[{"publist_id":"7619","external_id":{"isi":["000435571000017"]},"year":"2018","isi":1,"acknowledgement":"We gratefully acknowledge funding from the Chinese Scholarship Council (CSC; project number 201206910025 to Z.G.), the Fonds Wetenschappelijk Onderzoek (FWO; project number G005112N to A.D.; fellowship number 12I7417N to Z.L.), the Belgian Federal Science Policy Office (BELSPO; to Y.S.), the Agency for Innovation by Science and Technology of Belgium (IWT; fellowship number 121110 to M.V.D.), the Hercules foundation (grant AUGE-09-029 to K.D.), and the ERC StG PROCELLDEATH (project number 639234 to M.K.N.).","date_published":"2018-05-28T00:00:00Z","publication":"Nature Plants","status":"public","type":"journal_article","date_updated":"2023-09-13T08:24:17Z","_id":"280","publisher":"Nature Publishing Group","doi":"10.1038/s41477-018-0160-7","article_processing_charge":"No","quality_controlled":"1","page":"365 - 375","department":[{"_id":"JiFr"}],"month":"05","user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","issue":"6","citation":{"chicago":"Gao, Zhen, Anna Daneva, Yuliya Salanenka, Matthias Van Durme, Marlies Huysmans, Zongcheng Lin, Freya De Winter, et al. “KIRA1 and ORESARA1 Terminate Flower Receptivity by Promoting Cell Death in the Stigma of Arabidopsis.” <i>Nature Plants</i>. Nature Publishing Group, 2018. <a href=\"https://doi.org/10.1038/s41477-018-0160-7\">https://doi.org/10.1038/s41477-018-0160-7</a>.","ista":"Gao Z, Daneva A, Salanenka Y, Van Durme M, Huysmans M, Lin Z, De Winter F, Vanneste S, Karimi M, Van De Velde J, Vandepoele K, Van De Walle D, Dewettinck K, Lambrecht B, Nowack M. 2018. KIRA1 and ORESARA1 terminate flower receptivity by promoting cell death in the stigma of Arabidopsis. Nature Plants. 4(6), 365–375.","mla":"Gao, Zhen, et al. “KIRA1 and ORESARA1 Terminate Flower Receptivity by Promoting Cell Death in the Stigma of Arabidopsis.” <i>Nature Plants</i>, vol. 4, no. 6, Nature Publishing Group, 2018, pp. 365–75, doi:<a href=\"https://doi.org/10.1038/s41477-018-0160-7\">10.1038/s41477-018-0160-7</a>.","apa":"Gao, Z., Daneva, A., Salanenka, Y., Van Durme, M., Huysmans, M., Lin, Z., … Nowack, M. (2018). KIRA1 and ORESARA1 terminate flower receptivity by promoting cell death in the stigma of Arabidopsis. <i>Nature Plants</i>. Nature Publishing Group. <a href=\"https://doi.org/10.1038/s41477-018-0160-7\">https://doi.org/10.1038/s41477-018-0160-7</a>","ama":"Gao Z, Daneva A, Salanenka Y, et al. KIRA1 and ORESARA1 terminate flower receptivity by promoting cell death in the stigma of Arabidopsis. <i>Nature Plants</i>. 2018;4(6):365-375. doi:<a href=\"https://doi.org/10.1038/s41477-018-0160-7\">10.1038/s41477-018-0160-7</a>","short":"Z. Gao, A. Daneva, Y. Salanenka, M. Van Durme, M. Huysmans, Z. Lin, F. De Winter, S. Vanneste, M. Karimi, J. Van De Velde, K. Vandepoele, D. Van De Walle, K. Dewettinck, B. Lambrecht, M. Nowack, Nature Plants 4 (2018) 365–375.","ieee":"Z. Gao <i>et al.</i>, “KIRA1 and ORESARA1 terminate flower receptivity by promoting cell death in the stigma of Arabidopsis,” <i>Nature Plants</i>, vol. 4, no. 6. Nature Publishing Group, pp. 365–375, 2018."},"language":[{"iso":"eng"}],"date_created":"2018-12-11T11:45:35Z","volume":4,"title":"KIRA1 and ORESARA1 terminate flower receptivity by promoting cell death in the stigma of Arabidopsis","oa_version":"None","author":[{"first_name":"Zhen","full_name":"Gao, Zhen","last_name":"Gao"},{"full_name":"Daneva, Anna","last_name":"Daneva","first_name":"Anna"},{"last_name":"Salanenka","id":"46DAAE7E-F248-11E8-B48F-1D18A9856A87","full_name":"Salanenka, Yuliya","first_name":"Yuliya"},{"first_name":"Matthias","last_name":"Van Durme","full_name":"Van Durme, Matthias"},{"full_name":"Huysmans, Marlies","last_name":"Huysmans","first_name":"Marlies"},{"last_name":"Lin","full_name":"Lin, Zongcheng","first_name":"Zongcheng"},{"first_name":"Freya","full_name":"De Winter, Freya","last_name":"De Winter"},{"first_name":"Steffen","last_name":"Vanneste","full_name":"Vanneste, Steffen"},{"first_name":"Mansour","full_name":"Karimi, Mansour","last_name":"Karimi"},{"last_name":"Van De Velde","full_name":"Van De Velde, Jan","first_name":"Jan"},{"last_name":"Vandepoele","full_name":"Vandepoele, Klaas","first_name":"Klaas"},{"first_name":"Davy","last_name":"Van De Walle","full_name":"Van De Walle, Davy"},{"full_name":"Dewettinck, Koen","last_name":"Dewettinck","first_name":"Koen"},{"full_name":"Lambrecht, Bart","last_name":"Lambrecht","first_name":"Bart"},{"full_name":"Nowack, Moritz","last_name":"Nowack","first_name":"Moritz"}],"scopus_import":"1","day":"28","publication_status":"published","intvolume":"         4","abstract":[{"lang":"eng","text":"Flowers have a species-specific functional life span that determines the time window in which pollination, fertilization and seed set can occur. The stigma tissue plays a key role in flower receptivity by intercepting pollen and initiating pollen tube growth toward the ovary. In this article, we show that a developmentally controlled cell death programme terminates the functional life span of stigma cells in Arabidopsis. We identified the leaf senescence regulator ORESARA1 (also known as ANAC092) and the previously uncharacterized KIRA1 (also known as ANAC074) as partially redundant transcription factors that modulate stigma longevity by controlling the expression of programmed cell death-associated genes. KIRA1 expression is sufficient to induce cell death and terminate floral receptivity, whereas lack of both KIRA1 and ORESARA1 substantially increases stigma life span. Surprisingly, the extension of stigma longevity is accompanied by only a moderate extension of flower receptivity, suggesting that additional processes participate in the control of the flower's receptive life span."}]},{"oa":1,"language":[{"iso":"eng"}],"citation":{"short":"Y. Salanenka, I. Verstraeten, C. Löfke, K. Tabata, S. Naramoto, M. Glanc, J. Friml, PNAS 115 (2018) 3716–3721.","ieee":"Y. Salanenka <i>et al.</i>, “Gibberellin DELLA signaling targets the retromer complex to redirect protein trafficking to the plasma membrane,” <i>PNAS</i>, vol. 115, no. 14. National Academy of Sciences, pp. 3716–3721, 2018.","ama":"Salanenka Y, Verstraeten I, Löfke C, et al. Gibberellin DELLA signaling targets the retromer complex to redirect protein trafficking to the plasma membrane. <i>PNAS</i>. 2018;115(14):3716-3721. doi:<a href=\"https://doi.org/10.1073/pnas.1721760115\">10.1073/pnas.1721760115</a>","mla":"Salanenka, Yuliya, et al. “Gibberellin DELLA Signaling Targets the Retromer Complex to Redirect Protein Trafficking to the Plasma Membrane.” <i>PNAS</i>, vol. 115, no. 14, National Academy of Sciences, 2018, pp. 3716–21, doi:<a href=\"https://doi.org/10.1073/pnas.1721760115\">10.1073/pnas.1721760115</a>.","apa":"Salanenka, Y., Verstraeten, I., Löfke, C., Tabata, K., Naramoto, S., Glanc, M., &#38; Friml, J. (2018). Gibberellin DELLA signaling targets the retromer complex to redirect protein trafficking to the plasma membrane. <i>PNAS</i>. National Academy of Sciences. <a href=\"https://doi.org/10.1073/pnas.1721760115\">https://doi.org/10.1073/pnas.1721760115</a>","chicago":"Salanenka, Yuliya, Inge Verstraeten, Christian Löfke, Kaori Tabata, Satoshi Naramoto, Matous Glanc, and Jiří Friml. “Gibberellin DELLA Signaling Targets the Retromer Complex to Redirect Protein Trafficking to the Plasma Membrane.” <i>PNAS</i>. National Academy of Sciences, 2018. <a href=\"https://doi.org/10.1073/pnas.1721760115\">https://doi.org/10.1073/pnas.1721760115</a>.","ista":"Salanenka Y, Verstraeten I, Löfke C, Tabata K, Naramoto S, Glanc M, Friml J. 2018. Gibberellin DELLA signaling targets the retromer complex to redirect protein trafficking to the plasma membrane. PNAS. 115(14), 3716–3721."},"issue":"14","user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","month":"04","department":[{"_id":"JiFr"}],"file":[{"file_name":"2018_PNAS_Salanenka.pdf","access_level":"open_access","content_type":"application/pdf","relation":"main_file","checksum":"1fcf7223fb8f99559cfa80bd6f24ce44","file_size":1924101,"date_created":"2018-12-17T12:30:14Z","date_updated":"2020-07-14T12:46:26Z","creator":"dernst","file_id":"5700"}],"has_accepted_license":"1","tmp":{"image":"/images/cc_by_nc_nd.png","name":"Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0)","legal_code_url":"https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode","short":"CC BY-NC-ND (4.0)"},"abstract":[{"text":"The plant hormone gibberellic acid (GA) is a crucial regulator of growth and development. The main paradigm of GA signaling puts forward transcriptional regulation via the degradation of DELLA transcriptional repressors. GA has also been shown to regulate tropic responses by modulation of the plasma membrane incidence of PIN auxin transporters by an unclear mechanism. Here we uncovered the cellular and molecular mechanisms by which GA redirects protein trafficking and thus regulates cell surface functionality. Photoconvertible reporters revealed that GA balances the protein traffic between the vacuole degradation route and recycling back to the cell surface. Low GA levels promote vacuolar delivery and degradation of multiple cargos, including PIN proteins, whereas high GA levels promote their recycling to the plasma membrane. This GA effect requires components of the retromer complex, such as Sorting Nexin 1 (SNX1) and its interacting, microtubule (MT)-associated protein, the Cytoplasmic Linker-Associated Protein (CLASP1). Accordingly, GA regulates the subcellular distribution of SNX1 and CLASP1, and the intact MT cytoskeleton is essential for the GA effect on trafficking. This GA cellular action occurs through DELLA proteins that regulate the MT and retromer presumably via their interaction partners Prefoldins (PFDs). Our study identified a branching of the GA signaling pathway at the level of DELLA proteins, which, in parallel to regulating transcription, also target by a nontranscriptional mechanism the retromer complex acting at the intersection of the degradation and recycling trafficking routes. By this mechanism, GA can redirect receptors and transporters to the cell surface, thus coregulating multiple processes, including PIN-dependent auxin fluxes during tropic responses.","lang":"eng"}],"intvolume":"       115","file_date_updated":"2020-07-14T12:46:26Z","publication_status":"published","day":"03","scopus_import":"1","author":[{"id":"46DAAE7E-F248-11E8-B48F-1D18A9856A87","full_name":"Salanenka, Yuliya","last_name":"Salanenka","first_name":"Yuliya"},{"id":"362BF7FE-F248-11E8-B48F-1D18A9856A87","full_name":"Verstraeten, Inge","last_name":"Verstraeten","first_name":"Inge","orcid":"0000-0001-7241-2328"},{"first_name":"Christian","last_name":"Löfke","full_name":"Löfke, Christian"},{"full_name":"Tabata, Kaori","id":"7DAAEDA4-02D0-11E9-B11A-A5A4D7DFFFD0","last_name":"Tabata","first_name":"Kaori"},{"last_name":"Naramoto","full_name":"Naramoto, Satoshi","first_name":"Satoshi"},{"first_name":"Matous","orcid":"0000-0003-0619-7783","last_name":"Glanc","full_name":"Glanc, Matous","id":"1AE1EA24-02D0-11E9-9BAA-DAF4881429F2"},{"last_name":"Friml","full_name":"Friml, Jirí","id":"4159519E-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-8302-7596","first_name":"Jirí"}],"title":"Gibberellin DELLA signaling targets the retromer complex to redirect protein trafficking to the plasma membrane","oa_version":"Published Version","volume":115,"date_created":"2018-12-11T11:46:25Z","publication":"PNAS","status":"public","project":[{"_id":"25716A02-B435-11E9-9278-68D0E5697425","grant_number":"282300","name":"Polarity and subcellular dynamics in plants","call_identifier":"FP7"}],"ec_funded":1,"date_published":"2018-04-03T00:00:00Z","acknowledgement":"We gratefully acknowledge M. Blázquez (Instituto de Biología Molecular y Celular de Plantas), M. Fendrych, C. Cuesta Moliner (Institute of Science and Technology Austria), M. Vanstraelen, M. Nowack (Center for Plant Systems Biology, Ghent), C. Luschnig (Universitat fur Bodenkultur Wien, Vienna), S. Simon (Central European Institute of Technology, Brno), C. Sommerville (Carnegie Institution for Science), and Y. Gu (Penn State University) for making available the materials used in this study;\r\n...funding from the European Research Council (ERC) under the European Union’s Seventh Framework Programme (FP7/2007-2013)/ERC Grant Agreement 282300.\r\nCC BY NC ND","isi":1,"year":"2018","external_id":{"isi":["000429012500073"]},"publist_id":"7395","page":" 3716 - 3721","ddc":["580"],"quality_controlled":"1","article_processing_charge":"No","doi":"10.1073/pnas.1721760115","publisher":"National Academy of Sciences","_id":"428","date_updated":"2025-05-07T11:12:27Z","type":"journal_article"}]