[{"citation":{"short":"M. Nagano, J.Y. Toshima, D.E. Siekhaus, J. Toshima, Communications Biology 2 (2019).","ieee":"M. Nagano, J. Y. Toshima, D. E. Siekhaus, and J. Toshima, “Rab5-mediated endosome formation is regulated at the trans-Golgi network,” Communications Biology, vol. 2, no. 1. Springer Nature, 2019.","apa":"Nagano, M., Toshima, J. Y., Siekhaus, D. E., & Toshima, J. (2019). Rab5-mediated endosome formation is regulated at the trans-Golgi network. Communications Biology. Springer Nature. https://doi.org/10.1038/s42003-019-0670-5","ama":"Nagano M, Toshima JY, Siekhaus DE, Toshima J. Rab5-mediated endosome formation is regulated at the trans-Golgi network. Communications Biology. 2019;2(1). doi:10.1038/s42003-019-0670-5","mla":"Nagano, Makoto, et al. “Rab5-Mediated Endosome Formation Is Regulated at the Trans-Golgi Network.” Communications Biology, vol. 2, no. 1, 419, Springer Nature, 2019, doi:10.1038/s42003-019-0670-5.","ista":"Nagano M, Toshima JY, Siekhaus DE, Toshima J. 2019. Rab5-mediated endosome formation is regulated at the trans-Golgi network. Communications Biology. 2(1), 419.","chicago":"Nagano, Makoto, Junko Y. Toshima, Daria E Siekhaus, and Jiro Toshima. “Rab5-Mediated Endosome Formation Is Regulated at the Trans-Golgi Network.” Communications Biology. Springer Nature, 2019. https://doi.org/10.1038/s42003-019-0670-5."},"user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","external_id":{"isi":["000496767800005"]},"article_processing_charge":"No","author":[{"first_name":"Makoto","full_name":"Nagano, Makoto","last_name":"Nagano"},{"full_name":"Toshima, Junko Y.","last_name":"Toshima","first_name":"Junko Y."},{"id":"3D224B9E-F248-11E8-B48F-1D18A9856A87","first_name":"Daria E","full_name":"Siekhaus, Daria E","orcid":"0000-0001-8323-8353","last_name":"Siekhaus"},{"first_name":"Jiro","last_name":"Toshima","full_name":"Toshima, Jiro"}],"title":"Rab5-mediated endosome formation is regulated at the trans-Golgi network","article_number":"419","year":"2019","has_accepted_license":"1","isi":1,"publication":"Communications Biology","day":"15","date_created":"2019-11-25T07:55:01Z","date_published":"2019-11-15T00:00:00Z","doi":"10.1038/s42003-019-0670-5","oa":1,"quality_controlled":"1","publisher":"Springer Nature","date_updated":"2023-08-30T07:27:55Z","ddc":["570"],"department":[{"_id":"DaSi"}],"file_date_updated":"2020-07-14T12:47:49Z","_id":"7097","tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","image":"/images/cc_by.png","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","short":"CC BY (4.0)"},"type":"journal_article","article_type":"original","status":"public","publication_status":"published","publication_identifier":{"issn":["2399-3642"]},"language":[{"iso":"eng"}],"file":[{"file_name":"2019_CommunicBiology_Nagano.pdf","date_created":"2019-11-25T07:58:05Z","file_size":2626069,"date_updated":"2020-07-14T12:47:49Z","creator":"dernst","file_id":"7098","checksum":"c63c69a264fc8a0e52f2b0d482f3bdae","content_type":"application/pdf","relation":"main_file","access_level":"open_access"}],"volume":2,"issue":"1","abstract":[{"text":"Early endosomes, also called sorting endosomes, are known to mature into late endosomesvia the Rab5-mediated endolysosomal trafficking pathway. Thus, early endosome existence isthought to be maintained by the continual fusion of transport vesicles from the plasmamembrane and thetrans-Golgi network (TGN). Here we show instead that endocytosis isdispensable and post-Golgi vesicle transport is crucial for the formation of endosomes andthe subsequent endolysosomal traffic regulated by yeast Rab5 Vps21p. Fittingly, all threeproteins required for endosomal nucleotide exchange on Vps21p arefirst recruited to theTGN before transport to the endosome, namely the GEF Vps9p and the epsin-relatedadaptors Ent3/5p. The TGN recruitment of these components is distinctly controlled, withVps9p appearing to require the Arf1p GTPase, and the Rab11s, Ypt31p/32p. These resultsprovide a different view of endosome formation and identify the TGN as a critical location forregulating progress through the endolysosomal trafficking pathway.","lang":"eng"}],"oa_version":"Published Version","scopus_import":"1","intvolume":" 2","month":"11"},{"article_number":"5516","project":[{"call_identifier":"FWF","_id":"264CBBAC-B435-11E9-9278-68D0E5697425","name":"Modeling epithelial tissue mechanics during cell invasion","grant_number":"M02379"}],"user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","citation":{"chicago":"Retzer, Katarzyna, Maria Akhmanova, Nataliia Konstantinova, Kateřina Malínská, Johannes Leitner, Jan Petrášek, and Christian Luschnig. “Brassinosteroid Signaling Delimits Root Gravitropism via Sorting of the Arabidopsis PIN2 Auxin Transporter.” Nature Communications. Springer Nature, 2019. https://doi.org/10.1038/s41467-019-13543-1.","ista":"Retzer K, Akhmanova M, Konstantinova N, Malínská K, Leitner J, Petrášek J, Luschnig C. 2019. Brassinosteroid signaling delimits root gravitropism via sorting of the Arabidopsis PIN2 auxin transporter. Nature Communications. 10, 5516.","mla":"Retzer, Katarzyna, et al. “Brassinosteroid Signaling Delimits Root Gravitropism via Sorting of the Arabidopsis PIN2 Auxin Transporter.” Nature Communications, vol. 10, 5516, Springer Nature, 2019, doi:10.1038/s41467-019-13543-1.","ama":"Retzer K, Akhmanova M, Konstantinova N, et al. Brassinosteroid signaling delimits root gravitropism via sorting of the Arabidopsis PIN2 auxin transporter. Nature Communications. 2019;10. doi:10.1038/s41467-019-13543-1","apa":"Retzer, K., Akhmanova, M., Konstantinova, N., Malínská, K., Leitner, J., Petrášek, J., & Luschnig, C. (2019). Brassinosteroid signaling delimits root gravitropism via sorting of the Arabidopsis PIN2 auxin transporter. Nature Communications. Springer Nature. https://doi.org/10.1038/s41467-019-13543-1","ieee":"K. Retzer et al., “Brassinosteroid signaling delimits root gravitropism via sorting of the Arabidopsis PIN2 auxin transporter,” Nature Communications, vol. 10. Springer Nature, 2019.","short":"K. Retzer, M. Akhmanova, N. Konstantinova, K. Malínská, J. Leitner, J. Petrášek, C. Luschnig, Nature Communications 10 (2019)."},"title":"Brassinosteroid signaling delimits root gravitropism via sorting of the Arabidopsis PIN2 auxin transporter","author":[{"first_name":"Katarzyna","last_name":"Retzer","full_name":"Retzer, Katarzyna"},{"id":"3425EC26-F248-11E8-B48F-1D18A9856A87","first_name":"Maria","full_name":"Akhmanova, Maria","orcid":"0000-0003-1522-3162","last_name":"Akhmanova"},{"full_name":"Konstantinova, Nataliia","last_name":"Konstantinova","first_name":"Nataliia"},{"first_name":"Kateřina","full_name":"Malínská, Kateřina","last_name":"Malínská"},{"full_name":"Leitner, Johannes","last_name":"Leitner","first_name":"Johannes"},{"last_name":"Petrášek","full_name":"Petrášek, Jan","first_name":"Jan"},{"first_name":"Christian","full_name":"Luschnig, Christian","last_name":"Luschnig"}],"external_id":{"pmid":["31797871"],"isi":["000500508100001"]},"article_processing_charge":"No","publisher":"Springer Nature","quality_controlled":"1","oa":1,"day":"01","publication":"Nature Communications","isi":1,"has_accepted_license":"1","year":"2019","date_published":"2019-12-01T00:00:00Z","doi":"10.1038/s41467-019-13543-1","date_created":"2019-12-15T23:00:43Z","_id":"7180","status":"public","article_type":"original","type":"journal_article","tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","image":"/images/cc_by.png","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","short":"CC BY (4.0)"},"ddc":["570"],"date_updated":"2023-09-06T14:08:21Z","file_date_updated":"2020-07-14T12:47:52Z","department":[{"_id":"DaSi"}],"pmid":1,"oa_version":"Published Version","abstract":[{"lang":"eng","text":"Arabidopsis PIN2 protein directs transport of the phytohormone auxin from the root tip into the root elongation zone. Variation in hormone transport, which depends on a delicate interplay between PIN2 sorting to and from polar plasma membrane domains, determines root growth. By employing a constitutively degraded version of PIN2, we identify brassinolides as antagonists of PIN2 endocytosis. This response does not require de novo protein synthesis, but involves early events in canonical brassinolide signaling. Brassinolide-controlled adjustments in PIN2 sorting and intracellular distribution governs formation of a lateral PIN2 gradient in gravistimulated roots, coinciding with adjustments in auxin signaling and directional root growth. Strikingly, simulations indicate that PIN2 gradient formation is no prerequisite for root bending but rather dampens asymmetric auxin flow and signaling. Crosstalk between brassinolide signaling and endocytic PIN2 sorting, thus, appears essential for determining the rate of gravity-induced root curvature via attenuation of differential cell elongation."}],"month":"12","intvolume":" 10","scopus_import":"1","file":[{"file_name":"2019_NatureComm_Retzer.pdf","date_created":"2019-12-16T07:37:50Z","file_size":5156533,"date_updated":"2020-07-14T12:47:52Z","creator":"dernst","file_id":"7184","checksum":"77e8720a8e0f3091b98159f85be40893","content_type":"application/pdf","relation":"main_file","access_level":"open_access"}],"language":[{"iso":"eng"}],"publication_identifier":{"eissn":["20411723"]},"publication_status":"published","volume":10},{"page":"238-255","date_published":"2019-01-09T00:00:00Z","doi":"10.1523/JNEUROSCI.1059-18.2018","date_created":"2018-12-11T11:44:07Z","has_accepted_license":"1","isi":1,"year":"2019","day":"09","publication":"Journal of Neuroscience","quality_controlled":"1","publisher":"Society for Neuroscience","oa":1,"acknowledgement":"This work was supported by INSERM, CNRS, UDS, Ligue Régionale contre le Cancer, Hôpital de Strasbourg, Association pour la Recherche sur le Cancer (ARC) and Agence Nationale de la Recherche (ANR) grants. P.B.C. was funded by the ANR and by the ARSEP (Fondation pour l'Aide à la Recherche sur la Sclérose en Plaques), and G.T. by governmental and ARC fellowships. This work was also supported by grants from the Ataxia UK (2491) and the NC3R (NC/L000199/1) awarded to M.F. The Institut de Génétique et de Biologie Moléculaire et Cellulaire was also supported by a French state fund through the ANR labex. D.E.S. was funded by Marie Curie Grant CIG 334077/IRTIM. We thank B. Altenhein, K. Brückner, M. Crozatier, L. Waltzer, M. Logan, E. Kurant, R. Reuter, E. Kurucz, J.L Dimarcq, J. Hoffmann, C. Goodman, the DHSB, and the BDSC for reagents and flies. We also thank all of the laboratory members for comments on the manuscript; C. Diebold, C. Delaporte, M. Pezze, the fly, and imaging and antibody facilities for technical assistance; and D. Dembele for help with statistics. In addition, we thank Alison Brewer for help with Luciferase assays.","author":[{"last_name":"Trébuchet","full_name":"Trébuchet, Guillaume","first_name":"Guillaume"},{"full_name":"Cattenoz, Pierre B","last_name":"Cattenoz","first_name":"Pierre B"},{"last_name":"Zsámboki","full_name":"Zsámboki, János","first_name":"János"},{"last_name":"Mazaud","full_name":"Mazaud, David","first_name":"David"},{"last_name":"Siekhaus","full_name":"Siekhaus, Daria E","orcid":"0000-0001-8323-8353","id":"3D224B9E-F248-11E8-B48F-1D18A9856A87","first_name":"Daria E"},{"first_name":"Manolis","last_name":"Fanto","full_name":"Fanto, Manolis"},{"first_name":"Angela","full_name":"Giangrande, Angela","last_name":"Giangrande"}],"publist_id":"8048","external_id":{"isi":["000455189900006"],"pmid":["30504274"]},"article_processing_charge":"No","title":"The Repo homeodomain transcription factor suppresses hematopoiesis in Drosophila and preserves the glial fate","citation":{"mla":"Trébuchet, Guillaume, et al. “The Repo Homeodomain Transcription Factor Suppresses Hematopoiesis in Drosophila and Preserves the Glial Fate.” Journal of Neuroscience, vol. 39, no. 2, Society for Neuroscience, 2019, pp. 238–55, doi:10.1523/JNEUROSCI.1059-18.2018.","ieee":"G. Trébuchet et al., “The Repo homeodomain transcription factor suppresses hematopoiesis in Drosophila and preserves the glial fate,” Journal of Neuroscience, vol. 39, no. 2. Society for Neuroscience, pp. 238–255, 2019.","short":"G. Trébuchet, P.B. Cattenoz, J. Zsámboki, D. Mazaud, D.E. Siekhaus, M. Fanto, A. Giangrande, Journal of Neuroscience 39 (2019) 238–255.","apa":"Trébuchet, G., Cattenoz, P. B., Zsámboki, J., Mazaud, D., Siekhaus, D. E., Fanto, M., & Giangrande, A. (2019). The Repo homeodomain transcription factor suppresses hematopoiesis in Drosophila and preserves the glial fate. Journal of Neuroscience. Society for Neuroscience. https://doi.org/10.1523/JNEUROSCI.1059-18.2018","ama":"Trébuchet G, Cattenoz PB, Zsámboki J, et al. The Repo homeodomain transcription factor suppresses hematopoiesis in Drosophila and preserves the glial fate. Journal of Neuroscience. 2019;39(2):238-255. doi:10.1523/JNEUROSCI.1059-18.2018","chicago":"Trébuchet, Guillaume, Pierre B Cattenoz, János Zsámboki, David Mazaud, Daria E Siekhaus, Manolis Fanto, and Angela Giangrande. “The Repo Homeodomain Transcription Factor Suppresses Hematopoiesis in Drosophila and Preserves the Glial Fate.” Journal of Neuroscience. Society for Neuroscience, 2019. https://doi.org/10.1523/JNEUROSCI.1059-18.2018.","ista":"Trébuchet G, Cattenoz PB, Zsámboki J, Mazaud D, Siekhaus DE, Fanto M, Giangrande A. 2019. The Repo homeodomain transcription factor suppresses hematopoiesis in Drosophila and preserves the glial fate. Journal of Neuroscience. 39(2), 238–255."},"user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","project":[{"_id":"2536F660-B435-11E9-9278-68D0E5697425","call_identifier":"FP7","name":"Investigating the role of transporters in invasive migration through junctions","grant_number":"334077"}],"issue":"2","volume":39,"ec_funded":1,"publication_status":"published","file":[{"success":1,"checksum":"8f6925eb4cd1e8747d8ea25929c68de6","file_id":"8596","relation":"main_file","access_level":"open_access","content_type":"application/pdf","file_name":"2019_JournNeuroscience_Trebuchet.pdf","date_created":"2020-10-02T09:33:28Z","creator":"dernst","file_size":9455414,"date_updated":"2020-10-02T09:33:28Z"}],"language":[{"iso":"eng"}],"scopus_import":"1","month":"01","intvolume":" 39","abstract":[{"lang":"eng","text":"Despite their different origins, Drosophila glia and hemocytes are related cell populations that provide an immune function. Drosophila hemocytes patrol the body cavity and act as macrophages outside the nervous system whereas glia originate from the neuroepithelium and provide the scavenger population of the nervous system. Drosophila glia are hence the functional orthologs of vertebrate microglia, even though the latter are cells of immune origin that subsequently move into the brain during development. Interestingly, the Drosophila immune cells within (glia) and outside the nervous system (hemocytes) require the same transcription factor Glide/Gcm for their development. This raises the issue of how do glia specifically differentiate in the nervous system and hemocytes in the procephalic mesoderm. The Repo homeodomain transcription factor and pan-glial direct target of Glide/Gcm is known to ensure glial terminal differentiation. Here we show that Repo also takes center stage in the process that discriminates between glia and hemocytes. First, Repo expression is repressed in the hemocyte anlagen by mesoderm-specific factors. Second, Repo ectopic activation in the procephalic mesoderm is sufficient to repress the expression of hemocyte-specific genes. Third, the lack of Repo triggers the expression of hemocyte markers in glia. Thus, a complex network of tissue-specific cues biases the potential of Glide/Gcm. These data allow us to revise the concept of fate determinants and help us understand the bases of cell specification. Both sexes were analyzed.SIGNIFICANCE STATEMENTDistinct cell types often require the same pioneer transcription factor, raising the issue of how does one factor trigger different fates. In Drosophila, glia and hemocytes provide a scavenger activity within and outside the nervous system, respectively. While they both require the Glide/Gcm transcription factor, glia originate from the ectoderm, hemocytes from the mesoderm. Here we show that tissue-specific factors inhibit the gliogenic potential of Glide/Gcm in the mesoderm by repressing the expression of the homeodomain protein Repo, a major glial-specific target of Glide/Gcm. Repo expression in turn inhibits the expression of hemocyte-specific genes in the nervous system. These cell-specific networks secure the establishment of the glial fate only in the nervous system and allow cell diversification."}],"pmid":1,"oa_version":"Published Version","file_date_updated":"2020-10-02T09:33:28Z","department":[{"_id":"DaSi"}],"date_updated":"2023-09-19T10:10:55Z","ddc":["570"],"type":"journal_article","article_type":"original","status":"public","_id":"8"},{"article_number":"e41801","project":[{"_id":"253CDE40-B435-11E9-9278-68D0E5697425","name":"Examination of the role of a MFS transporter in the migration of Drosophila immune cells","grant_number":"24283"},{"grant_number":"P29638","name":"The role of Drosophila TNF alpha in immune cell invasion","_id":"253B6E48-B435-11E9-9278-68D0E5697425","call_identifier":"FWF"},{"call_identifier":"FP7","_id":"2536F660-B435-11E9-9278-68D0E5697425","name":"Investigating the role of transporters in invasive migration through junctions","grant_number":"334077"},{"call_identifier":"FP7","_id":"25388084-B435-11E9-9278-68D0E5697425","grant_number":"329540","name":"Breaking barriers: Investigating the junctional and mechanobiological changes underlying the ability of Drosophila immune cells to invade an epithelium"},{"_id":"2564DBCA-B435-11E9-9278-68D0E5697425","call_identifier":"H2020","grant_number":"665385","name":"International IST Doctoral Program"}],"user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","citation":{"chicago":"Valosková, Katarina, Julia Bicher, Marko Roblek, Shamsi Emtenani, Attila György, Michaela Misova, Aparna Ratheesh, et al. “A Conserved Major Facilitator Superfamily Member Orchestrates a Subset of O-Glycosylation to Aid Macrophage Tissue Invasion.” ELife. eLife Sciences Publications, 2019. https://doi.org/10.7554/elife.41801.","ista":"Valosková K, Bicher J, Roblek M, Emtenani S, György A, Misova M, Ratheesh A, Rodrigues P, Shkarina K, Larsen ISB, Vakhrushev SY, Clausen H, Siekhaus DE. 2019. A conserved major facilitator superfamily member orchestrates a subset of O-glycosylation to aid macrophage tissue invasion. eLife. 8, e41801.","mla":"Valosková, Katarina, et al. “A Conserved Major Facilitator Superfamily Member Orchestrates a Subset of O-Glycosylation to Aid Macrophage Tissue Invasion.” ELife, vol. 8, e41801, eLife Sciences Publications, 2019, doi:10.7554/elife.41801.","short":"K. Valosková, J. Bicher, M. Roblek, S. Emtenani, A. György, M. Misova, A. Ratheesh, P. Rodrigues, K. Shkarina, I.S.B. Larsen, S.Y. Vakhrushev, H. Clausen, D.E. Siekhaus, ELife 8 (2019).","ieee":"K. Valosková et al., “A conserved major facilitator superfamily member orchestrates a subset of O-glycosylation to aid macrophage tissue invasion,” eLife, vol. 8. eLife Sciences Publications, 2019.","ama":"Valosková K, Bicher J, Roblek M, et al. A conserved major facilitator superfamily member orchestrates a subset of O-glycosylation to aid macrophage tissue invasion. eLife. 2019;8. doi:10.7554/elife.41801","apa":"Valosková, K., Bicher, J., Roblek, M., Emtenani, S., György, A., Misova, M., … Siekhaus, D. E. (2019). A conserved major facilitator superfamily member orchestrates a subset of O-glycosylation to aid macrophage tissue invasion. ELife. eLife Sciences Publications. https://doi.org/10.7554/elife.41801"},"title":"A conserved major facilitator superfamily member orchestrates a subset of O-glycosylation to aid macrophage tissue invasion","author":[{"first_name":"Katarina","id":"46F146FC-F248-11E8-B48F-1D18A9856A87","full_name":"Valosková, Katarina","last_name":"Valosková"},{"full_name":"Biebl, Julia","last_name":"Biebl","id":"3CCBB46E-F248-11E8-B48F-1D18A9856A87","first_name":"Julia"},{"orcid":"0000-0001-9588-1389","full_name":"Roblek, Marko","last_name":"Roblek","first_name":"Marko","id":"3047D808-F248-11E8-B48F-1D18A9856A87"},{"first_name":"Shamsi","id":"49D32318-F248-11E8-B48F-1D18A9856A87","full_name":"Emtenani, Shamsi","orcid":"0000-0001-6981-6938","last_name":"Emtenani"},{"id":"3BCEDBE0-F248-11E8-B48F-1D18A9856A87","first_name":"Attila","last_name":"György","orcid":"0000-0002-1819-198X","full_name":"György, Attila"},{"id":"495A3C32-F248-11E8-B48F-1D18A9856A87","first_name":"Michaela","last_name":"Misova","orcid":"0000-0003-2427-6856","full_name":"Misova, Michaela"},{"id":"2F064CFE-F248-11E8-B48F-1D18A9856A87","first_name":"Aparna","full_name":"Ratheesh, Aparna","orcid":"0000-0001-7190-0776","last_name":"Ratheesh"},{"first_name":"Patricia","id":"2CE4065A-F248-11E8-B48F-1D18A9856A87","full_name":"Rodrigues, Patricia","last_name":"Rodrigues"},{"last_name":"Shkarina","full_name":"Shkarina, Katerina","first_name":"Katerina"},{"last_name":"Larsen","full_name":"Larsen, Ida Signe Bohse","first_name":"Ida Signe Bohse"},{"last_name":"Vakhrushev","full_name":"Vakhrushev, Sergey Y","first_name":"Sergey Y"},{"full_name":"Clausen, Henrik","last_name":"Clausen","first_name":"Henrik"},{"last_name":"Siekhaus","full_name":"Siekhaus, Daria E","orcid":"0000-0001-8323-8353","first_name":"Daria E","id":"3D224B9E-F248-11E8-B48F-1D18A9856A87"}],"article_processing_charge":"No","external_id":{"isi":["000462530200001"]},"quality_controlled":"1","publisher":"eLife Sciences Publications","oa":1,"day":"26","publication":"eLife","isi":1,"has_accepted_license":"1","year":"2019","date_published":"2019-03-26T00:00:00Z","doi":"10.7554/elife.41801","date_created":"2019-03-28T13:37:45Z","_id":"6187","status":"public","type":"journal_article","tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","image":"/images/cc_by.png","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","short":"CC BY (4.0)"},"ddc":["570"],"date_updated":"2024-03-27T23:30:29Z","file_date_updated":"2020-07-14T12:47:23Z","department":[{"_id":"DaSi"}],"oa_version":"Published Version","abstract":[{"lang":"eng","text":"Aberrant display of the truncated core1 O-glycan T-antigen is a common feature of human cancer cells that correlates with metastasis. Here we show that T-antigen in Drosophila melanogaster macrophages is involved in their developmentally programmed tissue invasion. Higher macrophage T-antigen levels require an atypical major facilitator superfamily (MFS) member that we named Minerva which enables macrophage dissemination and invasion. We characterize for the first time the T and Tn glycoform O-glycoproteome of the Drosophila melanogaster embryo, and determine that Minerva increases the presence of T-antigen on proteins in pathways previously linked to cancer, most strongly on the sulfhydryl oxidase Qsox1 which we show is required for macrophage tissue entry. Minerva’s vertebrate ortholog, MFSD1, rescues the minerva mutant’s migration and T-antigen glycosylation defects. We thus identify a key conserved regulator that orchestrates O-glycosylation on a protein subset to activate a program governing migration steps important for both development and cancer metastasis."}],"acknowledged_ssus":[{"_id":"LifeSc"}],"month":"03","intvolume":" 8","scopus_import":"1","file":[{"date_created":"2019-03-28T14:00:41Z","file_name":"2019_eLife_Valoskova.pdf","creator":"dernst","date_updated":"2020-07-14T12:47:23Z","file_size":4496017,"checksum":"cc0d1a512559d52e7e7cb0e9b9854b40","file_id":"6188","access_level":"open_access","relation":"main_file","content_type":"application/pdf"}],"language":[{"iso":"eng"}],"publication_identifier":{"issn":["2050-084X"]},"publication_status":"published","related_material":{"link":[{"url":"https://ist.ac.at/en/news/new-gene-potentially-involved-in-metastasis-identified/","relation":"press_release","description":"News on IST Homepage"}],"record":[{"relation":"dissertation_contains","id":"6530"},{"status":"public","id":"8983","relation":"dissertation_contains"},{"relation":"dissertation_contains","status":"public","id":"6546"}]},"volume":8,"ec_funded":1},{"project":[{"name":"Examination of the role of a MFS transporter in the migration of Drosophila immune cells","grant_number":"24283","_id":"253CDE40-B435-11E9-9278-68D0E5697425"}],"article_processing_charge":"No","author":[{"last_name":"Valosková","full_name":"Valosková, Katarina","first_name":"Katarina","id":"46F146FC-F248-11E8-B48F-1D18A9856A87"}],"title":"The role of a highly conserved major facilitator superfamily member in Drosophila embryonic macrophage migration","citation":{"chicago":"Valosková, Katarina. “The Role of a Highly Conserved Major Facilitator Superfamily Member in Drosophila Embryonic Macrophage Migration.” Institute of Science and Technology Austria, 2019. https://doi.org/10.15479/AT:ISTA:6546.","ista":"Valosková K. 2019. The role of a highly conserved major facilitator superfamily member in Drosophila embryonic macrophage migration. Institute of Science and Technology Austria.","mla":"Valosková, Katarina. The Role of a Highly Conserved Major Facilitator Superfamily Member in Drosophila Embryonic Macrophage Migration. Institute of Science and Technology Austria, 2019, doi:10.15479/AT:ISTA:6546.","ieee":"K. Valosková, “The role of a highly conserved major facilitator superfamily member in Drosophila embryonic macrophage migration,” Institute of Science and Technology Austria, 2019.","short":"K. Valosková, The Role of a Highly Conserved Major Facilitator Superfamily Member in Drosophila Embryonic Macrophage Migration, Institute of Science and Technology Austria, 2019.","ama":"Valosková K. The role of a highly conserved major facilitator superfamily member in Drosophila embryonic macrophage migration. 2019. doi:10.15479/AT:ISTA:6546","apa":"Valosková, K. (2019). The role of a highly conserved major facilitator superfamily member in Drosophila embryonic macrophage migration. Institute of Science and Technology Austria. https://doi.org/10.15479/AT:ISTA:6546"},"user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","oa":1,"publisher":"Institute of Science and Technology Austria","page":"141","date_created":"2019-06-07T12:49:19Z","doi":"10.15479/AT:ISTA:6546","date_published":"2019-06-07T00:00:00Z","year":"2019","has_accepted_license":"1","day":"07","type":"dissertation","status":"public","_id":"6546","department":[{"_id":"DaSi"}],"file_date_updated":"2021-02-11T11:17:14Z","date_updated":"2023-09-19T10:15:54Z","supervisor":[{"last_name":"Siekhaus","full_name":"Siekhaus, Daria E","orcid":"0000-0001-8323-8353","id":"3D224B9E-F248-11E8-B48F-1D18A9856A87","first_name":"Daria E"}],"ddc":["570"],"alternative_title":["ISTA Thesis"],"month":"06","acknowledged_ssus":[{"_id":"Bio"}],"abstract":[{"text":"Invasive migration plays a crucial role not only during development and homeostasis but also in pathological states, such as tumor metastasis. Drosophila macrophage migration into the extended germband is an interesting system to study invasive migration. It carries similarities to immune cell transmigration and cancer cell invasion, therefore studying this process could also bring new understanding of invasion in higher organisms. In our work, we uncover a highly conserved member of the major facilitator family that plays a role in tissue invasion through regulation of glycosylation on a subgroup of proteins and/or by aiding the precise timing of DN-Cadherin downregulation. \r\n\r\nAberrant display of the truncated core1 O-glycan T-antigen is a common feature of human cancer cells that correlates with metastasis. Here we show that T-antigen in Drosophila melanogaster macrophages is involved in their developmentally programmed tissue invasion. Higher macrophage T-antigen levels require an atypical major facilitator superfamily (MFS) member that we named Minerva which enables macrophage dissemination and invasion. We characterize for the first time the T and Tn glycoform O-glycoproteome of the Drosophila melanogaster embryo, and determine that Minerva increases the presence of T-antigen on proteins in pathways previously linked to cancer, most strongly on the sulfhydryl oxidase Qsox1 which we show is required for macrophage tissue entry. Minerva’s vertebrate ortholog, MFSD1, rescues the minerva mutant’s migration and T-antigen glycosylation defects. We thus identify \r\na key conserved regulator that orchestrates O-glycosylation on a protein subset to activate \r\na program governing migration steps important for both development and cancer metastasis. \r\n","lang":"eng"}],"oa_version":"Published Version","related_material":{"record":[{"status":"public","id":"6187","relation":"part_of_dissertation"},{"status":"public","id":"544","relation":"part_of_dissertation"}]},"degree_awarded":"PhD","publication_status":"published","publication_identifier":{"issn":["2663-337X"]},"language":[{"iso":"eng"}],"file":[{"checksum":"68949c2d96210b45b981a23e9c9cd93c","file_id":"6549","relation":"source_file","access_level":"closed","embargo_to":"open_access","content_type":"application/vnd.openxmlformats-officedocument.wordprocessingml.document","file_name":"Katarina Valoskova_PhD thesis_final version.docx","date_created":"2019-06-07T13:00:04Z","creator":"khribikova","file_size":14110626,"date_updated":"2020-07-14T12:47:33Z"},{"access_level":"open_access","relation":"main_file","content_type":"application/pdf","checksum":"555329cd76e196c96f5278c480ee2e6e","file_id":"6550","embargo":"2020-06-07","creator":"khribikova","date_updated":"2021-02-11T11:17:14Z","file_size":10054156,"date_created":"2019-06-07T13:00:08Z","file_name":"Katarina Valoskova_PhD thesis_final version.pdf"}]},{"publisher":"Elsevier","quality_controlled":"1","oa":1,"page":"331 - 346","date_published":"2018-05-07T00:00:00Z","doi":"10.1016/j.devcel.2018.04.002","date_created":"2018-12-11T11:45:44Z","isi":1,"year":"2018","day":"07","publication":"Developmental Cell","project":[{"name":"Drosophila TNFa´s Funktion in Immunzellen","grant_number":"P29638","_id":"253B6E48-B435-11E9-9278-68D0E5697425","call_identifier":"FWF"},{"call_identifier":"FP7","_id":"2536F660-B435-11E9-9278-68D0E5697425","grant_number":"334077","name":"Investigating the role of transporters in invasive migration through junctions"}],"author":[{"id":"2F064CFE-F248-11E8-B48F-1D18A9856A87","first_name":"Aparna","last_name":"Ratheesh","orcid":"0000-0001-7190-0776","full_name":"Ratheesh, Aparna"},{"first_name":"Julia","id":"3CCBB46E-F248-11E8-B48F-1D18A9856A87","full_name":"Biebl, Julia","last_name":"Biebl"},{"last_name":"Smutny","full_name":"Smutny, Michael","first_name":"Michael"},{"last_name":"Veselá","full_name":"Veselá, Jana","id":"433253EE-F248-11E8-B48F-1D18A9856A87","first_name":"Jana"},{"full_name":"Papusheva, Ekaterina","last_name":"Papusheva","id":"41DB591E-F248-11E8-B48F-1D18A9856A87","first_name":"Ekaterina"},{"first_name":"Gabriel","id":"2B819732-F248-11E8-B48F-1D18A9856A87","full_name":"Krens, Gabriel","orcid":"0000-0003-4761-5996","last_name":"Krens"},{"id":"3F99E422-F248-11E8-B48F-1D18A9856A87","first_name":"Walter","last_name":"Kaufmann","full_name":"Kaufmann, Walter","orcid":"0000-0001-9735-5315"},{"last_name":"György","full_name":"György, Attila","orcid":"0000-0002-1819-198X","first_name":"Attila","id":"3BCEDBE0-F248-11E8-B48F-1D18A9856A87"},{"first_name":"Alessandra M","id":"3DBA3F4E-F248-11E8-B48F-1D18A9856A87","last_name":"Casano","full_name":"Casano, Alessandra M","orcid":"0000-0002-6009-6804"},{"orcid":"0000-0001-8323-8353","full_name":"Siekhaus, Daria E","last_name":"Siekhaus","first_name":"Daria E","id":"3D224B9E-F248-11E8-B48F-1D18A9856A87"}],"article_processing_charge":"No","external_id":{"isi":["000432461400009"],"pmid":["29738712"]},"title":"Drosophila TNF modulates tissue tension in the embryo to facilitate macrophage invasive migration","citation":{"chicago":"Ratheesh, Aparna, Julia Bicher, Michael Smutny, Jana Veselá, Ekaterina Papusheva, Gabriel Krens, Walter Kaufmann, Attila György, Alessandra M Casano, and Daria E Siekhaus. “Drosophila TNF Modulates Tissue Tension in the Embryo to Facilitate Macrophage Invasive Migration.” Developmental Cell. Elsevier, 2018. https://doi.org/10.1016/j.devcel.2018.04.002.","ista":"Ratheesh A, Bicher J, Smutny M, Veselá J, Papusheva E, Krens G, Kaufmann W, György A, Casano AM, Siekhaus DE. 2018. Drosophila TNF modulates tissue tension in the embryo to facilitate macrophage invasive migration. Developmental Cell. 45(3), 331–346.","mla":"Ratheesh, Aparna, et al. “Drosophila TNF Modulates Tissue Tension in the Embryo to Facilitate Macrophage Invasive Migration.” Developmental Cell, vol. 45, no. 3, Elsevier, 2018, pp. 331–46, doi:10.1016/j.devcel.2018.04.002.","apa":"Ratheesh, A., Bicher, J., Smutny, M., Veselá, J., Papusheva, E., Krens, G., … Siekhaus, D. E. (2018). Drosophila TNF modulates tissue tension in the embryo to facilitate macrophage invasive migration. Developmental Cell. Elsevier. https://doi.org/10.1016/j.devcel.2018.04.002","ama":"Ratheesh A, Bicher J, Smutny M, et al. Drosophila TNF modulates tissue tension in the embryo to facilitate macrophage invasive migration. Developmental Cell. 2018;45(3):331-346. doi:10.1016/j.devcel.2018.04.002","ieee":"A. Ratheesh et al., “Drosophila TNF modulates tissue tension in the embryo to facilitate macrophage invasive migration,” Developmental Cell, vol. 45, no. 3. Elsevier, pp. 331–346, 2018.","short":"A. Ratheesh, J. Bicher, M. Smutny, J. Veselá, E. Papusheva, G. Krens, W. Kaufmann, A. György, A.M. Casano, D.E. Siekhaus, Developmental Cell 45 (2018) 331–346."},"user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","scopus_import":"1","main_file_link":[{"open_access":"1","url":"https://doi.org/10.1016/j.devcel.2018.04.002"}],"month":"05","intvolume":" 45","abstract":[{"text":"Migrating cells penetrate tissue barriers during development, inflammatory responses, and tumor metastasis. We study if migration in vivo in such three-dimensionally confined environments requires changes in the mechanical properties of the surrounding cells using embryonic Drosophila melanogaster hemocytes, also called macrophages, as a model. We find that macrophage invasion into the germband through transient separation of the apposing ectoderm and mesoderm requires cell deformations and reductions in apical tension in the ectoderm. Interestingly, the genetic pathway governing these mechanical shifts acts downstream of the only known tumor necrosis factor superfamily member in Drosophila, Eiger, and its receptor, Grindelwald. Eiger-Grindelwald signaling reduces levels of active Myosin in the germband ectodermal cortex through the localization of a Crumbs complex component, Patj (Pals-1-associated tight junction protein). We therefore elucidate a distinct molecular pathway that controls tissue tension and demonstrate the importance of such regulation for invasive migration in vivo.","lang":"eng"}],"acknowledged_ssus":[{"_id":"SSU"}],"oa_version":"Published Version","pmid":1,"volume":45,"issue":"3","related_material":{"link":[{"description":"News on IST Homepage","url":"https://ist.ac.at/en/news/cells-change-tension-to-make-tissue-barriers-easier-to-get-through/","relation":"press_release"}]},"ec_funded":1,"publication_status":"published","language":[{"iso":"eng"}],"article_type":"original","type":"journal_article","status":"public","_id":"308","department":[{"_id":"DaSi"},{"_id":"CaHe"},{"_id":"Bio"},{"_id":"EM-Fac"},{"_id":"MiSi"}],"date_updated":"2023-09-11T13:22:13Z"},{"oa_version":"Published Version","pmid":1,"abstract":[{"text":"Clathrin-mediated endocytosis requires the coordinated assembly of various endocytic proteins and lipids at the plasma membrane. Accumulating evidence demonstrates a crucial role for phosphatidylinositol-4,5-bisphosphate (PtdIns(4,5)P2) in endocytosis, but specific roles for PtdIns(4)P other than as the biosynthetic precursor of PtdIns(4,5)P2 have not been clarified. In this study we investigated the role of PtdIns(4)P or PtdIns(4,5)P2 in receptor-mediated endocytosis through the construction of temperature-sensitive (ts) mutants for the PI 4-kinases Stt4p and Pik1p and the PtdIns(4) 5-kinase Mss4p. Quantitative analyses of endocytosis revealed that both the stt4(ts)pik1(ts) and mss4(ts) mutants have a severe defect in endocytic internalization. Live-cell imaging of endocytic protein dynamics in stt4(ts)pik1(ts) and mss4(ts) mutants revealed that PtdIns(4)P is required for the recruitment of the alpha-factor receptor Ste2p to clathrin-coated pits whereas PtdIns(4,5)P2 is required for membrane internalization. We also found that the localization to endocytic sites of the ENTH/ANTH domain-bearing clathrin adaptors, Ent1p/Ent2p and Yap1801p/Yap1802p, is significantly impaired in the stt4(ts)pik1(ts) mutant, but not in the mss4(ts) mutant. These results suggest distinct roles in successive steps for PtdIns(4)P and PtdIns(4,5)P2 during receptor-mediated endocytosis.","lang":"eng"}],"month":"01","intvolume":" 131","scopus_import":"1","main_file_link":[{"url":"https://www.ncbi.nlm.nih.gov/pubmed/29192062","open_access":"1"}],"language":[{"iso":"eng"}],"publication_status":"published","issue":"1","volume":131,"_id":"620","status":"public","type":"journal_article","date_updated":"2023-09-11T12:57:13Z","department":[{"_id":"DaSi"}],"publisher":"Company of Biologists","quality_controlled":"1","oa":1,"day":"04","publication":"Journal of Cell Science","isi":1,"year":"2018","date_published":"2018-01-04T00:00:00Z","doi":"10.1242/jcs.207696","date_created":"2018-12-11T11:47:32Z","article_number":"jcs207696","user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","citation":{"ista":"Yamamoto W, Wada S, Nagano M, Aoshima K, Siekhaus DE, Toshima J, Toshima J. 2018. Distinct roles for plasma membrane PtdIns 4 P and PtdIns 4 5 P2 during yeast receptor mediated endocytosis. Journal of Cell Science. 131(1), jcs207696.","chicago":"Yamamoto, Wataru, Suguru Wada, Makoto Nagano, Kaito Aoshima, Daria E Siekhaus, Junko Toshima, and Jiro Toshima. “Distinct Roles for Plasma Membrane PtdIns 4 P and PtdIns 4 5 P2 during Yeast Receptor Mediated Endocytosis.” Journal of Cell Science. Company of Biologists, 2018. https://doi.org/10.1242/jcs.207696.","ieee":"W. Yamamoto et al., “Distinct roles for plasma membrane PtdIns 4 P and PtdIns 4 5 P2 during yeast receptor mediated endocytosis,” Journal of Cell Science, vol. 131, no. 1. Company of Biologists, 2018.","short":"W. Yamamoto, S. Wada, M. Nagano, K. Aoshima, D.E. Siekhaus, J. Toshima, J. Toshima, Journal of Cell Science 131 (2018).","apa":"Yamamoto, W., Wada, S., Nagano, M., Aoshima, K., Siekhaus, D. E., Toshima, J., & Toshima, J. (2018). Distinct roles for plasma membrane PtdIns 4 P and PtdIns 4 5 P2 during yeast receptor mediated endocytosis. Journal of Cell Science. Company of Biologists. https://doi.org/10.1242/jcs.207696","ama":"Yamamoto W, Wada S, Nagano M, et al. Distinct roles for plasma membrane PtdIns 4 P and PtdIns 4 5 P2 during yeast receptor mediated endocytosis. Journal of Cell Science. 2018;131(1). doi:10.1242/jcs.207696","mla":"Yamamoto, Wataru, et al. “Distinct Roles for Plasma Membrane PtdIns 4 P and PtdIns 4 5 P2 during Yeast Receptor Mediated Endocytosis.” Journal of Cell Science, vol. 131, no. 1, jcs207696, Company of Biologists, 2018, doi:10.1242/jcs.207696."},"title":"Distinct roles for plasma membrane PtdIns 4 P and PtdIns 4 5 P2 during yeast receptor mediated endocytosis","publist_id":"7184","author":[{"first_name":"Wataru","last_name":"Yamamoto","full_name":"Yamamoto, Wataru"},{"last_name":"Wada","full_name":"Wada, Suguru","first_name":"Suguru"},{"full_name":"Nagano, Makoto","last_name":"Nagano","first_name":"Makoto"},{"last_name":"Aoshima","full_name":"Aoshima, Kaito","first_name":"Kaito"},{"id":"3D224B9E-F248-11E8-B48F-1D18A9856A87","first_name":"Daria E","full_name":"Siekhaus, Daria E","orcid":"0000-0001-8323-8353","last_name":"Siekhaus"},{"first_name":"Junko","last_name":"Toshima","full_name":"Toshima, Junko"},{"full_name":"Toshima, Jiro","last_name":"Toshima","first_name":"Jiro"}],"external_id":{"pmid":["29192062"],"isi":["000424786900012"]},"article_processing_charge":"No"},{"citation":{"mla":"Fendrych, Matyas, et al. “Rapid and Reversible Root Growth Inhibition by TIR1 Auxin Signalling.” Nature Plants, vol. 4, no. 7, Springer Nature, 2018, pp. 453–59, doi:10.1038/s41477-018-0190-1.","apa":"Fendrych, M., Akhmanova, M., Merrin, J., Glanc, M., Hagihara, S., Takahashi, K., … Friml, J. (2018). Rapid and reversible root growth inhibition by TIR1 auxin signalling. Nature Plants. Springer Nature. https://doi.org/10.1038/s41477-018-0190-1","ama":"Fendrych M, Akhmanova M, Merrin J, et al. Rapid and reversible root growth inhibition by TIR1 auxin signalling. Nature Plants. 2018;4(7):453-459. doi:10.1038/s41477-018-0190-1","ieee":"M. Fendrych et al., “Rapid and reversible root growth inhibition by TIR1 auxin signalling,” Nature Plants, vol. 4, no. 7. Springer Nature, pp. 453–459, 2018.","short":"M. Fendrych, M. Akhmanova, J. Merrin, M. Glanc, S. Hagihara, K. Takahashi, N. Uchida, K.U. Torii, J. Friml, Nature Plants 4 (2018) 453–459.","chicago":"Fendrych, Matyas, Maria Akhmanova, Jack Merrin, Matous Glanc, Shinya Hagihara, Koji Takahashi, Naoyuki Uchida, Keiko U Torii, and Jiří Friml. “Rapid and Reversible Root Growth Inhibition by TIR1 Auxin Signalling.” Nature Plants. Springer Nature, 2018. https://doi.org/10.1038/s41477-018-0190-1.","ista":"Fendrych M, Akhmanova M, Merrin J, Glanc M, Hagihara S, Takahashi K, Uchida N, Torii KU, Friml J. 2018. Rapid and reversible root growth inhibition by TIR1 auxin signalling. Nature Plants. 4(7), 453–459."},"user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","author":[{"first_name":"Matyas","id":"43905548-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-9767-8699","full_name":"Fendrych, Matyas","last_name":"Fendrych"},{"first_name":"Maria","id":"3425EC26-F248-11E8-B48F-1D18A9856A87","last_name":"Akhmanova","orcid":"0000-0003-1522-3162","full_name":"Akhmanova, Maria"},{"id":"4515C308-F248-11E8-B48F-1D18A9856A87","first_name":"Jack","orcid":"0000-0001-5145-4609","full_name":"Merrin, Jack","last_name":"Merrin"},{"last_name":"Glanc","full_name":"Glanc, Matous","first_name":"Matous"},{"last_name":"Hagihara","full_name":"Hagihara, Shinya","first_name":"Shinya"},{"full_name":"Takahashi, Koji","last_name":"Takahashi","first_name":"Koji"},{"last_name":"Uchida","full_name":"Uchida, Naoyuki","first_name":"Naoyuki"},{"last_name":"Torii","full_name":"Torii, Keiko U","first_name":"Keiko U"},{"last_name":"Friml","orcid":"0000-0002-8302-7596","full_name":"Friml, Jirí","id":"4159519E-F248-11E8-B48F-1D18A9856A87","first_name":"Jirí"}],"publist_id":"7728","article_processing_charge":"No","external_id":{"isi":["000443221200017"],"pmid":["29942048"]},"title":"Rapid and reversible root growth inhibition by TIR1 auxin signalling","isi":1,"year":"2018","day":"25","publication":"Nature Plants","page":"453 - 459","date_published":"2018-06-25T00:00:00Z","doi":"10.1038/s41477-018-0190-1","date_created":"2018-12-11T11:45:07Z","publisher":"Springer Nature","quality_controlled":"1","oa":1,"date_updated":"2023-09-15T12:11:03Z","department":[{"_id":"JiFr"},{"_id":"DaSi"},{"_id":"NanoFab"}],"_id":"192","article_type":"original","type":"journal_article","status":"public","publication_status":"published","language":[{"iso":"eng"}],"related_material":{"link":[{"description":"News on IST Homepage","url":"https://ist.ac.at/en/news/new-mechanism-for-the-plant-hormone-auxin-discovered/","relation":"press_release"}]},"volume":4,"issue":"7","abstract":[{"text":"The phytohormone auxin is the information carrier in a plethora of developmental and physiological processes in plants(1). It has been firmly established that canonical, nuclear auxin signalling acts through regulation of gene transcription(2). Here, we combined microfluidics, live imaging, genetic engineering and computational modelling to reanalyse the classical case of root growth inhibition(3) by auxin. We show that Arabidopsis roots react to addition and removal of auxin by extremely rapid adaptation of growth rate. This process requires intracellular auxin perception but not transcriptional reprogramming. The formation of the canonical TIR1/AFB-Aux/IAA co-receptor complex is required for the growth regulation, hinting to a novel, non-transcriptional branch of this signalling pathway. Our results challenge the current understanding of root growth regulation by auxin and suggest another, presumably non-transcriptional, signalling output of the canonical auxin pathway.","lang":"eng"}],"oa_version":"Submitted Version","pmid":1,"scopus_import":"1","main_file_link":[{"open_access":"1","url":"https://www.ncbi.nlm.nih.gov/pubmed/29942048"}],"month":"06","intvolume":" 4"},{"project":[{"name":"Tracing Evolution of Auxin Transport and Polarity in Plants","grant_number":"742985","_id":"261099A6-B435-11E9-9278-68D0E5697425","call_identifier":"H2020"},{"name":"Molecular mechanisms of endocytic cargo recognition in plants","grant_number":"I03630","call_identifier":"FWF","_id":"26538374-B435-11E9-9278-68D0E5697425"}],"title":"Relative contribution of PIN-containing secretory vesicles and plasma membrane PINs to the directed auxin transport: Theoretical estimation","article_processing_charge":"No","external_id":{"isi":["000451528500282"]},"publist_id":"8042","author":[{"last_name":"Hille","full_name":"Hille, Sander","first_name":"Sander"},{"id":"3425EC26-F248-11E8-B48F-1D18A9856A87","first_name":"Maria","last_name":"Akhmanova","full_name":"Akhmanova, Maria","orcid":"0000-0003-1522-3162"},{"first_name":"Matous","id":"1AE1EA24-02D0-11E9-9BAA-DAF4881429F2","full_name":"Glanc, Matous","orcid":"0000-0003-0619-7783","last_name":"Glanc"},{"orcid":"0000-0002-2739-8843","full_name":"Johnson, Alexander J","last_name":"Johnson","id":"46A62C3A-F248-11E8-B48F-1D18A9856A87","first_name":"Alexander J"},{"id":"4159519E-F248-11E8-B48F-1D18A9856A87","first_name":"Jirí","last_name":"Friml","full_name":"Friml, Jirí","orcid":"0000-0002-8302-7596"}],"user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","citation":{"mla":"Hille, Sander, et al. “Relative Contribution of PIN-Containing Secretory Vesicles and Plasma Membrane PINs to the Directed Auxin Transport: Theoretical Estimation.” International Journal of Molecular Sciences, vol. 19, no. 11, MDPI, 2018, doi:10.3390/ijms19113566.","apa":"Hille, S., Akhmanova, M., Glanc, M., Johnson, A. J., & Friml, J. (2018). Relative contribution of PIN-containing secretory vesicles and plasma membrane PINs to the directed auxin transport: Theoretical estimation. International Journal of Molecular Sciences. MDPI. https://doi.org/10.3390/ijms19113566","ama":"Hille S, Akhmanova M, Glanc M, Johnson AJ, Friml J. Relative contribution of PIN-containing secretory vesicles and plasma membrane PINs to the directed auxin transport: Theoretical estimation. International Journal of Molecular Sciences. 2018;19(11). doi:10.3390/ijms19113566","short":"S. Hille, M. Akhmanova, M. Glanc, A.J. Johnson, J. Friml, International Journal of Molecular Sciences 19 (2018).","ieee":"S. Hille, M. Akhmanova, M. Glanc, A. J. Johnson, and J. Friml, “Relative contribution of PIN-containing secretory vesicles and plasma membrane PINs to the directed auxin transport: Theoretical estimation,” International Journal of Molecular Sciences, vol. 19, no. 11. MDPI, 2018.","chicago":"Hille, Sander, Maria Akhmanova, Matous Glanc, Alexander J Johnson, and Jiří Friml. “Relative Contribution of PIN-Containing Secretory Vesicles and Plasma Membrane PINs to the Directed Auxin Transport: Theoretical Estimation.” International Journal of Molecular Sciences. MDPI, 2018. https://doi.org/10.3390/ijms19113566.","ista":"Hille S, Akhmanova M, Glanc M, Johnson AJ, Friml J. 2018. Relative contribution of PIN-containing secretory vesicles and plasma membrane PINs to the directed auxin transport: Theoretical estimation. International Journal of Molecular Sciences. 19(11)."},"oa":1,"publisher":"MDPI","quality_controlled":"1","acknowledgement":"European Research Council (ERC): 742985 to Jiri Friml; M.A. was supported by the Austrian Science Fund (FWF) (M2379-B28); AJ was supported by the Austria Science Fund (FWF): I03630 to Jiri Friml.","date_created":"2018-12-11T11:44:09Z","date_published":"2018-11-12T00:00:00Z","doi":"10.3390/ijms19113566","publication":"International Journal of Molecular Sciences","day":"12","year":"2018","has_accepted_license":"1","isi":1,"status":"public","tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","image":"/images/cc_by.png","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","short":"CC BY (4.0)"},"article_type":"original","type":"journal_article","_id":"14","file_date_updated":"2020-07-14T12:44:50Z","department":[{"_id":"DaSi"},{"_id":"JiFr"}],"ddc":["580"],"date_updated":"2023-09-18T08:09:32Z","intvolume":" 19","month":"11","scopus_import":"1","oa_version":"Published Version","abstract":[{"text":"The intercellular transport of auxin is driven by PIN-formed (PIN) auxin efflux carriers. PINs are localized at the plasma membrane (PM) and on constitutively recycling endomembrane vesicles. Therefore, PINs can mediate auxin transport either by direct translocation across the PM or by pumping auxin into secretory vesicles (SVs), leading to its secretory release upon fusion with the PM. Which of these two mechanisms dominates is a matter of debate. Here, we addressed the issue with a mathematical modeling approach. We demonstrate that the efficiency of secretory transport depends on SV size, half-life of PINs on the PM, pH, exocytosis frequency and PIN density. 3D structured illumination microscopy (SIM) was used to determine PIN density on the PM. Combining this data with published values of the other parameters, we show that the transport activity of PINs in SVs would have to be at least 1000× greater than on the PM in order to produce a comparable macroscopic auxin transport. If both transport mechanisms operated simultaneously and PINs were equally active on SVs and PM, the contribution of secretion to the total auxin flux would be negligible. In conclusion, while secretory vesicle-mediated transport of auxin is an intriguing and theoretically possible model, it is unlikely to be a major mechanism of auxin transport inplanta.","lang":"eng"}],"ec_funded":1,"issue":"11","volume":19,"language":[{"iso":"eng"}],"file":[{"file_name":"2018_IJMS_Hille.pdf","date_created":"2018-12-17T16:04:11Z","creator":"dernst","file_size":2200593,"date_updated":"2020-07-14T12:44:50Z","file_id":"5719","checksum":"e4b59c2599b0ca26ebf5b8434bcde94a","relation":"main_file","access_level":"open_access","content_type":"application/pdf"}],"publication_status":"published","publication_identifier":{"eissn":["1422-0067"]}},{"language":[{"iso":"eng"}],"file":[{"creator":"dernst","date_updated":"2020-07-14T12:48:14Z","file_size":102737483,"date_created":"2019-04-08T14:13:12Z","file_name":"2018_Thesis_Belyaeva_source.docx","access_level":"closed","relation":"source_file","content_type":"application/vnd.openxmlformats-officedocument.wordprocessingml.document","embargo_to":"open_access","checksum":"d27b2465cb70d0c9678a0381b9b6ced1","file_id":"6243"},{"embargo":"2019-11-19","file_id":"6244","checksum":"a2939b61bde2de7b8ced77bbae0eaaed","relation":"main_file","access_level":"open_access","content_type":"application/pdf","file_name":"2018_Thesis_Belyaeva.pdf","date_created":"2019-04-08T14:14:08Z","creator":"dernst","file_size":88077843,"date_updated":"2021-02-11T11:17:16Z"}],"degree_awarded":"PhD","publication_status":"published","publication_identifier":{"issn":["2663-337X"]},"month":"07","alternative_title":["ISTA Thesis"],"oa_version":"Published Version","abstract":[{"lang":"eng","text":"Immune cells migrating to the sites of infection navigate through diverse tissue architectures and switch their migratory mechanisms upon demand. However, little is known about systemic regulators that could allow the acquisition of these mechanisms. We performed a genetic screen in Drosophila melanogaster to identify regulators of germband invasion by embryonic macrophages into the confined space between the ectoderm and mesoderm. We have found that bZIP circadian transcription factors (TFs) Kayak (dFos) and Vrille (dNFIL3) have opposite effects on macrophage germband infiltration: Kayak facilitated and Vrille inhibited it. These TFs are enriched in the macrophages during migration and genetically interact to control it. Kayak sets a less coordinated mode of migration of the macrophage group and increases the probability and length of Levy walks. Intriguingly, the motility of kayak mutant macrophages was also strongly affected during initial germband invasion but not along another less confined route. Inhibiting Rho1 signaling within the tail ectoderm partially rescued the Kayak mutant phenotype, strongly suggesting that migrating macrophages have to overcome a barrier imposed by the stiffness of the ectoderm. Also, Kayak appeared to be important for the maintenance of the round cell shape and the rear edge translocation of the macrophages invading the germband. Complementary to this, the cortical actin cytoskeleton of Kayak- deficient macrophages was strongly affected. RNA sequencing revealed the filamin Cheerio and tetraspanin TM4SF to be downstream of Kayak. Chromatin immunoprecipitation and immunostaining revealed that the formin Diaphanous is another downstream target of Kayak. Immunostaining revealed that the formin Diaphanous is another downstream target of Kayak. Indeed, Cheerio, TM4SF and Diaphanous are required within macrophages for germband invasion, and expression of constitutively active Diaphanous in macrophages was able to rescue the kayak mutant phenotype. Moreover, Cher and Diaphanous are also reduced in the macrophages overexpressing Vrille. We hypothesize that Kayak, through its targets, increases actin polymerization and cortical tension in macrophages and thus allows extra force generation necessary for macrophage dissemination and migration through confined stiff tissues, while Vrille counterbalances it."}],"file_date_updated":"2021-02-11T11:17:16Z","department":[{"_id":"DaSi"}],"ddc":["570"],"date_updated":"2023-09-07T12:43:10Z","supervisor":[{"last_name":"Siekhaus","orcid":"0000-0001-8323-8353","full_name":"Siekhaus, Daria E","first_name":"Daria E","id":"3D224B9E-F248-11E8-B48F-1D18A9856A87"}],"pubrep_id":"1064","status":"public","type":"dissertation","_id":"9","date_created":"2018-12-11T11:44:08Z","date_published":"2018-07-01T00:00:00Z","doi":"10.15479/AT:ISTA:th1064","page":"96","day":"01","year":"2018","has_accepted_license":"1","oa":1,"publisher":"Institute of Science and Technology Austria","title":"Transcriptional regulation of macrophage migration in the Drosophila melanogaster embryo ","article_processing_charge":"No","publist_id":"8047","author":[{"id":"47F080FE-F248-11E8-B48F-1D18A9856A87","first_name":"Vera","last_name":"Belyaeva","full_name":"Belyaeva, Vera"}],"user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","citation":{"mla":"Belyaeva, Vera. Transcriptional Regulation of Macrophage Migration in the Drosophila Melanogaster Embryo . Institute of Science and Technology Austria, 2018, doi:10.15479/AT:ISTA:th1064.","short":"V. Belyaeva, Transcriptional Regulation of Macrophage Migration in the Drosophila Melanogaster Embryo , Institute of Science and Technology Austria, 2018.","ieee":"V. Belyaeva, “Transcriptional regulation of macrophage migration in the Drosophila melanogaster embryo ,” Institute of Science and Technology Austria, 2018.","apa":"Belyaeva, V. (2018). Transcriptional regulation of macrophage migration in the Drosophila melanogaster embryo . Institute of Science and Technology Austria. https://doi.org/10.15479/AT:ISTA:th1064","ama":"Belyaeva V. Transcriptional regulation of macrophage migration in the Drosophila melanogaster embryo . 2018. doi:10.15479/AT:ISTA:th1064","chicago":"Belyaeva, Vera. “Transcriptional Regulation of Macrophage Migration in the Drosophila Melanogaster Embryo .” Institute of Science and Technology Austria, 2018. https://doi.org/10.15479/AT:ISTA:th1064.","ista":"Belyaeva V. 2018. Transcriptional regulation of macrophage migration in the Drosophila melanogaster embryo . Institute of Science and Technology Austria."}}]