Author ValidYN="Y"><LastName>Misra</LastName><ForeName>Santosh</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></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2005</Year><Month>04</Month><Day>29</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>J Exp Bot</MedlineTA><NlmUniqueID>9882906</NlmUniqueID><ISSNLinking>0022-0957</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D023181">Antimicrobial Cationic Peptides</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D011993">Recombinant Fusion Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>20449-79-0</RegistryNumber><NameOfSubstance UI="D008555">Melitten</NameOfSubstance></Chemical><Chemical><RegistryNumber>80451-04-3</RegistryNumber><NameOfSubstance UI="C031161">cecropin A</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D023181" MajorTopicYN="N">Antimicrobial Cationic Peptides</DescriptorName><QualifierName UI="Q000096" MajorTopicYN="Y">biosynthesis</QualifierName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005670" MajorTopicYN="N">Fusarium</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007113" MajorTopicYN="N">Immunity, Innate</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008555" MajorTopicYN="N">Melitten</DescriptorName><QualifierName UI="Q000096" MajorTopicYN="Y">biosynthesis</QualifierName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010935" MajorTopicYN="N">Plant Diseases</DescriptorName><QualifierName UI="Q000382" MajorTopicYN="N">microbiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D030821" MajorTopicYN="N">Plants, Genetically Modified</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D011401" MajorTopicYN="N">Promoter Regions, Genetic</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D011993" MajorTopicYN="N">Recombinant Fusion Proteins</DescriptorName><QualifierName UI="Q000096" MajorTopicYN="N">biosynthesis</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D014026" MajorTopicYN="N">Tobacco</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName><QualifierName UI="Q000382" MajorTopicYN="N">microbiology</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2005</Year><Month>5</Month><Day>3</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2005</Year><Month>7</Month><Day>8</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2005</Year><Month>5</Month><Day>3</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">15863447</ArticleId><ArticleId IdType="pii">eri165</ArticleId><ArticleId IdType="doi">10.1093/jxb/eri165</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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