Thurow, Corinna

[["dc.bibliographiccitation.firstpage","507"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","The Plant Journal"],["dc.bibliographiccitation.lastpage","519"],["dc.bibliographiccitation.volume","68"],["dc.contributor.author","La Camera, Sylvain"],["dc.contributor.author","L'Haridon, Floriane"],["dc.contributor.author","Astier, Jeremy"],["dc.contributor.author","Zander, Mark"],["dc.contributor.author","Abou-Mansour, Eliane"],["dc.contributor.author","Page, Gonzague"],["dc.contributor.author","Thurow, Corinna"],["dc.contributor.author","Wendehenne, David"],["dc.contributor.author","Gatz, Christiane"],["dc.contributor.author","Metraux, Jean-Pierre"],["dc.contributor.author","Lamotte, Olivier"],["dc.date.accessioned","2018-11-07T08:50:30Z"],["dc.date.available","2018-11-07T08:50:30Z"],["dc.date.issued","2011"],["dc.description.abstract","Botrytis cinerea is a major pre- and post-harvest necrotrophic pathogen with a broad host range that causes substantial crop losses. The plant hormone jasmonic acid (JA) is involved in the basal resistance against this fungus. Despite basal resistance, virulent strains of B. cinerea can cause disease on Arabidopsis thaliana and virulent pathogens can interfere with the metabolism of the host in a way to facilitate infection of the plant. However, plant genes that are required by the pathogen for infection remain poorly described. To find such genes, we have compared the changes in gene expression induced in A. thaliana by JA with those induced after B. cinerea using genome-wide microarrays. We have identified genes that are repressed by JA but that are induced by B. cinerea. In this study, we describe one candidate gene, ATGRXS13, that encodes for a putative glutaredoxin and that exhibits such a crossed expression. In plants that are infected by this necrotrophic fungus, ATGRXS13 expression was negatively controlled by JA and TGA transcription factors but also through a JA-salicylic acid (SA) cross-talk mechanism as B. cinerea induced SA production that positively controlled ATGRXS13 expression. Furthermore, plants impaired in ATGRXS13 exhibited resistance to B. cinerea. Finally, we present a model whereby B. cinerea takes advantage of defence signalling pathways of the plant to help the colonization of its host."],["dc.description.sponsorship","CNRS; Swiss NSF [125370]; Deutsche Forschungsgemeinschaft"],["dc.identifier.doi","10.1111/j.1365-313X.2011.04706.x"],["dc.identifier.isi","000296299800011"],["dc.identifier.pmid","21756272"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/21708"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.relation.issn","0960-7412"],["dc.title","The glutaredoxin ATGRXS13 is required to facilitate Botrytis cinerea infection of Arabidopsis thaliana plants"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","128"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","The Plant Journal"],["dc.bibliographiccitation.lastpage","139"],["dc.bibliographiccitation.volume","50"],["dc.contributor.author","Ndamukong, Ivan"],["dc.contributor.author","Al Abdallat, Ayed"],["dc.contributor.author","Thurow, Corinna"],["dc.contributor.author","Fode, Benjamin"],["dc.contributor.author","Zander, Mark"],["dc.contributor.author","Weigel, Ralf"],["dc.contributor.author","Gatz, Christiane"],["dc.date.accessioned","2018-11-07T11:03:56Z"],["dc.date.available","2018-11-07T11:03:56Z"],["dc.date.issued","2007"],["dc.description.abstract","Salicylic acid (SA) is a plant signaling molecule that mediates the induction of defense responses upon attack by a variety of pathogens. Moreover, it antagonizes gene induction by the stress signaling molecule jasmonic acid (JA). Several SA-responsive genes are regulated by basic/leucine zipper-type transcription factors of the TGA family. TGA factors interact with NPR1, a central regulator of many SA-induced defense responses including SA/JA antagonism. In order to identify further regulatory proteins of SA-dependent signaling pathways, a yeast protein interaction screen with tobacco TGA2.2 as bait and an Arabidopsis thaliana cDNA prey library was performed and led to the identification of a member of the glutaredoxin family (GRX480, encoded by At1g28480). Glutaredoxins are candidates for mediating redox regulation of proteins because of their capacity to catalyze disulfide transitions. This agrees with previous findings that the redox state of both TGA1 and NPR1 changes under inducing conditions. Transgenic Arabidopsis plants ectopically expressing GRX480 show near wild-type expression of standard marker genes for SA- and xenobiotic-inducible responses. In contrast, transcription of the JA-dependent defensin gene PDF1.2 was antagonized by transgenic GRX480. This, together with the observation that GRX480 transcription is SA-inducible and requires NPR1, suggests a role of GRX480 in SA/JA cross-talk. Suppression of PDF1.2 by GRX480 depends on the presence of TGA factors, indicating that the GRX480/TGA interaction is effective in planta."],["dc.identifier.doi","10.1111/j.1365-313X.2007.03039.x"],["dc.identifier.isi","000245258300011"],["dc.identifier.pmid","17397508"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/51719"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Blackwell Publishing"],["dc.relation.issn","0960-7412"],["dc.title","SA-inducible Arabidopsis glutaredoxin interacts with TGA factors and suppresses JA-responsive PDF1.2 transcription"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1671"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","PLANT PHYSIOLOGY"],["dc.bibliographiccitation.lastpage","1683"],["dc.bibliographiccitation.volume","165"],["dc.contributor.author","Zander, Mark"],["dc.contributor.author","Thurow, Corinna"],["dc.contributor.author","Gatz, Christiane"],["dc.date.accessioned","2018-11-07T09:36:56Z"],["dc.date.available","2018-11-07T09:36:56Z"],["dc.date.issued","2014"],["dc.description.abstract","Salicylic acid (SA), a hormone essential for defense against biotrophic pathogens, triggers increased susceptibility of plants against necrotrophic attackers by suppressing the jasmonic acid-ethylene (ET) defense response. Here, we show that this disease-promoting SA effect is abolished in plants lacking the three related TGACG sequence-specific binding proteins TGA2, TGA5, and TGA6 (class II TGAs). After treatment of plants with the ET precursor 1-aminocyclopropane-1-carboxylic acid (ACC), activation of all those genes that are suppressed by SA depended on class II TGAs. Rather than TGA binding sites, GCC-box motifs were significantly enriched in the corresponding promoters. GCC-box motifs are recognized by members of the superfamily of APETALA2/ETHYLENE RESPONSE FACTORs (ERFs). Of 11 activating ACC-induced APETALA2/ERFs, only ORA59 (for OCTADECANOID-RESPONSIVE ARABIDOPSIS APETALA2/ETHYLENE RESPONSE FACTOR domain protein59) and ERF96 were strongly suppressed by SA. ORA59 is the master regulator of the jasmonic acid-ET-induced defense program. ORA59 transcript levels do not reach maximal levels in the tga2 tga5 tga6 triple mutant, and this residual activity cannot be suppressed by SA. The ORA59 promoter contains an essential TGA binding site and is a direct target of class II TGAs as revealed by chromatin immunoprecipitation experiments. We suggest that class II TGAs at the ORA59 promoter constitute an important regulatory hub for the activation and SA suppression of ACC-induced genes."],["dc.identifier.doi","10.1104/pp.114.243360"],["dc.identifier.isi","000341648600023"],["dc.identifier.pmid","24989234"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/32725"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Soc Plant Biologists"],["dc.relation.issn","1532-2548"],["dc.relation.issn","0032-0889"],["dc.title","TGA Transcription Factors Activate the Salicylic Acid-Suppressible Branch of the Ethylene-Induced Defense Program by Regulating ORA59 Expression"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","831"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Molecular Plant"],["dc.bibliographiccitation.lastpage","840"],["dc.bibliographiccitation.volume","5"],["dc.contributor.author","Zander, Mark"],["dc.contributor.author","Chen, Shuxia"],["dc.contributor.author","Imkampe, Julia"],["dc.contributor.author","Thurow, Corinna"],["dc.contributor.author","Gatz, Christiane"],["dc.date.accessioned","2018-11-07T09:08:22Z"],["dc.date.available","2018-11-07T09:08:22Z"],["dc.date.issued","2012"],["dc.description.abstract","Glutaredoxins are small heat-stable oxidoreductases that transfer electrons from glutathione (GSH) to oxidized cysteine residues, thereby contributing to protein integrity and regulation. In Arabidopsis thaliana, floral glutaredoxins ROXY1 and ROXY2 and pathogen-induced ROXY19/GRX480 interact with bZIP transcription factors of the TGACG (TGA) motif-binding family. ROXY1, ROXY2, and TGA factors PERIANTHIA, TGA9, and TGA10 play essential roles in floral development. In contrast, ectopically expressed ROXY19/GRX480 negatively regulates expression of jasmonic acid (JA)/ethylene (ET)-induced defense genes through an unknown mechanism that requires clade II transcription factors TGA2, TGA5, and/or TGA6. Here, we report that at least 17 of the 21 land plant-specific glutaredoxins encoded in the Arabidopsis genome interact with TGA2 in a yeast-two-hybrid system. To investigate their capacity to interfere with the expression of JA/ET-induced genes, we developed a transient expression system. Activation of the ORA59 (OCTADECANOID-RESPONSIVE ARABIDOPSIS AP2/ERF-domain protein 59) promoter by transcription factor EIN3 (ETHYLENE INSENSITVE 3) was suppressed by co-expressed ROXY19/GRX480. Suppression depended on the L LL motif in the C-terminus of ROXY19/ GRX480. This putative protein interaction domain was recently described as being essential for the TGA/ROXY interaction. Ten of the 17 tested ROXY proteins suppressed ORA59 promoter activity, which correlated with the presence of the C-terminal ALWL motif, which is essential for ROXY1 function in flower development. ROXY19/GRX480-mediated repression depended on the GSH binding site, suggesting that redox modification of either TGA factors or as yet unknown target proteins is important for the suppression of ORA59 promoter activity."],["dc.identifier.doi","10.1093/mp/ssr113"],["dc.identifier.isi","000306668400008"],["dc.identifier.pmid","22207719"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/26016"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Oxford Univ Press"],["dc.relation.issn","1674-2052"],["dc.title","Repression of the Arabidopsis thaliana Jasmonic Acid/Ethylene-Induced Defense Pathway by TGA-Interacting Glutaredoxins Depends on Their C-Terminal ALWL Motif"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]