dc.contributor.author | Wallmeroth, Niklas | |
dc.contributor.author | Jeschke, Daniel | |
dc.contributor.author | Slane, Daniel | |
dc.contributor.author | Nägele, Janine | |
dc.contributor.author | Veerabagu, Manikandan | |
dc.contributor.author | Mira-Rodado, Virtudes | |
dc.contributor.author | Berendzen, Kenneth Wayne | |
dc.date.accessioned | 2021-04-26T11:06:26Z | |
dc.date.available | 2021-04-26T11:06:26Z | |
dc.date.created | 2019-06-13T08:21:59Z | |
dc.date.issued | 2019 | |
dc.identifier.issn | 1932-6203 | |
dc.identifier.uri | https://hdl.handle.net/11250/2739551 | |
dc.description.abstract | In plants, several developmental processes are co-coordinated by cytokinins via phosphorylation dependent processes of the Two-Component System (TCS). An outstanding challenge is to track phosphorelay flow from cytokinin perception to its molecular outputs, of which gene activation plays a major role. To address this issue, a kinetic-based reporter system was expounded to track TCS phosphorelay activity in vivo that can distinguish between basal and cytokinin dependent effects of overexpressed TCS members. The TCS phosphorelay can be positively activated by cytokinin and inhibited by pharmaceuticals or naturally interfering components. In this case we took advantage of the phosphohistidinephosphatase Arabidopsis Response Regulator (ARR) 22 and investigated its phosphocompetition with other TCS members in regulating promoters of ARR5 and WUS in Arabidopsis thaliana cell culture protoplasts. In congruency with the proposed function of ARR22, overexpression of ARR22 blocked the activation of all B-type ARRs in this study in a TCS dependent manner. Furthermore, this effect could not be mimicked by A-type response regulator overexpression or compensated by AHP overexpression. Compared to other reporter assays, ours mimicked effects previously observed only in transgenic plants for all of the
TCS proteins studied, suggesting that it is possible to expose phosphocompetition. Thus,
our approach can be used to investigate gene signaling networks involving the TCS by
leveraging ARR22 as a TCS inhibitor along with B-type ARR overexpression. | en_US |
dc.language.iso | eng | en_US |
dc.rights | Navngivelse 4.0 Internasjonal | * |
dc.rights.uri | http://creativecommons.org/licenses/by/4.0/deed.no | * |
dc.title | ARR22 overexpression can suppress plant Two-Component Regulatory Systems | en_US |
dc.type | Peer reviewed | en_US |
dc.type | Journal article | en_US |
dc.description.version | publishedVersion | en_US |
dc.source.volume | 14 | en_US |
dc.source.journal | PLOS ONE | en_US |
dc.source.issue | 2 | en_US |
dc.identifier.doi | 10.1371/journal.pone.0212056 | |
dc.identifier.cristin | 1704509 | |
dc.relation.project | Andre: German Research Foundation (CRC 1101) | en_US |
dc.relation.project | Andre: Eberhard Karls Universität Tübingen (DE) | en_US |
cristin.unitcode | 192,10,2,0 | |
cristin.unitname | Institutt for plantevitenskap | |
cristin.ispublished | true | |
cristin.fulltext | original | |
cristin.qualitycode | 1 | |