[{"day":"08","publication":"Frontiers in Oncology","isi":1,"has_accepted_license":"1","year":"2022","date_published":"2022-02-08T00:00:00Z","doi":"10.3389/fonc.2022.777634","date_created":"2022-02-01T10:33:50Z","acknowledgement":"We thank M. Sixt, A. Leithner, and J. Alanko for helpful advice and the BioImaging Facility at IST Austria for technical support and assistance. We thank the Siekhaus Lab for the careful review of the manuscript and their input. MR and DS were funded by the NO Forschungs- und Bildungsges.m.b.H. (LS16-021) and IST core funding. MD was funded by Deutsche Forschungsgemeinschaft (DA 1785-1).","quality_controlled":"1","publisher":"Frontiers","oa":1,"user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","citation":{"mla":"Roblek, Marko, et al. “The Solute Carrier MFSD1 Decreases Β1 Integrin’s Activation Status and Thus Tumor Metastasis.” Frontiers in Oncology, vol. 12, 777634, Frontiers, 2022, doi:10.3389/fonc.2022.777634.","ama":"Roblek M, Bicher J, van Gogh M, et al. The solute carrier MFSD1 decreases β1 integrin’s activation status and thus tumor metastasis. Frontiers in Oncology. 2022;12. doi:10.3389/fonc.2022.777634","apa":"Roblek, M., Bicher, J., van Gogh, M., György, A., Seeböck, R., Szulc, B., … Siekhaus, D. E. (2022). The solute carrier MFSD1 decreases β1 integrin’s activation status and thus tumor metastasis. Frontiers in Oncology. Frontiers. https://doi.org/10.3389/fonc.2022.777634","short":"M. Roblek, J. Bicher, M. van Gogh, A. György, R. Seeböck, B. Szulc, M. Damme, M. Olczak, L. Borsig, D.E. Siekhaus, Frontiers in Oncology 12 (2022).","ieee":"M. Roblek et al., “The solute carrier MFSD1 decreases β1 integrin’s activation status and thus tumor metastasis,” Frontiers in Oncology, vol. 12. Frontiers, 2022.","chicago":"Roblek, Marko, Julia Bicher, Merel van Gogh, Attila György, Rita Seeböck, Bozena Szulc, Markus Damme, Mariusz Olczak, Lubor Borsig, and Daria E Siekhaus. “The Solute Carrier MFSD1 Decreases Β1 Integrin’s Activation Status and Thus Tumor Metastasis.” Frontiers in Oncology. Frontiers, 2022. https://doi.org/10.3389/fonc.2022.777634.","ista":"Roblek M, Bicher J, van Gogh M, György A, Seeböck R, Szulc B, Damme M, Olczak M, Borsig L, Siekhaus DE. 2022. The solute carrier MFSD1 decreases β1 integrin’s activation status and thus tumor metastasis. Frontiers in Oncology. 12, 777634."},"title":"The solute carrier MFSD1 decreases β1 integrin’s activation status and thus tumor metastasis","author":[{"first_name":"Marko","id":"3047D808-F248-11E8-B48F-1D18A9856A87","last_name":"Roblek","orcid":"0000-0001-9588-1389","full_name":"Roblek, Marko"},{"first_name":"Julia","id":"3CCBB46E-F248-11E8-B48F-1D18A9856A87","full_name":"Bicher, Julia","last_name":"Bicher"},{"full_name":"van Gogh, Merel","last_name":"van Gogh","first_name":"Merel"},{"last_name":"György","orcid":"0000-0002-1819-198X","full_name":"György, Attila","first_name":"Attila","id":"3BCEDBE0-F248-11E8-B48F-1D18A9856A87"},{"first_name":"Rita","last_name":"Seeböck","full_name":"Seeböck, Rita"},{"full_name":"Szulc, Bozena","last_name":"Szulc","first_name":"Bozena"},{"first_name":"Markus","full_name":"Damme, Markus","last_name":"Damme"},{"last_name":"Olczak","full_name":"Olczak, Mariusz","first_name":"Mariusz"},{"full_name":"Borsig, Lubor","last_name":"Borsig","first_name":"Lubor"},{"first_name":"Daria E","id":"3D224B9E-F248-11E8-B48F-1D18A9856A87","last_name":"Siekhaus","full_name":"Siekhaus, Daria E","orcid":"0000-0001-8323-8353"}],"article_processing_charge":"Yes (via OA deal)","external_id":{"isi":["000760618800001"]},"article_number":"777634","project":[{"_id":"2637E9C0-B435-11E9-9278-68D0E5697425","name":"Investigating the role of the novel major superfamily facilitator transporter family member MFSD1 in metastasis","grant_number":"LSC16-021 "}],"file":[{"success":1,"file_id":"10751","checksum":"63dfecf30c5bbf9408b3512bd603f78c","content_type":"application/pdf","relation":"main_file","access_level":"open_access","file_name":"2022_FrontiersOncol_Roblek.pdf","date_created":"2022-02-08T13:26:40Z","file_size":6303227,"date_updated":"2022-02-08T13:26:40Z","creator":"cchlebak"}],"language":[{"iso":"eng"}],"publication_identifier":{"issn":["2234-943X"]},"publication_status":"published","volume":12,"related_material":{"link":[{"url":"https://ist.ac.at/en/news/suppressing-the-spread-of-tumors/","relation":"confirmation","description":"News on IST Homepage"}]},"oa_version":"Published Version","acknowledged_ssus":[{"_id":"Bio"}],"abstract":[{"lang":"eng","text":"Solute carriers are increasingly recognized as participating in a plethora of pathologies, including cancer. We describe here the involvement of the orphan solute carrier MFSD1 in the regulation of tumor cell migration. Loss of MFSD1 enabled higher levels of metastasis in a mouse model. We identified an increased migratory potential in MFSD1-/- tumor cells which was mediated by increased focal adhesion turn-over, reduced stability of mature inactive β1 integrin, and the resulting increased integrin activation index. We show that MFSD1 promoted recycling to the cell surface of endocytosed inactive β1 integrin and thereby protected β1 integrin from proteolytic degradation; this led to dampening of the integrin activation index. Furthermore, down-regulation of MFSD1 expression was observed during early steps of tumorigenesis and higher MFSD1 expression levels correlate with a better cancer patient prognosis. In sum, we describe a requirement for endolysosomal MFSD1 in efficient β1 integrin recycling to suppress tumor spread."}],"month":"02","intvolume":" 12","scopus_import":"1","ddc":["570"],"date_updated":"2023-08-02T14:05:44Z","file_date_updated":"2022-02-08T13:26:40Z","department":[{"_id":"DaSi"}],"_id":"10712","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)"}},{"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":"10918","department":[{"_id":"DaSi"},{"_id":"LoSw"}],"file_date_updated":"2022-03-24T13:22:41Z","ddc":["570"],"date_updated":"2023-08-03T06:13:14Z","intvolume":" 41","month":"03","scopus_import":"1","oa_version":"Published Version","acknowledged_ssus":[{"_id":"Bio"}],"abstract":[{"lang":"eng","text":"Cellular metabolism must adapt to changing demands to enable homeostasis. During immune responses or cancer metastasis, cells leading migration into challenging environments require an energy boost, but what controls this capacity is unclear. Here, we study a previously uncharacterized nuclear protein, Atossa (encoded by CG9005), which supports macrophage invasion into the germband of Drosophila by controlling cellular metabolism. First, nuclear Atossa increases mRNA levels of Porthos, a DEAD-box protein, and of two metabolic enzymes, lysine-α-ketoglutarate reductase (LKR/SDH) and NADPH glyoxylate reductase (GR/HPR), thus enhancing mitochondrial bioenergetics. Then Porthos supports ribosome assembly and thereby raises the translational efficiency of a subset of mRNAs, including those affecting mitochondrial functions, the electron transport chain, and metabolism. Mitochondrial respiration measurements, metabolomics, and live imaging indicate that Atossa and Porthos power up OxPhos and energy production to promote the forging of a path into tissues by leading macrophages. Since many crucial physiological responses require increases in mitochondrial energy output, this previously undescribed genetic program may modulate a wide range of cellular behaviors."}],"ec_funded":1,"volume":41,"language":[{"iso":"eng"}],"file":[{"file_size":4344585,"date_updated":"2022-03-24T13:22:41Z","creator":"siekhaus","file_name":"Macrophage mitochondrial bioenergetics and tissue invasion are boosted by an Atossa-Porthos axis in Drosopila.pdf","date_created":"2022-03-24T13:22:41Z","content_type":"application/pdf","relation":"main_file","access_level":"open_access","file_id":"10919","checksum":"dba48580fe0fefaa4c63078d1d2a35df"}],"publication_status":"published","publication_identifier":{"eissn":["1460-2075"]},"project":[{"grant_number":"334077","name":"Investigating the role of transporters in invasive migration through junctions","call_identifier":"FP7","_id":"2536F660-B435-11E9-9278-68D0E5697425"},{"grant_number":"M02379","name":"Modeling epithelial tissue mechanics during cell invasion","_id":"264CBBAC-B435-11E9-9278-68D0E5697425","call_identifier":"FWF"},{"_id":"253B6E48-B435-11E9-9278-68D0E5697425","call_identifier":"FWF","name":"Drosophila TNFa´s Funktion in Immunzellen","grant_number":"P29638"}],"article_number":"e109049","title":"Macrophage mitochondrial bioenergetics and tissue invasion are boosted by an Atossa-Porthos axis in Drosophila","article_processing_charge":"Yes (via OA deal)","external_id":{"isi":["000771957000001"]},"author":[{"id":"49D32318-F248-11E8-B48F-1D18A9856A87","first_name":"Shamsi","full_name":"Emtenani, Shamsi","orcid":"0000-0001-6981-6938","last_name":"Emtenani"},{"full_name":"Martin, Elliot T","last_name":"Martin","first_name":"Elliot T"},{"first_name":"Attila","id":"3BCEDBE0-F248-11E8-B48F-1D18A9856A87","last_name":"György","orcid":"0000-0002-1819-198X","full_name":"György, Attila"},{"first_name":"Julia","id":"3CCBB46E-F248-11E8-B48F-1D18A9856A87","full_name":"Bicher, Julia","last_name":"Bicher"},{"last_name":"Genger","full_name":"Genger, Jakob-Wendelin","first_name":"Jakob-Wendelin"},{"full_name":"Köcher, Thomas","last_name":"Köcher","first_name":"Thomas"},{"first_name":"Maria","id":"3425EC26-F248-11E8-B48F-1D18A9856A87","last_name":"Akhmanova","full_name":"Akhmanova, Maria","orcid":"0000-0003-1522-3162"},{"full_name":"Pereira Guarda, Mariana","last_name":"Pereira Guarda","id":"6de81d9d-e2f2-11eb-945a-af8bc2a60b26","first_name":"Mariana"},{"last_name":"Roblek","full_name":"Roblek, Marko","orcid":"0000-0001-9588-1389","first_name":"Marko","id":"3047D808-F248-11E8-B48F-1D18A9856A87"},{"full_name":"Bergthaler, Andreas","last_name":"Bergthaler","first_name":"Andreas"},{"last_name":"Hurd","full_name":"Hurd, Thomas R","first_name":"Thomas R"},{"first_name":"Prashanth","full_name":"Rangan, Prashanth","last_name":"Rangan"},{"id":"3D224B9E-F248-11E8-B48F-1D18A9856A87","first_name":"Daria E","last_name":"Siekhaus","orcid":"0000-0001-8323-8353","full_name":"Siekhaus, Daria E"}],"user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","citation":{"ista":"Emtenani S, Martin ET, György A, Bicher J, Genger J-W, Köcher T, Akhmanova M, Pereira Guarda M, Roblek M, Bergthaler A, Hurd TR, Rangan P, Siekhaus DE. 2022. Macrophage mitochondrial bioenergetics and tissue invasion are boosted by an Atossa-Porthos axis in Drosophila. The Embo Journal. 41, e109049.","chicago":"Emtenani, Shamsi, Elliot T Martin, Attila György, Julia Bicher, Jakob-Wendelin Genger, Thomas Köcher, Maria Akhmanova, et al. “Macrophage Mitochondrial Bioenergetics and Tissue Invasion Are Boosted by an Atossa-Porthos Axis in Drosophila.” The Embo Journal. Embo Press, 2022. https://doi.org/10.15252/embj.2021109049.","short":"S. Emtenani, E.T. Martin, A. György, J. Bicher, J.-W. Genger, T. Köcher, M. Akhmanova, M. Pereira Guarda, M. Roblek, A. Bergthaler, T.R. Hurd, P. Rangan, D.E. Siekhaus, The Embo Journal 41 (2022).","ieee":"S. Emtenani et al., “Macrophage mitochondrial bioenergetics and tissue invasion are boosted by an Atossa-Porthos axis in Drosophila,” The Embo Journal, vol. 41. Embo Press, 2022.","apa":"Emtenani, S., Martin, E. T., György, A., Bicher, J., Genger, J.-W., Köcher, T., … Siekhaus, D. E. (2022). Macrophage mitochondrial bioenergetics and tissue invasion are boosted by an Atossa-Porthos axis in Drosophila. The Embo Journal. Embo Press. https://doi.org/10.15252/embj.2021109049","ama":"Emtenani S, Martin ET, György A, et al. Macrophage mitochondrial bioenergetics and tissue invasion are boosted by an Atossa-Porthos axis in Drosophila. The Embo Journal. 2022;41. doi:10.15252/embj.2021109049","mla":"Emtenani, Shamsi, et al. “Macrophage Mitochondrial Bioenergetics and Tissue Invasion Are Boosted by an Atossa-Porthos Axis in Drosophila.” The Embo Journal, vol. 41, e109049, Embo Press, 2022, doi:10.15252/embj.2021109049."},"oa":1,"quality_controlled":"1","publisher":"Embo Press","acknowledgement":"We thank the DGRC (NIH grant 2P40OD010949-10A1) for plasmids, the BDSC (NIH grant P40OD018537) and the VDRC for fly stocks, FlyBase for essential genomic information, the BDGP in situ database for data (Tomancak et al, 2007), the IST Austria Bioimaging facility for support, the VBC Core Facilities for RNA sequencing and analysis, and C. Guet, C. Navarro, C. Desplan, T. Lecuit, I. Miguel-Aliaga, and Siekhaus group members for comments on the manuscript. The VBCF Metabolomics Facility is funded by the City of Vienna through the Vienna Business Agency. This work was supported by the Marie Curie CIG 334077/IRTIM (DES), Austrian Science Fund (FWF) Lise Meitner Fellowship M2379-B28 (MA and DES), Austrian Science Fund (FWF) grant ASI_FWF01_P29638S (DES), NIH/NIGMS (R01GM111779-06 (PR), RO1GM135628-01 (PR), European Research Council (ERC) grant no. 677006 “CMIL” (AB), and Natural Sciences and Engineering Research Council of Canada\r\n(RGPIN-2019-06766) (TRH). ","date_created":"2022-03-24T13:23:09Z","doi":"10.15252/embj.2021109049","date_published":"2022-03-23T00:00:00Z","publication":"The Embo Journal","day":"23","year":"2022","isi":1,"has_accepted_license":"1"},{"acknowledgement":"We thank R. Cagan, A. Whitworth and J. Nagpal for fly lines and advice, S. Herlitze for provision of a tissue culture illuminator, and Verian Bader for help with statistical analysis.","oa":1,"quality_controlled":"1","publisher":"Public Library of Science","publication":"PLoS genetics","day":"01","year":"2021","has_accepted_license":"1","isi":1,"date_created":"2021-05-02T22:01:29Z","doi":"10.1371/journal.pgen.1009479","date_published":"2021-04-01T00:00:00Z","page":"e1009479","user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","citation":{"ista":"Inglés Prieto Á, Furthmann N, Crossman SH, Tichy AM, Hoyer N, Petersen M, Zheden V, Bicher J, Gschaider-Reichhart E, György A, Siekhaus DE, Soba P, Winklhofer KF, Janovjak HL. 2021. Optogenetic delivery of trophic signals in a genetic model of Parkinson’s disease. PLoS genetics. 17(4), e1009479.","chicago":"Inglés Prieto, Álvaro, Nikolas Furthmann, Samuel H. Crossman, Alexandra Madelaine Tichy, Nina Hoyer, Meike Petersen, Vanessa Zheden, et al. “Optogenetic Delivery of Trophic Signals in a Genetic Model of Parkinson’s Disease.” PLoS Genetics. Public Library of Science, 2021. https://doi.org/10.1371/journal.pgen.1009479.","ama":"Inglés Prieto Á, Furthmann N, Crossman SH, et al. Optogenetic delivery of trophic signals in a genetic model of Parkinson’s disease. PLoS genetics. 2021;17(4):e1009479. doi:10.1371/journal.pgen.1009479","apa":"Inglés Prieto, Á., Furthmann, N., Crossman, S. H., Tichy, A. M., Hoyer, N., Petersen, M., … Janovjak, H. L. (2021). Optogenetic delivery of trophic signals in a genetic model of Parkinson’s disease. PLoS Genetics. Public Library of Science. https://doi.org/10.1371/journal.pgen.1009479","ieee":"Á. Inglés Prieto et al., “Optogenetic delivery of trophic signals in a genetic model of Parkinson’s disease,” PLoS genetics, vol. 17, no. 4. Public Library of Science, p. e1009479, 2021.","short":"Á. Inglés Prieto, N. Furthmann, S.H. Crossman, A.M. Tichy, N. Hoyer, M. Petersen, V. Zheden, J. Bicher, E. Gschaider-Reichhart, A. György, D.E. Siekhaus, P. Soba, K.F. Winklhofer, H.L. Janovjak, PLoS Genetics 17 (2021) e1009479.","mla":"Inglés Prieto, Álvaro, et al. “Optogenetic Delivery of Trophic Signals in a Genetic Model of Parkinson’s Disease.” PLoS Genetics, vol. 17, no. 4, Public Library of Science, 2021, p. e1009479, doi:10.1371/journal.pgen.1009479."},"title":"Optogenetic delivery of trophic signals in a genetic model of Parkinson's disease","external_id":{"isi":["000640606700001"]},"article_processing_charge":"No","author":[{"id":"2A9DB292-F248-11E8-B48F-1D18A9856A87","first_name":"Álvaro","last_name":"Inglés Prieto","orcid":"0000-0002-5409-8571","full_name":"Inglés Prieto, Álvaro"},{"first_name":"Nikolas","full_name":"Furthmann, Nikolas","last_name":"Furthmann"},{"first_name":"Samuel H.","last_name":"Crossman","full_name":"Crossman, Samuel H."},{"first_name":"Alexandra Madelaine","last_name":"Tichy","full_name":"Tichy, Alexandra Madelaine"},{"full_name":"Hoyer, Nina","last_name":"Hoyer","first_name":"Nina"},{"first_name":"Meike","full_name":"Petersen, Meike","last_name":"Petersen"},{"last_name":"Zheden","full_name":"Zheden, Vanessa","first_name":"Vanessa","id":"39C5A68A-F248-11E8-B48F-1D18A9856A87"},{"full_name":"Bicher, Julia","last_name":"Bicher","first_name":"Julia","id":"3CCBB46E-F248-11E8-B48F-1D18A9856A87"},{"id":"3FEE232A-F248-11E8-B48F-1D18A9856A87","first_name":"Eva","last_name":"Gschaider-Reichhart","full_name":"Gschaider-Reichhart, Eva","orcid":"0000-0002-7218-7738"},{"id":"3BCEDBE0-F248-11E8-B48F-1D18A9856A87","first_name":"Attila","last_name":"György","orcid":"0000-0002-1819-198X","full_name":"György, Attila"},{"last_name":"Siekhaus","full_name":"Siekhaus, Daria E","orcid":"0000-0001-8323-8353","first_name":"Daria E","id":"3D224B9E-F248-11E8-B48F-1D18A9856A87"},{"last_name":"Soba","full_name":"Soba, Peter","first_name":"Peter"},{"full_name":"Winklhofer, Konstanze F.","last_name":"Winklhofer","first_name":"Konstanze F."},{"id":"33BA6C30-F248-11E8-B48F-1D18A9856A87","first_name":"Harald L","last_name":"Janovjak","full_name":"Janovjak, Harald L","orcid":"0000-0002-8023-9315"}],"oa_version":"Published Version","abstract":[{"text":"Optogenetics has been harnessed to shed new mechanistic light on current and future therapeutic strategies. This has been to date achieved by the regulation of ion flow and electrical signals in neuronal cells and neural circuits that are known to be affected by disease. In contrast, the optogenetic delivery of trophic biochemical signals, which support cell survival and are implicated in degenerative disorders, has never been demonstrated in an animal model of disease. Here, we reengineered the human and Drosophila melanogaster REarranged during Transfection (hRET and dRET) receptors to be activated by light, creating one-component optogenetic tools termed Opto-hRET and Opto-dRET. Upon blue light stimulation, these receptors robustly induced the MAPK/ERK proliferative signaling pathway in cultured cells. In PINK1B9 flies that exhibit loss of PTEN-induced putative kinase 1 (PINK1), a kinase associated with familial Parkinson’s disease (PD), light activation of Opto-dRET suppressed mitochondrial defects, tissue degeneration and behavioral deficits. In human cells with PINK1 loss-of-function, mitochondrial fragmentation was rescued using Opto-dRET via the PI3K/NF-кB pathway. Our results demonstrate that a light-activated receptor can ameliorate disease hallmarks in a genetic model of PD. The optogenetic delivery of trophic signals is cell type-specific and reversible and thus has the potential to inspire novel strategies towards a spatio-temporal regulation of tissue repair.","lang":"eng"}],"intvolume":" 17","month":"04","scopus_import":"1","language":[{"iso":"eng"}],"file":[{"content_type":"application/pdf","access_level":"open_access","relation":"main_file","checksum":"82a74668f863e8dfb22fdd4f845c92ce","file_id":"9369","success":1,"date_updated":"2021-05-04T09:05:27Z","file_size":3072764,"creator":"kschuh","date_created":"2021-05-04T09:05:27Z","file_name":"2021_PLOS_Ingles-Prieto.pdf"}],"publication_status":"published","publication_identifier":{"eissn":["15537404"]},"volume":17,"issue":"4","_id":"9363","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)"},"type":"journal_article","ddc":["570"],"date_updated":"2023-08-08T13:17:47Z","file_date_updated":"2021-05-04T09:05:27Z","department":[{"_id":"EM-Fac"},{"_id":"LoSw"},{"_id":"DaSi"}]},{"year":"2019","has_accepted_license":"1","isi":1,"publication":"eLife","day":"26","date_created":"2019-03-28T13:37:45Z","date_published":"2019-03-26T00:00:00Z","doi":"10.7554/elife.41801","oa":1,"publisher":"eLife Sciences Publications","quality_controlled":"1","citation":{"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.","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.","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.","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).","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","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","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."},"user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","article_processing_charge":"No","external_id":{"isi":["000462530200001"]},"author":[{"full_name":"Valosková, Katarina","last_name":"Valosková","first_name":"Katarina","id":"46F146FC-F248-11E8-B48F-1D18A9856A87"},{"first_name":"Julia","id":"3CCBB46E-F248-11E8-B48F-1D18A9856A87","full_name":"Biebl, Julia","last_name":"Biebl"},{"full_name":"Roblek, Marko","orcid":"0000-0001-9588-1389","last_name":"Roblek","id":"3047D808-F248-11E8-B48F-1D18A9856A87","first_name":"Marko"},{"last_name":"Emtenani","orcid":"0000-0001-6981-6938","full_name":"Emtenani, Shamsi","id":"49D32318-F248-11E8-B48F-1D18A9856A87","first_name":"Shamsi"},{"first_name":"Attila","id":"3BCEDBE0-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-1819-198X","full_name":"György, Attila","last_name":"György"},{"id":"495A3C32-F248-11E8-B48F-1D18A9856A87","first_name":"Michaela","orcid":"0000-0003-2427-6856","full_name":"Misova, Michaela","last_name":"Misova"},{"first_name":"Aparna","id":"2F064CFE-F248-11E8-B48F-1D18A9856A87","last_name":"Ratheesh","orcid":"0000-0001-7190-0776","full_name":"Ratheesh, Aparna"},{"first_name":"Patricia","id":"2CE4065A-F248-11E8-B48F-1D18A9856A87","full_name":"Rodrigues, Patricia","last_name":"Rodrigues"},{"first_name":"Katerina","last_name":"Shkarina","full_name":"Shkarina, Katerina"},{"last_name":"Larsen","full_name":"Larsen, Ida Signe Bohse","first_name":"Ida Signe Bohse"},{"first_name":"Sergey Y","full_name":"Vakhrushev, Sergey Y","last_name":"Vakhrushev"},{"first_name":"Henrik","last_name":"Clausen","full_name":"Clausen, Henrik"},{"id":"3D224B9E-F248-11E8-B48F-1D18A9856A87","first_name":"Daria E","full_name":"Siekhaus, Daria E","orcid":"0000-0001-8323-8353","last_name":"Siekhaus"}],"title":"A conserved major facilitator superfamily member orchestrates a subset of O-glycosylation to aid macrophage tissue invasion","article_number":"e41801","project":[{"grant_number":"24283","name":"Examination of the role of a MFS transporter in the migration of Drosophila immune cells","_id":"253CDE40-B435-11E9-9278-68D0E5697425"},{"grant_number":"P29638","name":"The role of Drosophila TNF alpha in immune cell invasion","_id":"253B6E48-B435-11E9-9278-68D0E5697425","call_identifier":"FWF"},{"grant_number":"334077","name":"Investigating the role of transporters in invasive migration through junctions","call_identifier":"FP7","_id":"2536F660-B435-11E9-9278-68D0E5697425"},{"name":"Breaking barriers: Investigating the junctional and mechanobiological changes underlying the ability of Drosophila immune cells to invade an epithelium","grant_number":"329540","call_identifier":"FP7","_id":"25388084-B435-11E9-9278-68D0E5697425"},{"_id":"2564DBCA-B435-11E9-9278-68D0E5697425","call_identifier":"H2020","grant_number":"665385","name":"International IST Doctoral Program"}],"publication_status":"published","publication_identifier":{"issn":["2050-084X"]},"language":[{"iso":"eng"}],"file":[{"creator":"dernst","date_updated":"2020-07-14T12:47:23Z","file_size":4496017,"date_created":"2019-03-28T14:00:41Z","file_name":"2019_eLife_Valoskova.pdf","access_level":"open_access","relation":"main_file","content_type":"application/pdf","checksum":"cc0d1a512559d52e7e7cb0e9b9854b40","file_id":"6188"}],"ec_funded":1,"related_material":{"record":[{"id":"6530","relation":"dissertation_contains"},{"relation":"dissertation_contains","id":"8983","status":"public"},{"status":"public","id":"6546","relation":"dissertation_contains"}],"link":[{"url":"https://ist.ac.at/en/news/new-gene-potentially-involved-in-metastasis-identified/","relation":"press_release","description":"News on IST Homepage"}]},"volume":8,"acknowledged_ssus":[{"_id":"LifeSc"}],"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."}],"oa_version":"Published Version","scopus_import":"1","intvolume":" 8","month":"03","date_updated":"2024-03-27T23:30:29Z","ddc":["570"],"department":[{"_id":"DaSi"}],"file_date_updated":"2020-07-14T12:47:23Z","_id":"6187","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","status":"public"},{"date_created":"2018-12-11T11:45:44Z","date_published":"2018-05-07T00:00:00Z","doi":"10.1016/j.devcel.2018.04.002","page":"331 - 346","publication":"Developmental Cell","day":"07","year":"2018","isi":1,"oa":1,"quality_controlled":"1","publisher":"Elsevier","title":"Drosophila TNF modulates tissue tension in the embryo to facilitate macrophage invasive migration","article_processing_charge":"No","external_id":{"pmid":["29738712"],"isi":["000432461400009"]},"author":[{"last_name":"Ratheesh","orcid":"0000-0001-7190-0776","full_name":"Ratheesh, Aparna","first_name":"Aparna","id":"2F064CFE-F248-11E8-B48F-1D18A9856A87"},{"full_name":"Biebl, Julia","last_name":"Biebl","first_name":"Julia","id":"3CCBB46E-F248-11E8-B48F-1D18A9856A87"},{"first_name":"Michael","last_name":"Smutny","full_name":"Smutny, 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"},{"last_name":"Krens","full_name":"Krens, Gabriel","orcid":"0000-0003-4761-5996","first_name":"Gabriel","id":"2B819732-F248-11E8-B48F-1D18A9856A87"},{"last_name":"Kaufmann","full_name":"Kaufmann, Walter","orcid":"0000-0001-9735-5315","first_name":"Walter","id":"3F99E422-F248-11E8-B48F-1D18A9856A87"},{"first_name":"Attila","id":"3BCEDBE0-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-1819-198X","full_name":"György, Attila","last_name":"György"},{"last_name":"Casano","full_name":"Casano, Alessandra M","orcid":"0000-0002-6009-6804","first_name":"Alessandra M","id":"3DBA3F4E-F248-11E8-B48F-1D18A9856A87"},{"id":"3D224B9E-F248-11E8-B48F-1D18A9856A87","first_name":"Daria E","last_name":"Siekhaus","full_name":"Siekhaus, Daria E","orcid":"0000-0001-8323-8353"}],"user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","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.","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.","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"},"project":[{"grant_number":"P29638","name":"Drosophila TNFa´s Funktion in Immunzellen","call_identifier":"FWF","_id":"253B6E48-B435-11E9-9278-68D0E5697425"},{"call_identifier":"FP7","_id":"2536F660-B435-11E9-9278-68D0E5697425","grant_number":"334077","name":"Investigating the role of transporters in invasive migration through junctions"}],"ec_funded":1,"volume":45,"issue":"3","related_material":{"link":[{"description":"News on IST Homepage","relation":"press_release","url":"https://ist.ac.at/en/news/cells-change-tension-to-make-tissue-barriers-easier-to-get-through/"}]},"language":[{"iso":"eng"}],"publication_status":"published","intvolume":" 45","month":"05","main_file_link":[{"url":"https://doi.org/10.1016/j.devcel.2018.04.002","open_access":"1"}],"scopus_import":"1","pmid":1,"oa_version":"Published Version","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"}],"department":[{"_id":"DaSi"},{"_id":"CaHe"},{"_id":"Bio"},{"_id":"EM-Fac"},{"_id":"MiSi"}],"date_updated":"2023-09-11T13:22:13Z","status":"public","article_type":"original","type":"journal_article","_id":"308"}]