[{"doi":"10.3389/fonc.2022.777634","language":[{"iso":"eng"}],"acknowledged_ssus":[{"_id":"Bio"}],"tmp":{"name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","short":"CC BY (4.0)","image":"/images/cc_by.png"},"external_id":{"isi":["000760618800001"]},"oa":1,"project":[{"grant_number":"LSC16-021 ","_id":"2637E9C0-B435-11E9-9278-68D0E5697425","name":"Investigating the role of the novel major superfamily facilitator transporter family member MFSD1 in metastasis"}],"quality_controlled":"1","isi":1,"publication_identifier":{"issn":["2234-943X"]},"month":"02","related_material":{"link":[{"description":"News on IST Homepage","relation":"confirmation","url":"https://ist.ac.at/en/news/suppressing-the-spread-of-tumors/"}]},"author":[{"first_name":"Marko","last_name":"Roblek","id":"3047D808-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0001-9588-1389","full_name":"Roblek, Marko"},{"first_name":"Julia","last_name":"Bicher","id":"3CCBB46E-F248-11E8-B48F-1D18A9856A87","full_name":"Bicher, Julia"},{"full_name":"van Gogh, Merel","first_name":"Merel","last_name":"van Gogh"},{"full_name":"György, Attila","last_name":"György","first_name":"Attila","orcid":"0000-0002-1819-198X","id":"3BCEDBE0-F248-11E8-B48F-1D18A9856A87"},{"full_name":"Seeböck, Rita","last_name":"Seeböck","first_name":"Rita"},{"full_name":"Szulc, Bozena","last_name":"Szulc","first_name":"Bozena"},{"full_name":"Damme, Markus","first_name":"Markus","last_name":"Damme"},{"first_name":"Mariusz","last_name":"Olczak","full_name":"Olczak, Mariusz"},{"full_name":"Borsig, Lubor","first_name":"Lubor","last_name":"Borsig"},{"id":"3D224B9E-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0001-8323-8353","first_name":"Daria E","last_name":"Siekhaus","full_name":"Siekhaus, Daria E"}],"volume":12,"date_updated":"2023-08-02T14:05:44Z","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).","year":"2022","publisher":"Frontiers","department":[{"_id":"DaSi"}],"publication_status":"published","file_date_updated":"2022-02-08T13:26:40Z","article_number":"777634","date_published":"2022-02-08T00:00:00Z","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.","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).","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.","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","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.","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.","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"},"publication":"Frontiers in Oncology","article_type":"original","has_accepted_license":"1","article_processing_charge":"Yes (via OA deal)","day":"08","scopus_import":"1","oa_version":"Published Version","file":[{"creator":"cchlebak","file_size":6303227,"content_type":"application/pdf","file_name":"2022_FrontiersOncol_Roblek.pdf","access_level":"open_access","date_created":"2022-02-08T13:26:40Z","date_updated":"2022-02-08T13:26:40Z","success":1,"checksum":"63dfecf30c5bbf9408b3512bd603f78c","file_id":"10751","relation":"main_file"}],"user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","_id":"10712","intvolume":" 12","ddc":["570"],"title":"The solute carrier MFSD1 decreases β1 integrin’s activation status and thus tumor metastasis","status":"public","abstract":[{"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.","lang":"eng"}],"type":"journal_article"},{"oa_version":"Published Version","file":[{"file_name":"Macrophage mitochondrial bioenergetics and tissue invasion are boosted by an Atossa-Porthos axis in Drosopila.pdf","access_level":"open_access","content_type":"application/pdf","file_size":4344585,"creator":"siekhaus","relation":"main_file","file_id":"10919","date_created":"2022-03-24T13:22:41Z","date_updated":"2022-03-24T13:22:41Z","checksum":"dba48580fe0fefaa4c63078d1d2a35df"}],"intvolume":" 41","title":"Macrophage mitochondrial bioenergetics and tissue invasion are boosted by an Atossa-Porthos axis in Drosophila","status":"public","ddc":["570"],"user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","_id":"10918","abstract":[{"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.","lang":"eng"}],"type":"journal_article","date_published":"2022-03-23T00:00:00Z","article_type":"original","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.","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","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.","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.","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)."},"publication":"The Embo Journal","has_accepted_license":"1","article_processing_charge":"Yes (via OA deal)","day":"23","scopus_import":"1","volume":41,"date_updated":"2023-08-03T06:13:14Z","date_created":"2022-03-24T13:23:09Z","author":[{"orcid":"0000-0001-6981-6938","id":"49D32318-F248-11E8-B48F-1D18A9856A87","last_name":"Emtenani","first_name":"Shamsi","full_name":"Emtenani, Shamsi"},{"full_name":"Martin, Elliot T","last_name":"Martin","first_name":"Elliot T"},{"id":"3BCEDBE0-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-1819-198X","first_name":"Attila","last_name":"György","full_name":"György, Attila"},{"id":"3CCBB46E-F248-11E8-B48F-1D18A9856A87","last_name":"Bicher","first_name":"Julia","full_name":"Bicher, Julia"},{"full_name":"Genger, Jakob-Wendelin","first_name":"Jakob-Wendelin","last_name":"Genger"},{"first_name":"Thomas","last_name":"Köcher","full_name":"Köcher, Thomas"},{"full_name":"Akhmanova, Maria","last_name":"Akhmanova","first_name":"Maria","orcid":"0000-0003-1522-3162","id":"3425EC26-F248-11E8-B48F-1D18A9856A87"},{"full_name":"Pereira Guarda, Mariana","last_name":"Pereira Guarda","first_name":"Mariana","id":"6de81d9d-e2f2-11eb-945a-af8bc2a60b26"},{"last_name":"Roblek","first_name":"Marko","orcid":"0000-0001-9588-1389","id":"3047D808-F248-11E8-B48F-1D18A9856A87","full_name":"Roblek, Marko"},{"full_name":"Bergthaler, Andreas","first_name":"Andreas","last_name":"Bergthaler"},{"full_name":"Hurd, Thomas R","first_name":"Thomas R","last_name":"Hurd"},{"full_name":"Rangan, Prashanth","last_name":"Rangan","first_name":"Prashanth"},{"full_name":"Siekhaus, Daria E","last_name":"Siekhaus","first_name":"Daria E","orcid":"0000-0001-8323-8353","id":"3D224B9E-F248-11E8-B48F-1D18A9856A87"}],"publisher":"Embo Press","department":[{"_id":"DaSi"},{"_id":"LoSw"}],"publication_status":"published","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). ","year":"2022","ec_funded":1,"file_date_updated":"2022-03-24T13:22:41Z","article_number":"e109049","language":[{"iso":"eng"}],"acknowledged_ssus":[{"_id":"Bio"}],"doi":"10.15252/embj.2021109049","project":[{"name":"Investigating the role of transporters in invasive migration through junctions","call_identifier":"FP7","grant_number":"334077","_id":"2536F660-B435-11E9-9278-68D0E5697425"},{"_id":"264CBBAC-B435-11E9-9278-68D0E5697425","grant_number":"M02379","name":"Modeling epithelial tissue mechanics during cell invasion","call_identifier":"FWF"},{"name":"Drosophila TNFa´s Funktion in Immunzellen","call_identifier":"FWF","grant_number":"P29638","_id":"253B6E48-B435-11E9-9278-68D0E5697425"}],"quality_controlled":"1","isi":1,"tmp":{"name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","short":"CC BY (4.0)","image":"/images/cc_by.png"},"oa":1,"external_id":{"isi":["000771957000001"]},"publication_identifier":{"eissn":["1460-2075"]},"month":"03"},{"article_processing_charge":"No","has_accepted_license":"1","day":"06","scopus_import":"1","date_published":"2022-01-06T00:00:00Z","citation":{"ista":"Belyaeva V, Wachner S, György A, Emtenani S, Gridchyn I, Akhmanova M, Linder M, Roblek M, Sibilia M, Siekhaus DE. 2022. Fos regulates macrophage infiltration against surrounding tissue resistance by a cortical actin-based mechanism in Drosophila. PLoS Biology. 20(1), e3001494.","ieee":"V. Belyaeva et al., “Fos regulates macrophage infiltration against surrounding tissue resistance by a cortical actin-based mechanism in Drosophila,” PLoS Biology, vol. 20, no. 1. Public Library of Science, p. e3001494, 2022.","apa":"Belyaeva, V., Wachner, S., György, A., Emtenani, S., Gridchyn, I., Akhmanova, M., … Siekhaus, D. E. (2022). Fos regulates macrophage infiltration against surrounding tissue resistance by a cortical actin-based mechanism in Drosophila. PLoS Biology. Public Library of Science. https://doi.org/10.1371/journal.pbio.3001494","ama":"Belyaeva V, Wachner S, György A, et al. Fos regulates macrophage infiltration against surrounding tissue resistance by a cortical actin-based mechanism in Drosophila. PLoS Biology. 2022;20(1):e3001494. doi:10.1371/journal.pbio.3001494","chicago":"Belyaeva, Vera, Stephanie Wachner, Attila György, Shamsi Emtenani, Igor Gridchyn, Maria Akhmanova, M Linder, Marko Roblek, M Sibilia, and Daria E Siekhaus. “Fos Regulates Macrophage Infiltration against Surrounding Tissue Resistance by a Cortical Actin-Based Mechanism in Drosophila.” PLoS Biology. Public Library of Science, 2022. https://doi.org/10.1371/journal.pbio.3001494.","mla":"Belyaeva, Vera, et al. “Fos Regulates Macrophage Infiltration against Surrounding Tissue Resistance by a Cortical Actin-Based Mechanism in Drosophila.” PLoS Biology, vol. 20, no. 1, Public Library of Science, 2022, p. e3001494, doi:10.1371/journal.pbio.3001494.","short":"V. Belyaeva, S. Wachner, A. György, S. Emtenani, I. Gridchyn, M. Akhmanova, M. Linder, M. Roblek, M. Sibilia, D.E. Siekhaus, PLoS Biology 20 (2022) e3001494."},"publication":"PLoS Biology","page":"e3001494","article_type":"original","issue":"1","abstract":[{"lang":"eng","text":"The infiltration of immune cells into tissues underlies the establishment of tissue-resident macrophages and responses to infections and tumors. Yet the mechanisms immune cells utilize to negotiate tissue barriers in living organisms are not well understood, and a role for cortical actin has not been examined. Here, we find that the tissue invasion of Drosophila macrophages, also known as plasmatocytes or hemocytes, utilizes enhanced cortical F-actin levels stimulated by the Drosophila member of the fos proto oncogene transcription factor family (Dfos, Kayak). RNA sequencing analysis and live imaging show that Dfos enhances F-actin levels around the entire macrophage surface by increasing mRNA levels of the membrane spanning molecular scaffold tetraspanin TM4SF, and the actin cross-linking filamin Cheerio, which are themselves required for invasion. Both the filamin and the tetraspanin enhance the cortical activity of Rho1 and the formin Diaphanous and thus the assembly of cortical actin, which is a critical function since expressing a dominant active form of Diaphanous can rescue the Dfos macrophage invasion defect. In vivo imaging shows that Dfos enhances the efficiency of the initial phases of macrophage tissue entry. Genetic evidence argues that this Dfos-induced program in macrophages counteracts the constraint produced by the tension of surrounding tissues and buffers the properties of the macrophage nucleus from affecting tissue entry. We thus identify strengthening the cortical actin cytoskeleton through Dfos as a key process allowing efficient forward movement of an immune cell into surrounding tissues. "}],"type":"journal_article","oa_version":"Published Version","file":[{"file_size":5426932,"content_type":"application/pdf","creator":"cchlebak","file_name":"2022_PLOSBio_Belyaeva.pdf","access_level":"open_access","date_updated":"2022-01-12T13:50:04Z","date_created":"2022-01-12T13:50:04Z","checksum":"f454212a5522a7818ba4b2892315c478","success":1,"relation":"main_file","file_id":"10615"}],"_id":"10614","user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","intvolume":" 20","title":"Fos regulates macrophage infiltration against surrounding tissue resistance by a cortical actin-based mechanism in Drosophila","ddc":["570"],"status":"public","publication_identifier":{"issn":["1544-9173"],"eissn":["1545-7885"]},"month":"01","doi":"10.1371/journal.pbio.3001494","language":[{"iso":"eng"}],"acknowledged_ssus":[{"_id":"LifeSc"}],"tmp":{"name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","short":"CC BY (4.0)","image":"/images/cc_by.png"},"external_id":{"isi":["000971223700001"],"pmid":["34990456"]},"oa":1,"project":[{"grant_number":"P29638","_id":"253B6E48-B435-11E9-9278-68D0E5697425","call_identifier":"FWF","name":"Drosophila TNFa´s Funktion in Immunzellen"},{"name":"Tissue barrier penetration is crucial for immunity and metastasis","grant_number":"24800","_id":"26199CA4-B435-11E9-9278-68D0E5697425"},{"call_identifier":"FP7","name":"Investigating the role of transporters in invasive migration through junctions","grant_number":"334077","_id":"2536F660-B435-11E9-9278-68D0E5697425"}],"quality_controlled":"1","isi":1,"ec_funded":1,"file_date_updated":"2022-01-12T13:50:04Z","related_material":{"record":[{"status":"public","relation":"earlier_version","id":"8557"},{"status":"public","relation":"dissertation_contains","id":"11193"}],"link":[{"url":"https://www.biorxiv.org/content/10.1101/2020.09.18.301481","relation":"earlier_version"},{"url":"https://ista.ac.at/en/news/resisting-the-pressure/","description":"News on the ISTA Website","relation":"press_release"}]},"author":[{"full_name":"Belyaeva, Vera","first_name":"Vera","last_name":"Belyaeva","id":"47F080FE-F248-11E8-B48F-1D18A9856A87"},{"id":"2A95E7B0-F248-11E8-B48F-1D18A9856A87","last_name":"Wachner","first_name":"Stephanie","full_name":"Wachner, Stephanie"},{"full_name":"György, Attila","last_name":"György","first_name":"Attila","orcid":"0000-0002-1819-198X","id":"3BCEDBE0-F248-11E8-B48F-1D18A9856A87"},{"id":"49D32318-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0001-6981-6938","first_name":"Shamsi","last_name":"Emtenani","full_name":"Emtenani, Shamsi"},{"full_name":"Gridchyn, Igor","last_name":"Gridchyn","first_name":"Igor","orcid":"0000-0002-1807-1929","id":"4B60654C-F248-11E8-B48F-1D18A9856A87"},{"full_name":"Akhmanova, Maria","id":"3425EC26-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0003-1522-3162","first_name":"Maria","last_name":"Akhmanova"},{"first_name":"M","last_name":"Linder","full_name":"Linder, M"},{"orcid":"0000-0001-9588-1389","id":"3047D808-F248-11E8-B48F-1D18A9856A87","last_name":"Roblek","first_name":"Marko","full_name":"Roblek, Marko"},{"first_name":"M","last_name":"Sibilia","full_name":"Sibilia, M"},{"orcid":"0000-0001-8323-8353","id":"3D224B9E-F248-11E8-B48F-1D18A9856A87","last_name":"Siekhaus","first_name":"Daria E","full_name":"Siekhaus, Daria E"}],"volume":20,"date_updated":"2024-03-28T23:30:29Z","date_created":"2022-01-12T10:18:17Z","pmid":1,"year":"2022","acknowledgement":"We thank the following for their contributions: Plasmids were supplied by the Drosophila Genomics Resource Center (NIH 2P40OD010949-10A1); fly stocks were provided by K. Brueckner, B. Stramer, M. Uhlirova, O. Schuldiner, the Bloomington Drosophila Stock Center (NIH P40OD018537) and the Vienna Drosophila Resource Center, FlyBase for essential genomic information, and the BDGP in situ database for data. For antibodies, we thank the Developmental Studies Hybridoma Bank, which was created by the Eunice Kennedy Shriver National Institute of Child Health and Human Development of the NIH and is maintained at the University of Iowa, as well as J. Zeitlinger for her generous gift of Dfos antibody. We thank the Vienna BioCenter Core Facilities for RNA sequencing and analysis and the Life Scientific Service Units at IST Austria for technical support and assistance with microscopy and FACS analysis. We thank C. P. Heisenberg, P. Martin, M. Sixt, and Siekhaus group members for discussions and T. Hurd, A. Ratheesh, and P. Rangan for comments on the manuscript.","publisher":"Public Library of Science","department":[{"_id":"DaSi"},{"_id":"JoCs"}],"publication_status":"published"},{"month":"11","publication_identifier":{"eissn":["2234-943X"]},"isi":1,"quality_controlled":"1","external_id":{"pmid":["34868988"],"isi":["000726603400001"]},"tmp":{"name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","short":"CC BY (4.0)","image":"/images/cc_by.png"},"oa":1,"language":[{"iso":"eng"}],"doi":"10.3389/fonc.2021.765151","article_number":"765151","file_date_updated":"2021-12-13T13:32:37Z","publication_status":"published","publisher":"Frontiers","department":[{"_id":"DaSi"}],"year":"2021","acknowledgement":"The authors acknowledge the assistance of the Laboratory Animal Services Center (LASC) – UZH, Center for Microscopy and Image Analysis, and the Flow Cytometry Center of the University of Zurich.","pmid":1,"date_created":"2021-12-12T23:01:27Z","date_updated":"2023-08-17T06:20:32Z","volume":11,"author":[{"first_name":"Cristina","last_name":"Stefanescu","full_name":"Stefanescu, Cristina"},{"full_name":"Van Gogh, Merel","last_name":"Van Gogh","first_name":"Merel"},{"full_name":"Roblek, Marko","first_name":"Marko","last_name":"Roblek","id":"3047D808-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0001-9588-1389"},{"first_name":"Mathias","last_name":"Heikenwalder","full_name":"Heikenwalder, Mathias"},{"first_name":"Lubor","last_name":"Borsig","full_name":"Borsig, Lubor"}],"scopus_import":"1","day":"18","has_accepted_license":"1","article_processing_charge":"No","article_type":"original","publication":"Frontiers in Oncology","citation":{"chicago":"Stefanescu, Cristina, Merel Van Gogh, Marko Roblek, Mathias Heikenwalder, and Lubor Borsig. “TGFβ Signaling in Myeloid Cells Promotes Lung and Liver Metastasis through Different Mechanisms.” Frontiers in Oncology. Frontiers, 2021. https://doi.org/10.3389/fonc.2021.765151.","short":"C. Stefanescu, M. Van Gogh, M. Roblek, M. Heikenwalder, L. Borsig, Frontiers in Oncology 11 (2021).","mla":"Stefanescu, Cristina, et al. “TGFβ Signaling in Myeloid Cells Promotes Lung and Liver Metastasis through Different Mechanisms.” Frontiers in Oncology, vol. 11, 765151, Frontiers, 2021, doi:10.3389/fonc.2021.765151.","ieee":"C. Stefanescu, M. Van Gogh, M. Roblek, M. Heikenwalder, and L. Borsig, “TGFβ signaling in myeloid cells promotes lung and liver metastasis through different mechanisms,” Frontiers in Oncology, vol. 11. Frontiers, 2021.","apa":"Stefanescu, C., Van Gogh, M., Roblek, M., Heikenwalder, M., & Borsig, L. (2021). TGFβ signaling in myeloid cells promotes lung and liver metastasis through different mechanisms. Frontiers in Oncology. Frontiers. https://doi.org/10.3389/fonc.2021.765151","ista":"Stefanescu C, Van Gogh M, Roblek M, Heikenwalder M, Borsig L. 2021. TGFβ signaling in myeloid cells promotes lung and liver metastasis through different mechanisms. Frontiers in Oncology. 11, 765151.","ama":"Stefanescu C, Van Gogh M, Roblek M, Heikenwalder M, Borsig L. TGFβ signaling in myeloid cells promotes lung and liver metastasis through different mechanisms. Frontiers in Oncology. 2021;11. doi:10.3389/fonc.2021.765151"},"date_published":"2021-11-18T00:00:00Z","type":"journal_article","abstract":[{"lang":"eng","text":"TGFβ overexpression is commonly detected in cancer patients and correlates with poor prognosis and metastasis. Cancer progression is often associated with an enhanced recruitment of myeloid-derived cells to the tumor microenvironment. Here we show that functional TGFβ-signaling in myeloid cells is required for metastasis to the lungs and the liver. Myeloid-specific deletion of Tgfbr2 resulted in reduced spontaneous lung metastasis, which was associated with a reduction of proinflammatory cytokines in the metastatic microenvironment. Notably, CD8+ T cell depletion in myeloid-specific Tgfbr2-deficient mice rescued lung metastasis. Myeloid-specific Tgfbr2-deficiency resulted in reduced liver metastasis with an almost complete absence of myeloid cells within metastatic foci. On contrary, an accumulation of Tgfβ-responsive myeloid cells was associated with an increased recruitment of monocytes and granulocytes and higher proinflammatory cytokine levels in control mice. Monocytic cells isolated from metastatic livers of Tgfbr2-deficient mice showed increased polarization towards the M1 phenotype, Tnfα and Il-1β expression, reduced levels of M2 markers and reduced production of chemokines responsible for myeloid-cell recruitment. No significant differences in Tgfβ levels were observed at metastatic sites of any model. These data demonstrate that Tgfβ signaling in monocytic myeloid cells suppresses CD8+ T cell activity during lung metastasis, while these cells actively contribute to tumor growth during liver metastasis. Thus, myeloid cells modulate metastasis through different mechanisms in a tissue-specific manner."}],"title":"TGFβ signaling in myeloid cells promotes lung and liver metastasis through different mechanisms","ddc":["610"],"status":"public","intvolume":" 11","user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","_id":"10536","file":[{"content_type":"application/pdf","file_size":9245199,"creator":"alisjak","access_level":"open_access","file_name":"2021_Frontiers_Stefanescu.pdf","checksum":"56cbac80e6891ce750511a30161b7792","success":1,"date_created":"2021-12-13T13:32:37Z","date_updated":"2021-12-13T13:32:37Z","relation":"main_file","file_id":"10539"}],"oa_version":"Published Version"},{"main_file_link":[{"open_access":"1","url":"https://doi.org/10.1158/1541-7786.MCR-18-0530"}],"external_id":{"pmid":["30552233"],"isi":["000460099800012"]},"oa":1,"quality_controlled":"1","isi":1,"doi":"10.1158/1541-7786.MCR-18-0530","language":[{"iso":"eng"}],"month":"03","publication_identifier":{"eissn":["15573125"],"issn":["15417786"]},"year":"2019","pmid":1,"publication_status":"published","publisher":"AACR","department":[{"_id":"DaSi"}],"author":[{"full_name":"Roblek, Marko","first_name":"Marko","last_name":"Roblek","id":"3047D808-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0001-9588-1389"},{"last_name":"Protsyuk","first_name":"Darya","full_name":"Protsyuk, Darya"},{"first_name":"Paul F.","last_name":"Becker","full_name":"Becker, Paul F."},{"full_name":"Stefanescu, Cristina","first_name":"Cristina","last_name":"Stefanescu"},{"full_name":"Gorzelanny, Christian","last_name":"Gorzelanny","first_name":"Christian"},{"full_name":"Glaus Garzon, Jesus F.","last_name":"Glaus Garzon","first_name":"Jesus F."},{"first_name":"Lucia","last_name":"Knopfova","full_name":"Knopfova, Lucia"},{"full_name":"Heikenwalder, Mathias","last_name":"Heikenwalder","first_name":"Mathias"},{"first_name":"Bruno","last_name":"Luckow","full_name":"Luckow, Bruno"},{"last_name":"Schneider","first_name":"Stefan W.","full_name":"Schneider, Stefan W."},{"last_name":"Borsig","first_name":"Lubor","full_name":"Borsig, Lubor"}],"date_created":"2019-03-31T21:59:12Z","date_updated":"2023-08-25T08:57:01Z","volume":17,"publication":"Molecular Cancer Research","citation":{"chicago":"Roblek, Marko, Darya Protsyuk, Paul F. Becker, Cristina Stefanescu, Christian Gorzelanny, Jesus F. Glaus Garzon, Lucia Knopfova, et al. “CCL2 Is a Vascular Permeability Factor Inducing CCR2-Dependent Endothelial Retraction during Lung Metastasis.” Molecular Cancer Research. AACR, 2019. https://doi.org/10.1158/1541-7786.MCR-18-0530.","short":"M. Roblek, D. Protsyuk, P.F. Becker, C. Stefanescu, C. Gorzelanny, J.F. Glaus Garzon, L. Knopfova, M. Heikenwalder, B. Luckow, S.W. Schneider, L. Borsig, Molecular Cancer Research 17 (2019) 783–793.","mla":"Roblek, Marko, et al. “CCL2 Is a Vascular Permeability Factor Inducing CCR2-Dependent Endothelial Retraction during Lung Metastasis.” Molecular Cancer Research, vol. 17, no. 3, AACR, 2019, pp. 783–93, doi:10.1158/1541-7786.MCR-18-0530.","apa":"Roblek, M., Protsyuk, D., Becker, P. F., Stefanescu, C., Gorzelanny, C., Glaus Garzon, J. F., … Borsig, L. (2019). CCL2 is a vascular permeability factor inducing CCR2-dependent endothelial retraction during lung metastasis. Molecular Cancer Research. AACR. https://doi.org/10.1158/1541-7786.MCR-18-0530","ieee":"M. Roblek et al., “CCL2 is a vascular permeability factor inducing CCR2-dependent endothelial retraction during lung metastasis,” Molecular Cancer Research, vol. 17, no. 3. AACR, pp. 783–793, 2019.","ista":"Roblek M, Protsyuk D, Becker PF, Stefanescu C, Gorzelanny C, Glaus Garzon JF, Knopfova L, Heikenwalder M, Luckow B, Schneider SW, Borsig L. 2019. CCL2 is a vascular permeability factor inducing CCR2-dependent endothelial retraction during lung metastasis. Molecular Cancer Research. 17(3), 783–793.","ama":"Roblek M, Protsyuk D, Becker PF, et al. CCL2 is a vascular permeability factor inducing CCR2-dependent endothelial retraction during lung metastasis. Molecular Cancer Research. 2019;17(3):783-793. doi:10.1158/1541-7786.MCR-18-0530"},"article_type":"original","page":"783-793","date_published":"2019-03-01T00:00:00Z","scopus_import":"1","day":"01","article_processing_charge":"No","_id":"6190","user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","title":"CCL2 is a vascular permeability factor inducing CCR2-dependent endothelial retraction during lung metastasis","status":"public","intvolume":" 17","oa_version":"Published Version","type":"journal_article","abstract":[{"lang":"eng","text":"Increased levels of the chemokine CCL2 in cancer patients are associated with poor prognosis. Experimental evidence suggests that CCL2 correlates with inflammatory monocyte recruitment and induction of vascular activation, but the functionality remains open. Here, we show that endothelial Ccr2 facilitates pulmonary metastasis using an endothelial-specific Ccr2-deficient mouse model (Ccr2ecKO). Similar levels of circulating monocytes and equal leukocyte recruitment to metastatic lesions of Ccr2ecKO and Ccr2fl/fl littermates were observed. The absence of endothelial Ccr2 strongly reduced pulmonary metastasis, while the primary tumor growth was unaffected. Despite a comparable cytokine milieu in Ccr2ecKO and Ccr2fl/fl littermates the absence of vascular permeability induction was observed only in Ccr2ecKO mice. CCL2 stimulation of pulmonary endothelial cells resulted in increased phosphorylation of MLC2, endothelial cell retraction, and vascular leakiness that was blocked by an addition of a CCR2 inhibitor. These data demonstrate that endothelial CCR2 expression is required for tumor cell extravasation and pulmonary metastasis.\r\n\r\nImplications: The findings provide mechanistic insight into how CCL2–CCR2 signaling in endothelial cells promotes their activation through myosin light chain phosphorylation, resulting in endothelial retraction and enhanced tumor cell migration and metastasis."}],"issue":"3"},{"type":"journal_article","abstract":[{"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.","lang":"eng"}],"title":"A conserved major facilitator superfamily member orchestrates a subset of O-glycosylation to aid macrophage tissue invasion","status":"public","ddc":["570"],"intvolume":" 8","_id":"6187","user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","oa_version":"Published Version","file":[{"relation":"main_file","file_id":"6188","checksum":"cc0d1a512559d52e7e7cb0e9b9854b40","date_updated":"2020-07-14T12:47:23Z","date_created":"2019-03-28T14:00:41Z","access_level":"open_access","file_name":"2019_eLife_Valoskova.pdf","content_type":"application/pdf","file_size":4496017,"creator":"dernst"}],"scopus_import":"1","day":"26","article_processing_charge":"No","has_accepted_license":"1","publication":"eLife","citation":{"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","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.","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.","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","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).","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."},"date_published":"2019-03-26T00:00:00Z","article_number":"e41801","file_date_updated":"2020-07-14T12:47:23Z","ec_funded":1,"publication_status":"published","department":[{"_id":"DaSi"}],"publisher":"eLife Sciences Publications","year":"2019","date_updated":"2024-03-28T23:30:30Z","date_created":"2019-03-28T13:37:45Z","volume":8,"author":[{"id":"46F146FC-F248-11E8-B48F-1D18A9856A87","last_name":"Valosková","first_name":"Katarina","full_name":"Valosková, Katarina"},{"full_name":"Biebl, Julia","id":"3CCBB46E-F248-11E8-B48F-1D18A9856A87","last_name":"Biebl","first_name":"Julia"},{"last_name":"Roblek","first_name":"Marko","orcid":"0000-0001-9588-1389","id":"3047D808-F248-11E8-B48F-1D18A9856A87","full_name":"Roblek, Marko"},{"last_name":"Emtenani","first_name":"Shamsi","orcid":"0000-0001-6981-6938","id":"49D32318-F248-11E8-B48F-1D18A9856A87","full_name":"Emtenani, Shamsi"},{"full_name":"György, Attila","first_name":"Attila","last_name":"György","id":"3BCEDBE0-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-1819-198X"},{"last_name":"Misova","first_name":"Michaela","orcid":"0000-0003-2427-6856","id":"495A3C32-F248-11E8-B48F-1D18A9856A87","full_name":"Misova, Michaela"},{"full_name":"Ratheesh, Aparna","last_name":"Ratheesh","first_name":"Aparna","orcid":"0000-0001-7190-0776","id":"2F064CFE-F248-11E8-B48F-1D18A9856A87"},{"full_name":"Rodrigues, Patricia","id":"2CE4065A-F248-11E8-B48F-1D18A9856A87","last_name":"Rodrigues","first_name":"Patricia"},{"full_name":"Shkarina, Katerina","first_name":"Katerina","last_name":"Shkarina"},{"full_name":"Larsen, Ida Signe Bohse","last_name":"Larsen","first_name":"Ida Signe Bohse"},{"first_name":"Sergey Y","last_name":"Vakhrushev","full_name":"Vakhrushev, Sergey Y"},{"full_name":"Clausen, Henrik","first_name":"Henrik","last_name":"Clausen"},{"full_name":"Siekhaus, Daria E","first_name":"Daria E","last_name":"Siekhaus","id":"3D224B9E-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0001-8323-8353"}],"related_material":{"record":[{"relation":"dissertation_contains","id":"6530"},{"status":"public","relation":"dissertation_contains","id":"8983"},{"id":"6546","relation":"dissertation_contains","status":"public"}],"link":[{"relation":"press_release","description":"News on IST Homepage","url":"https://ist.ac.at/en/news/new-gene-potentially-involved-in-metastasis-identified/"}]},"month":"03","publication_identifier":{"issn":["2050-084X"]},"quality_controlled":"1","isi":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"},{"_id":"253B6E48-B435-11E9-9278-68D0E5697425","grant_number":"P29638","name":"The role of Drosophila TNF alpha in immune cell invasion","call_identifier":"FWF"},{"grant_number":"334077","_id":"2536F660-B435-11E9-9278-68D0E5697425","call_identifier":"FP7","name":"Investigating the role of transporters in invasive migration through junctions"},{"call_identifier":"FP7","name":"Breaking barriers: Investigating the junctional and mechanobiological changes underlying the ability of Drosophila immune cells to invade an epithelium","_id":"25388084-B435-11E9-9278-68D0E5697425","grant_number":"329540"},{"_id":"2564DBCA-B435-11E9-9278-68D0E5697425","grant_number":"665385","name":"International IST Doctoral Program","call_identifier":"H2020"}],"oa":1,"tmp":{"name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","short":"CC BY (4.0)","image":"/images/cc_by.png"},"external_id":{"isi":["000462530200001"]},"acknowledged_ssus":[{"_id":"LifeSc"}],"language":[{"iso":"eng"}],"doi":"10.7554/elife.41801"},{"doi":"10.1534/g3.117.300452","language":[{"iso":"eng"}],"acknowledged_ssus":[{"_id":"LifeSc"}],"tmp":{"name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","short":"CC BY (4.0)","image":"/images/cc_by.png"},"oa":1,"external_id":{"isi":["000426693300011"]},"project":[{"call_identifier":"FWF","name":"Drosophila TNFa´s Funktion in Immunzellen","_id":"253B6E48-B435-11E9-9278-68D0E5697425","grant_number":"P29638"},{"grant_number":"P29638","_id":"253B6E48-B435-11E9-9278-68D0E5697425","name":"The role of Drosophila TNF alpha in immune cell invasion","call_identifier":"FWF"},{"grant_number":"LSC16-021 ","_id":"2637E9C0-B435-11E9-9278-68D0E5697425","name":"Investigating the role of the novel major superfamily facilitator transporter family member MFSD1 in metastasis"},{"call_identifier":"FP7","name":"Investigating the role of transporters in invasive migration through junctions","grant_number":"334077","_id":"2536F660-B435-11E9-9278-68D0E5697425"}],"quality_controlled":"1","isi":1,"month":"03","related_material":{"record":[{"id":"6530","relation":"research_paper"},{"id":"6543","relation":"research_paper"},{"status":"public","relation":"dissertation_contains","id":"11193"},{"id":"6546","status":"public","relation":"dissertation_contains"}]},"author":[{"full_name":"György, Attila","orcid":"0000-0002-1819-198X","id":"3BCEDBE0-F248-11E8-B48F-1D18A9856A87","last_name":"György","first_name":"Attila"},{"orcid":"0000-0001-9588-1389","id":"3047D808-F248-11E8-B48F-1D18A9856A87","last_name":"Roblek","first_name":"Marko","full_name":"Roblek, Marko"},{"full_name":"Ratheesh, Aparna","last_name":"Ratheesh","first_name":"Aparna","orcid":"0000-0001-7190-0776","id":"2F064CFE-F248-11E8-B48F-1D18A9856A87"},{"full_name":"Valosková, Katarina","last_name":"Valosková","first_name":"Katarina","id":"46F146FC-F248-11E8-B48F-1D18A9856A87"},{"full_name":"Belyaeva, Vera","first_name":"Vera","last_name":"Belyaeva","id":"47F080FE-F248-11E8-B48F-1D18A9856A87"},{"full_name":"Wachner, Stephanie","id":"2A95E7B0-F248-11E8-B48F-1D18A9856A87","first_name":"Stephanie","last_name":"Wachner"},{"last_name":"Matsubayashi","first_name":"Yutaka","full_name":"Matsubayashi, Yutaka"},{"full_name":"Sanchez Sanchez, Besaiz","last_name":"Sanchez Sanchez","first_name":"Besaiz"},{"first_name":"Brian","last_name":"Stramer","full_name":"Stramer, Brian"},{"orcid":"0000-0001-8323-8353","id":"3D224B9E-F248-11E8-B48F-1D18A9856A87","last_name":"Siekhaus","first_name":"Daria E","full_name":"Siekhaus, Daria E"}],"volume":8,"date_updated":"2024-03-28T23:30:30Z","date_created":"2018-12-11T11:47:05Z","acknowledgement":" A. Ratheesh also by Marie Curie IIF GA-2012-32950BB:DICJI, Marko Roblek by the provincial government of Lower Austria, K. Valoskova and S. Wachner by DOC Fellowships from the Austrian Academy of Sciences, ","year":"2018","department":[{"_id":"DaSi"}],"publisher":"Genetics Society of America","publication_status":"published","publist_id":"7271","ec_funded":1,"file_date_updated":"2020-07-14T12:46:56Z","date_published":"2018-03-01T00:00:00Z","citation":{"chicago":"György, Attila, Marko Roblek, Aparna Ratheesh, Katarina Valosková, Vera Belyaeva, Stephanie Wachner, Yutaka Matsubayashi, Besaiz Sanchez Sanchez, Brian Stramer, and Daria E Siekhaus. “Tools Allowing Independent Visualization and Genetic Manipulation of Drosophila Melanogaster Macrophages and Surrounding Tissues.” G3: Genes, Genomes, Genetics. Genetics Society of America, 2018. https://doi.org/10.1534/g3.117.300452.","mla":"György, Attila, et al. “Tools Allowing Independent Visualization and Genetic Manipulation of Drosophila Melanogaster Macrophages and Surrounding Tissues.” G3: Genes, Genomes, Genetics, vol. 8, no. 3, Genetics Society of America, 2018, pp. 845–57, doi:10.1534/g3.117.300452.","short":"A. György, M. Roblek, A. Ratheesh, K. Valosková, V. Belyaeva, S. Wachner, Y. Matsubayashi, B. Sanchez Sanchez, B. Stramer, D.E. Siekhaus, G3: Genes, Genomes, Genetics 8 (2018) 845–857.","ista":"György A, Roblek M, Ratheesh A, Valosková K, Belyaeva V, Wachner S, Matsubayashi Y, Sanchez Sanchez B, Stramer B, Siekhaus DE. 2018. Tools allowing independent visualization and genetic manipulation of Drosophila melanogaster macrophages and surrounding tissues. G3: Genes, Genomes, Genetics. 8(3), 845–857.","ieee":"A. György et al., “Tools allowing independent visualization and genetic manipulation of Drosophila melanogaster macrophages and surrounding tissues,” G3: Genes, Genomes, Genetics, vol. 8, no. 3. Genetics Society of America, pp. 845–857, 2018.","apa":"György, A., Roblek, M., Ratheesh, A., Valosková, K., Belyaeva, V., Wachner, S., … Siekhaus, D. E. (2018). Tools allowing independent visualization and genetic manipulation of Drosophila melanogaster macrophages and surrounding tissues. G3: Genes, Genomes, Genetics. Genetics Society of America. https://doi.org/10.1534/g3.117.300452","ama":"György A, Roblek M, Ratheesh A, et al. Tools allowing independent visualization and genetic manipulation of Drosophila melanogaster macrophages and surrounding tissues. G3: Genes, Genomes, Genetics. 2018;8(3):845-857. doi:10.1534/g3.117.300452"},"publication":"G3: Genes, Genomes, Genetics","page":"845 - 857","has_accepted_license":"1","article_processing_charge":"No","day":"01","scopus_import":"1","pubrep_id":"990","file":[{"checksum":"7d9d28b915159078a4ca7add568010e8","date_updated":"2020-07-14T12:46:56Z","date_created":"2018-12-12T10:11:48Z","relation":"main_file","file_id":"4905","content_type":"application/pdf","file_size":2251222,"creator":"system","access_level":"open_access","file_name":"IST-2018-990-v1+1_2018_Gyoergy_Tools_allowing.pdf"}],"oa_version":"Published Version","_id":"544","user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","intvolume":" 8","ddc":["570"],"title":"Tools allowing independent visualization and genetic manipulation of Drosophila melanogaster macrophages and surrounding tissues","status":"public","issue":"3","abstract":[{"lang":"eng","text":"Drosophila melanogaster plasmatocytes, the phagocytic cells among hemocytes, are essential for immune responses, but also play key roles from early development to death through their interactions with other cell types. They regulate homeostasis and signaling during development, stem cell proliferation, metabolism, cancer, wound responses and aging, displaying intriguing molecular and functional conservation with vertebrate macrophages. Given the relative ease of genetics in Drosophila compared to vertebrates, tools permitting visualization and genetic manipulation of plasmatocytes and surrounding tissues independently at all stages would greatly aid in fully understanding these processes, but are lacking. Here we describe a comprehensive set of transgenic lines that allow this. These include extremely brightly fluorescing mCherry-based lines that allow GAL4-independent visualization of plasmatocyte nuclei, cytoplasm or actin cytoskeleton from embryonic Stage 8 through adulthood in both live and fixed samples even as heterozygotes, greatly facilitating screening. These lines allow live visualization and tracking of embryonic plasmatocytes, as well as larval plasmatocytes residing at the body wall or flowing with the surrounding hemolymph. With confocal imaging, interactions of plasmatocytes and inner tissues can be seen in live or fixed embryos, larvae and adults. They permit efficient GAL4-independent FACS analysis/sorting of plasmatocytes throughout life. To facilitate genetic analysis of reciprocal signaling, we have also made a plasmatocyte-expressing QF2 line that in combination with extant GAL4 drivers allows independent genetic manipulation of both plasmatocytes and surrounding tissues, and a GAL80 line that blocks GAL4 drivers from affecting plasmatocytes, both of which function from the early embryo to the adult."}],"type":"journal_article"}]