Transcriptional Control of Glutaredoxin GRXC9 Expression by a Salicylic Acid-Dependent and NPR1-Independent Pathway in Arabidopsis.
Identifieur interne : 000490 ( Main/Exploration ); précédent : 000489; suivant : 000491Transcriptional Control of Glutaredoxin GRXC9 Expression by a Salicylic Acid-Dependent and NPR1-Independent Pathway in Arabidopsis.
Auteurs : Ariel Herrera-Vásquez [Chili] ; Loreto Carvallo [Chili] ; Francisca Blanco [Chili] ; Mariola Tobar [Chili] ; Eva Villarroel-Candia [Chili] ; Jesús Vicente-Carbajosa [Espagne] ; Paula Salinas [Chili] ; Loreto Holuigue [Chili]Source :
- Plant molecular biology reporter [ 0735-9640 ]
Abstract
Salicylic acid (SA) is a key hormone that mediates gene transcriptional reprogramming in the context of the defense response to stress. GRXC9, coding for a CC-type glutaredoxin from Arabidopsis, is an SA-responsive gene induced early and transiently by an NPR1-independent pathway. Here, we address the mechanism involved in this SA-dependent pathway, using GRXC9 as a model gene. We first established that GRXC9 expression is induced by UVB exposure through this pathway, validating its activation in a physiological stress condition. GRXC9 promoter analyses indicate that SA controls gene transcription through two activating sequence-1 (as-1)-like elements located in its proximal region. TGA2 and TGA3, but not TGA1, are constitutively bound to this promoter region. Accordingly, the transient recruitment of RNA polymerase II to the GRXC9 promoter, as well as the transient accumulation of gene transcripts detected in SA-treated WT plants, was abolished in a knockout mutant for the TGA class II factors. We conclude that constitutive binding of TGA2 is essential for controlling GRXC9 expression, while binding of TGA3 in a lesser extent contributes to this regulation. Finally, overexpression of GRXC9 indicates that the GRXC9 protein negatively controls its own gene expression, forming part of the complex bound to the as-1-containing promoter region. These findings are integrated in a model that explains how SA controls transcription of GRXC9 in the context of the defense response to stress.
DOI: 10.1007/s11105-014-0782-5
PubMed: 26696694
PubMed Central: PMC4677692
Affiliations:
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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Transcriptional Control of Glutaredoxin <i>GRXC9</i> Expression by a Salicylic Acid-Dependent and NPR1-Independent Pathway in <i>Arabidopsis</i>.</title><author><name sortKey="Herrera Vasquez, Ariel" sort="Herrera Vasquez, Ariel" uniqKey="Herrera Vasquez A" first="Ariel" last="Herrera-Vásquez">Ariel Herrera-Vásquez</name><affiliation wicri:level="1"><nlm:affiliation>Departamento de Genética Molecular y Microbiología, Facultad de Ciencias Biológicas, Pontificia Universidad Católica de Chile, Alameda 340, Santiago, Chile.</nlm:affiliation><country xml:lang="fr">Chili</country><wicri:regionArea>Departamento de Genética Molecular y Microbiología, Facultad de Ciencias Biológicas, Pontificia Universidad Católica de Chile, Alameda 340, Santiago</wicri:regionArea><wicri:noRegion>Santiago</wicri:noRegion></affiliation></author><author><name sortKey="Carvallo, Loreto" sort="Carvallo, Loreto" uniqKey="Carvallo L" first="Loreto" last="Carvallo">Loreto Carvallo</name><affiliation wicri:level="1"><nlm:affiliation>Departamento de Genética Molecular y Microbiología, Facultad de Ciencias Biológicas, Pontificia Universidad Católica de Chile, Alameda 340, Santiago, Chile.</nlm:affiliation><country xml:lang="fr">Chili</country><wicri:regionArea>Departamento de Genética Molecular y Microbiología, Facultad de Ciencias Biológicas, Pontificia Universidad Católica de Chile, Alameda 340, Santiago</wicri:regionArea><wicri:noRegion>Santiago</wicri:noRegion></affiliation></author><author><name sortKey="Blanco, Francisca" sort="Blanco, Francisca" uniqKey="Blanco F" first="Francisca" last="Blanco">Francisca Blanco</name><affiliation wicri:level="1"><nlm:affiliation>Departamento de Genética Molecular y Microbiología, Facultad de Ciencias Biológicas, Pontificia Universidad Católica de Chile, Alameda 340, Santiago, Chile.</nlm:affiliation><country xml:lang="fr">Chili</country><wicri:regionArea>Departamento de Genética Molecular y 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Santiago</wicri:regionArea><wicri:noRegion>Santiago</wicri:noRegion></affiliation></author><author><name sortKey="Carvallo, Loreto" sort="Carvallo, Loreto" uniqKey="Carvallo L" first="Loreto" last="Carvallo">Loreto Carvallo</name><affiliation wicri:level="1"><nlm:affiliation>Departamento de Genética Molecular y Microbiología, Facultad de Ciencias Biológicas, Pontificia Universidad Católica de Chile, Alameda 340, Santiago, Chile.</nlm:affiliation><country xml:lang="fr">Chili</country><wicri:regionArea>Departamento de Genética Molecular y Microbiología, Facultad de Ciencias Biológicas, Pontificia Universidad Católica de Chile, Alameda 340, Santiago</wicri:regionArea><wicri:noRegion>Santiago</wicri:noRegion></affiliation></author><author><name sortKey="Blanco, Francisca" sort="Blanco, Francisca" uniqKey="Blanco F" first="Francisca" last="Blanco">Francisca Blanco</name><affiliation wicri:level="1"><nlm:affiliation>Departamento de Genética Molecular y Microbiología, Facultad de Ciencias Biológicas, Pontificia Universidad Católica de Chile, Alameda 340, Santiago, Chile.</nlm:affiliation><country xml:lang="fr">Chili</country><wicri:regionArea>Departamento de Genética Molecular y Microbiología, Facultad de Ciencias Biológicas, Pontificia Universidad Católica de Chile, Alameda 340, Santiago</wicri:regionArea><wicri:noRegion>Santiago</wicri:noRegion></affiliation></author><author><name sortKey="Tobar, Mariola" sort="Tobar, Mariola" uniqKey="Tobar M" first="Mariola" last="Tobar">Mariola Tobar</name><affiliation wicri:level="1"><nlm:affiliation>Departamento de Genética Molecular y Microbiología, Facultad de Ciencias Biológicas, Pontificia Universidad Católica de Chile, Alameda 340, Santiago, Chile.</nlm:affiliation><country xml:lang="fr">Chili</country><wicri:regionArea>Departamento de Genética Molecular y Microbiología, Facultad de Ciencias Biológicas, Pontificia Universidad Católica de Chile, Alameda 340, Santiago</wicri:regionArea><wicri:noRegion>Santiago</wicri:noRegion></affiliation></author><author><name sortKey="Villarroel Candia, Eva" sort="Villarroel Candia, Eva" uniqKey="Villarroel Candia E" first="Eva" last="Villarroel-Candia">Eva Villarroel-Candia</name><affiliation wicri:level="1"><nlm:affiliation>Departamento de Genética Molecular y Microbiología, Facultad de Ciencias Biológicas, Pontificia Universidad Católica de Chile, Alameda 340, Santiago, Chile.</nlm:affiliation><country xml:lang="fr">Chili</country><wicri:regionArea>Departamento de Genética Molecular y Microbiología, Facultad de Ciencias Biológicas, Pontificia Universidad Católica de Chile, Alameda 340, Santiago</wicri:regionArea><wicri:noRegion>Santiago</wicri:noRegion></affiliation></author><author><name sortKey="Vicente Carbajosa, Jesus" sort="Vicente Carbajosa, Jesus" uniqKey="Vicente Carbajosa J" first="Jesús" last="Vicente-Carbajosa">Jesús Vicente-Carbajosa</name><affiliation wicri:level="3"><nlm:affiliation>Centro de Biotecnología y Genómica de Plantas (UPM-INIA), Universidad Politécnica de Madrid, 28223 Pozuelo de Alarcón, Madrid, Spain.</nlm:affiliation><country xml:lang="fr">Espagne</country><wicri:regionArea>Centro de Biotecnología y Genómica de Plantas (UPM-INIA), Universidad Politécnica de Madrid, 28223 Pozuelo de Alarcón, Madrid</wicri:regionArea><placeName><settlement type="city">Madrid</settlement><region nuts="2" type="region">Communauté de Madrid</region></placeName></affiliation></author><author><name sortKey="Salinas, Paula" sort="Salinas, Paula" uniqKey="Salinas P" first="Paula" last="Salinas">Paula Salinas</name><affiliation wicri:level="1"><nlm:affiliation>Departamento de Genética Molecular y Microbiología, Facultad de Ciencias Biológicas, Pontificia Universidad Católica de Chile, Alameda 340, Santiago, Chile.</nlm:affiliation><country xml:lang="fr">Chili</country><wicri:regionArea>Departamento de Genética Molecular y Microbiología, Facultad de Ciencias Biológicas, Pontificia Universidad Católica de Chile, Alameda 340, Santiago</wicri:regionArea><wicri:noRegion>Santiago</wicri:noRegion></affiliation></author><author><name sortKey="Holuigue, Loreto" sort="Holuigue, Loreto" uniqKey="Holuigue L" first="Loreto" last="Holuigue">Loreto Holuigue</name><affiliation wicri:level="1"><nlm:affiliation>Departamento de Genética Molecular y Microbiología, Facultad de Ciencias Biológicas, Pontificia Universidad Católica de Chile, Alameda 340, Santiago, Chile.</nlm:affiliation><country xml:lang="fr">Chili</country><wicri:regionArea>Departamento de Genética Molecular y Microbiología, Facultad de Ciencias Biológicas, Pontificia Universidad Católica de Chile, Alameda 340, Santiago</wicri:regionArea><wicri:noRegion>Santiago</wicri:noRegion></affiliation></author></analytic><series><title level="j">Plant molecular biology reporter</title><idno type="ISSN">0735-9640</idno></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Salicylic acid (SA) is a key hormone that mediates gene transcriptional reprogramming in the context of the defense response to stress. <i>GRXC9</i>, coding for a CC-type glutaredoxin from <i>Arabidopsis</i>, is an SA-responsive gene induced early and transiently by an NPR1-independent pathway. Here, we address the mechanism involved in this SA-dependent pathway, using <i>GRXC9</i> as a model gene. We first established that <i>GRXC9</i> expression is induced by UVB exposure through this pathway, validating its activation in a physiological stress condition. <i>GRXC9</i> promoter analyses indicate that SA controls gene transcription through two <i>activating sequence</i>-<i>1</i> (<i>as</i>-<i>1</i>)-like elements located in its proximal region. TGA2 and TGA3, but not TGA1, are constitutively bound to this promoter region. Accordingly, the transient recruitment of RNA polymerase II to the <i>GRXC9</i> promoter, as well as the transient accumulation of gene transcripts detected in SA-treated WT plants, was abolished in a <i>knockout</i> mutant for the TGA class II factors. We conclude that constitutive binding of TGA2 is essential for controlling <i>GRXC9</i> expression, while binding of TGA3 in a lesser extent contributes to this regulation. Finally, overexpression of <i>GRXC9</i> indicates that the <i>GRXC9</i> protein negatively controls its own gene expression, forming part of the complex bound to the <i>as</i>-<i>1</i>-containing promoter region. These findings are integrated in a model that explains how SA controls transcription of <i>GRXC9</i> in the context of the defense response to stress.</div></front></TEI><pubmed><MedlineCitation Status="PubMed-not-MEDLINE" Owner="NLM"><PMID Version="1">26696694</PMID><DateRevised><Year>2020</Year><Month>10</Month><Day>01</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Print">0735-9640</ISSN><JournalIssue CitedMedium="Print"><Volume>33</Volume><PubDate><MedlineDate>2015</MedlineDate></PubDate></JournalIssue><Title>Plant molecular biology reporter</Title><ISOAbbreviation>Plant Mol Biol Report</ISOAbbreviation></Journal><ArticleTitle>Transcriptional Control of Glutaredoxin <i>GRXC9</i> Expression by a Salicylic Acid-Dependent and NPR1-Independent Pathway in <i>Arabidopsis</i>.</ArticleTitle><Pagination><MedlinePgn>624-637</MedlinePgn></Pagination><Abstract><AbstractText>Salicylic acid (SA) is a key hormone that mediates gene transcriptional reprogramming in the context of the defense response to stress. <i>GRXC9</i>, coding for a CC-type glutaredoxin from <i>Arabidopsis</i>, is an SA-responsive gene induced early and transiently by an NPR1-independent pathway. Here, we address the mechanism involved in this SA-dependent pathway, using <i>GRXC9</i> as a model gene. We first established that <i>GRXC9</i> expression is induced by UVB exposure through this pathway, validating its activation in a physiological stress condition. <i>GRXC9</i> promoter analyses indicate that SA controls gene transcription through two <i>activating sequence</i>-<i>1</i> (<i>as</i>-<i>1</i>)-like elements located in its proximal region. TGA2 and TGA3, but not TGA1, are constitutively bound to this promoter region. Accordingly, the transient recruitment of RNA polymerase II to the <i>GRXC9</i> promoter, as well as the transient accumulation of gene transcripts detected in SA-treated WT plants, was abolished in a <i>knockout</i> mutant for the TGA class II factors. We conclude that constitutive binding of TGA2 is essential for controlling <i>GRXC9</i> expression, while binding of TGA3 in a lesser extent contributes to this regulation. Finally, overexpression of <i>GRXC9</i> indicates that the <i>GRXC9</i> protein negatively controls its own gene expression, forming part of the complex bound to the <i>as</i>-<i>1</i>-containing promoter region. These findings are integrated in a model that explains how SA controls transcription of <i>GRXC9</i> in the context of the defense response to stress.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Herrera-Vásquez</LastName><ForeName>Ariel</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Departamento de Genética Molecular y Microbiología, Facultad de Ciencias Biológicas, Pontificia Universidad Católica de Chile, Alameda 340, Santiago, Chile.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Carvallo</LastName><ForeName>Loreto</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>Departamento de Genética Molecular y Microbiología, Facultad de Ciencias Biológicas, Pontificia Universidad Católica de Chile, Alameda 340, Santiago, Chile.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Blanco</LastName><ForeName>Francisca</ForeName><Initials>F</Initials><AffiliationInfo><Affiliation>Departamento de Genética Molecular y Microbiología, Facultad de Ciencias Biológicas, Pontificia Universidad Católica de Chile, Alameda 340, Santiago, Chile.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Tobar</LastName><ForeName>Mariola</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Departamento de Genética Molecular y Microbiología, Facultad de Ciencias Biológicas, Pontificia Universidad Católica de Chile, Alameda 340, Santiago, Chile.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Villarroel-Candia</LastName><ForeName>Eva</ForeName><Initials>E</Initials><AffiliationInfo><Affiliation>Departamento de Genética Molecular y Microbiología, Facultad de Ciencias Biológicas, Pontificia Universidad Católica de Chile, Alameda 340, Santiago, Chile.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Vicente-Carbajosa</LastName><ForeName>Jesús</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Centro de Biotecnología y Genómica de Plantas (UPM-INIA), Universidad Politécnica de Madrid, 28223 Pozuelo de Alarcón, Madrid, Spain.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Salinas</LastName><ForeName>Paula</ForeName><Initials>P</Initials><AffiliationInfo><Affiliation>Departamento de Genética Molecular y Microbiología, Facultad de Ciencias Biológicas, Pontificia Universidad Católica de Chile, Alameda 340, Santiago, Chile.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Holuigue</LastName><ForeName>Loreto</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>Departamento de Genética Molecular y Microbiología, Facultad de Ciencias Biológicas, Pontificia Universidad Católica de Chile, Alameda 340, Santiago, Chile.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2014</Year><Month>08</Month><Day>14</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Plant Mol Biol Report</MedlineTA><NlmUniqueID>9880213</NlmUniqueID><ISSNLinking>0735-9640</ISSNLinking></MedlineJournalInfo><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Glutaredoxin GRXC9 (GRX480)</Keyword><Keyword MajorTopicYN="N">NPR1-independent</Keyword><Keyword MajorTopicYN="N">Salicylic acid</Keyword><Keyword MajorTopicYN="N">TGA transcription factors</Keyword><Keyword MajorTopicYN="N">as-1-like element</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="entrez"><Year>2015</Year><Month>12</Month><Day>24</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2015</Year><Month>12</Month><Day>24</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2015</Year><Month>12</Month><Day>24</Day><Hour>6</Hour><Minute>1</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">26696694</ArticleId><ArticleId IdType="doi">10.1007/s11105-014-0782-5</ArticleId><ArticleId IdType="pii">782</ArticleId><ArticleId IdType="pmc">PMC4677692</ArticleId></ArticleIdList><pmc-dir>pmcsd</pmc-dir>
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