[{"article_number":"jcs261448","author":[{"full_name":"Nagano, Makoto","first_name":"Makoto","last_name":"Nagano"},{"last_name":"Aoshima","full_name":"Aoshima, Kaito","first_name":"Kaito"},{"full_name":"Shimamura, Hiroki","first_name":"Hiroki","last_name":"Shimamura"},{"first_name":"Daria E","full_name":"Siekhaus, Daria E","orcid":"0000-0001-8323-8353","id":"3D224B9E-F248-11E8-B48F-1D18A9856A87","last_name":"Siekhaus"},{"last_name":"Toshima","first_name":"Junko Y.","full_name":"Toshima, Junko Y."},{"first_name":"Jiro","full_name":"Toshima, Jiro","last_name":"Toshima"}],"volume":136,"pmid":1,"department":[{"_id":"DaSi"}],"status":"public","day":"01","year":"2023","language":[{"iso":"eng"}],"article_type":"original","citation":{"chicago":"Nagano, Makoto, Kaito Aoshima, Hiroki Shimamura, Daria E Siekhaus, Junko Y. Toshima, and Jiro Toshima. “Distinct Role of TGN-Resident Clathrin Adaptors for Vps21p Activation in the TGN-Endosome Trafficking Pathway.” Journal of Cell Science. The Company of Biologists, 2023. https://doi.org/10.1242/jcs.261448.","short":"M. Nagano, K. Aoshima, H. Shimamura, D.E. Siekhaus, J.Y. Toshima, J. Toshima, Journal of Cell Science 136 (2023).","ama":"Nagano M, Aoshima K, Shimamura H, Siekhaus DE, Toshima JY, Toshima J. Distinct role of TGN-resident clathrin adaptors for Vps21p activation in the TGN-endosome trafficking pathway. Journal of Cell Science. 2023;136(17). doi:10.1242/jcs.261448","apa":"Nagano, M., Aoshima, K., Shimamura, H., Siekhaus, D. E., Toshima, J. Y., & Toshima, J. (2023). Distinct role of TGN-resident clathrin adaptors for Vps21p activation in the TGN-endosome trafficking pathway. Journal of Cell Science. The Company of Biologists. https://doi.org/10.1242/jcs.261448","ista":"Nagano M, Aoshima K, Shimamura H, Siekhaus DE, Toshima JY, Toshima J. 2023. Distinct role of TGN-resident clathrin adaptors for Vps21p activation in the TGN-endosome trafficking pathway. Journal of Cell Science. 136(17), jcs261448.","mla":"Nagano, Makoto, et al. “Distinct Role of TGN-Resident Clathrin Adaptors for Vps21p Activation in the TGN-Endosome Trafficking Pathway.” Journal of Cell Science, vol. 136, no. 17, jcs261448, The Company of Biologists, 2023, doi:10.1242/jcs.261448.","ieee":"M. Nagano, K. Aoshima, H. Shimamura, D. E. Siekhaus, J. Y. Toshima, and J. Toshima, “Distinct role of TGN-resident clathrin adaptors for Vps21p activation in the TGN-endosome trafficking pathway,” Journal of Cell Science, vol. 136, no. 17. The Company of Biologists, 2023."},"publication":"Journal of Cell Science","date_published":"2023-09-01T00:00:00Z","scopus_import":"1","oa_version":"Preprint","month":"09","intvolume":" 136","publication_status":"published","type":"journal_article","doi":"10.1242/jcs.261448","article_processing_charge":"No","title":"Distinct role of TGN-resident clathrin adaptors for Vps21p activation in the TGN-endosome trafficking pathway","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","_id":"14316","quality_controlled":"1","main_file_link":[{"open_access":"1","url":"https://doi.org/10.1101/2023.03.27.534325"}],"date_updated":"2023-09-20T09:14:15Z","external_id":{"pmid":["37539494"]},"date_created":"2023-09-10T22:01:12Z","publisher":"The Company of Biologists","issue":"17","oa":1,"abstract":[{"lang":"eng","text":"Clathrin-mediated vesicle trafficking plays central roles in post-Golgi transport. In yeast (Saccharomyces cerevisiae), the AP-1 complex and GGA adaptors are predicted to generate distinct transport vesicles at the trans-Golgi network (TGN), and the epsin-related proteins Ent3p and Ent5p (collectively Ent3p/5p) act as accessories for these adaptors. Recently, we showed that vesicle transport from the TGN is crucial for yeast Rab5 (Vps21p)-mediated endosome formation, and that Ent3p/5p are crucial for this process, whereas AP-1 and GGA adaptors are dispensable. However, these observations were incompatible with previous studies showing that these adaptors are required for Ent3p/5p recruitment to the TGN, and thus the overall mechanism responsible for regulation of Vps21p activity remains ambiguous. Here, we investigated the functional relationships between clathrin adaptors in post-Golgi-mediated Vps21p activation. We show that AP-1 disruption in the ent3Δ5Δ mutant impaired transport of the Vps21p guanine nucleotide exchange factor Vps9p transport to the Vps21p compartment and severely reduced Vps21p activity. Additionally, GGA adaptors, the phosphatidylinositol-4-kinase Pik1p and Rab11 GTPases Ypt31p and Ypt32p were found to have partially overlapping functions for recruitment of AP-1 and Ent3p/5p to the TGN. These findings suggest a distinct role of clathrin adaptors for Vps21p activation in the TGN–endosome trafficking pathway."}],"publication_identifier":{"eissn":["1477-9137"],"issn":["0021-9533"]}},{"publication":"eLife","date_published":"2023-07-21T00:00:00Z","citation":{"chicago":"Toshima, Junko Y., Ayana Tsukahara, Makoto Nagano, Takuro Tojima, Daria E Siekhaus, Akihiko Nakano, and Jiro Toshima. “The Yeast Endocytic Early/Sorting Compartment Exists as an Independent Sub-Compartment within the Trans-Golgi Network.” ELife. eLife Sciences Publications, 2023. https://doi.org/10.7554/eLife.84850.","short":"J.Y. Toshima, A. Tsukahara, M. Nagano, T. Tojima, D.E. Siekhaus, A. Nakano, J. Toshima, ELife 12 (2023).","apa":"Toshima, J. Y., Tsukahara, A., Nagano, M., Tojima, T., Siekhaus, D. E., Nakano, A., & Toshima, J. (2023). The yeast endocytic early/sorting compartment exists as an independent sub-compartment within the trans-Golgi network. ELife. eLife Sciences Publications. https://doi.org/10.7554/eLife.84850","ama":"Toshima JY, Tsukahara A, Nagano M, et al. The yeast endocytic early/sorting compartment exists as an independent sub-compartment within the trans-Golgi network. eLife. 2023;12. doi:10.7554/eLife.84850","ieee":"J. Y. Toshima et al., “The yeast endocytic early/sorting compartment exists as an independent sub-compartment within the trans-Golgi network,” eLife, vol. 12. eLife Sciences Publications, 2023.","mla":"Toshima, Junko Y., et al. “The Yeast Endocytic Early/Sorting Compartment Exists as an Independent Sub-Compartment within the Trans-Golgi Network.” ELife, vol. 12, e84850, eLife Sciences Publications, 2023, doi:10.7554/eLife.84850.","ista":"Toshima JY, Tsukahara A, Nagano M, Tojima T, Siekhaus DE, Nakano A, Toshima J. 2023. The yeast endocytic early/sorting compartment exists as an independent sub-compartment within the trans-Golgi network. eLife. 12, e84850."},"intvolume":" 12","month":"07","file_date_updated":"2023-07-31T07:43:00Z","oa_version":"Published Version","scopus_import":"1","type":"journal_article","doi":"10.7554/eLife.84850","article_processing_charge":"Yes","tmp":{"image":"/images/cc_by.png","legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","short":"CC BY (4.0)","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)"},"publication_status":"published","volume":12,"pmid":1,"department":[{"_id":"DaSi"}],"article_number":"e84850","author":[{"first_name":"Junko Y.","full_name":"Toshima, Junko Y.","last_name":"Toshima"},{"last_name":"Tsukahara","full_name":"Tsukahara, Ayana","first_name":"Ayana"},{"first_name":"Makoto","full_name":"Nagano, Makoto","last_name":"Nagano"},{"first_name":"Takuro","full_name":"Tojima, Takuro","last_name":"Tojima"},{"id":"3D224B9E-F248-11E8-B48F-1D18A9856A87","last_name":"Siekhaus","orcid":"0000-0001-8323-8353","first_name":"Daria E","full_name":"Siekhaus, Daria E"},{"last_name":"Nakano","full_name":"Nakano, Akihiko","first_name":"Akihiko"},{"last_name":"Toshima","full_name":"Toshima, Jiro","first_name":"Jiro"}],"article_type":"original","has_accepted_license":"1","year":"2023","day":"21","language":[{"iso":"eng"}],"status":"public","publisher":"eLife Sciences Publications","date_created":"2023-07-30T22:01:02Z","acknowledgement":"This work was supported by JSPS KAKENHI grant #18K062291, and the Takeda Science Foundation to JYT., as well as JSPS KAKENHI grant #19K065710, the Takeda Science Foundation, and Life Science Foundation of Japan to JT.","external_id":{"pmid":["37477116"],"isi":["001035372800001"]},"date_updated":"2023-12-13T11:37:36Z","ddc":["570"],"abstract":[{"text":"Although budding yeast has been extensively used as a model organism for studying organelle functions and intracellular vesicle trafficking, whether it possesses an independent endocytic early/sorting compartment that sorts endocytic cargos to the endo-lysosomal pathway or the recycling pathway has long been unclear. The structure and properties of the endocytic early/sorting compartment differ significantly between organisms; in plant cells, the trans-Golgi network (TGN) serves this role, whereas in mammalian cells a separate intracellular structure performs this function. The yeast syntaxin homolog Tlg2p, widely localizing to the TGN and endosomal compartments, is presumed to act as a Q-SNARE for endocytic vesicles, but which compartment is the direct target for endocytic vesicles remained unanswered. Here we demonstrate by high-speed and high-resolution 4D imaging of fluorescently labeled endocytic cargos that the Tlg2p-residing compartment within the TGN functions as the early/sorting compartment. After arriving here, endocytic cargos are recycled to the plasma membrane or transported to the yeast Rab5-residing endosomal compartment through the pathway requiring the clathrin adaptors GGAs. Interestingly, Gga2p predominantly localizes at the Tlg2p-residing compartment, and the deletion of GGAs has little effect on another TGN region where Sec7p is present but suppresses dynamics of the Tlg2-residing early/sorting compartment, indicating that the Tlg2p- and Sec7p-residing regions are discrete entities in the mutant. Thus, the Tlg2p-residing region seems to serve as an early/sorting compartment and function independently of the Sec7p-residing region within the TGN.","lang":"eng"}],"publication_identifier":{"eissn":["2050-084X"]},"oa":1,"file":[{"file_size":11980913,"date_created":"2023-07-31T07:43:00Z","checksum":"2af111a00cf5e3a956f7f0fd13199b15","relation":"main_file","date_updated":"2023-07-31T07:43:00Z","file_id":"13324","creator":"dernst","file_name":"2023_eLife_Toshima.pdf","access_level":"open_access","success":1,"content_type":"application/pdf"}],"isi":1,"title":"The yeast endocytic early/sorting compartment exists as an independent sub-compartment within the trans-Golgi network","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","quality_controlled":"1","_id":"13316"},{"date_updated":"2023-08-02T14:05:44Z","external_id":{"isi":["000760618800001"]},"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).","date_created":"2022-02-01T10:33:50Z","publisher":"Frontiers","oa":1,"project":[{"name":"Investigating the role of the novel major superfamily facilitator transporter family member MFSD1 in metastasis","grant_number":"LSC16-021 ","_id":"2637E9C0-B435-11E9-9278-68D0E5697425"}],"related_material":{"link":[{"relation":"confirmation","description":"News on IST Homepage","url":"https://ist.ac.at/en/news/suppressing-the-spread-of-tumors/"}]},"publication_identifier":{"issn":["2234-943X"]},"ddc":["570"],"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."}],"user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","title":"The solute carrier MFSD1 decreases β1 integrin’s activation status and thus tumor metastasis","isi":1,"file":[{"access_level":"open_access","success":1,"content_type":"application/pdf","file_name":"2022_FrontiersOncol_Roblek.pdf","date_updated":"2022-02-08T13:26:40Z","relation":"main_file","creator":"cchlebak","file_id":"10751","checksum":"63dfecf30c5bbf9408b3512bd603f78c","date_created":"2022-02-08T13:26:40Z","file_size":6303227}],"_id":"10712","quality_controlled":"1","scopus_import":"1","oa_version":"Published Version","file_date_updated":"2022-02-08T13:26:40Z","intvolume":" 12","month":"02","citation":{"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.","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.","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.","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.","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).","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","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"},"date_published":"2022-02-08T00:00:00Z","publication":"Frontiers in Oncology","publication_status":"published","tmp":{"image":"/images/cc_by.png","legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","short":"CC BY (4.0)","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)"},"acknowledged_ssus":[{"_id":"Bio"}],"article_processing_charge":"Yes (via OA deal)","doi":"10.3389/fonc.2022.777634","type":"journal_article","author":[{"orcid":"0000-0001-9588-1389","full_name":"Roblek, Marko","first_name":"Marko","last_name":"Roblek","id":"3047D808-F248-11E8-B48F-1D18A9856A87"},{"full_name":"Bicher, Julia","first_name":"Julia","last_name":"Bicher","id":"3CCBB46E-F248-11E8-B48F-1D18A9856A87"},{"full_name":"van Gogh, Merel","first_name":"Merel","last_name":"van Gogh"},{"id":"3BCEDBE0-F248-11E8-B48F-1D18A9856A87","last_name":"György","first_name":"Attila","full_name":"György, Attila","orcid":"0000-0002-1819-198X"},{"last_name":"Seeböck","full_name":"Seeböck, Rita","first_name":"Rita"},{"full_name":"Szulc, Bozena","first_name":"Bozena","last_name":"Szulc"},{"first_name":"Markus","full_name":"Damme, Markus","last_name":"Damme"},{"full_name":"Olczak, Mariusz","first_name":"Mariusz","last_name":"Olczak"},{"last_name":"Borsig","full_name":"Borsig, Lubor","first_name":"Lubor"},{"orcid":"0000-0001-8323-8353","first_name":"Daria E","full_name":"Siekhaus, Daria E","id":"3D224B9E-F248-11E8-B48F-1D18A9856A87","last_name":"Siekhaus"}],"article_number":"777634","department":[{"_id":"DaSi"}],"volume":12,"status":"public","language":[{"iso":"eng"}],"day":"08","year":"2022","has_accepted_license":"1","article_type":"original"},{"tmp":{"image":"/images/cc_by_nc_nd.png","short":"CC BY-NC-ND (4.0)","name":"Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0)","legal_code_url":"https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode"},"page":"883-900.e10","publication_status":"published","doi":"10.1016/j.devcel.2022.03.005","type":"journal_article","article_processing_charge":"No","license":"https://creativecommons.org/licenses/by-nc-nd/4.0/","date_published":"2022-04-11T00:00:00Z","publication":"Developmental Cell","citation":{"ista":"Martin ET, Blatt P, Ngyuen E, Lahr R, Selvam S, Yoon HAM, Pocchiari T, Emtenani S, Siekhaus DE, Berman A, Fuchs G, Rangan P. 2022. A translation control module coordinates germline stem cell differentiation with ribosome biogenesis during Drosophila oogenesis. Developmental Cell. 57(7), 883–900.e10.","mla":"Martin, Elliot T., et al. “A Translation Control Module Coordinates Germline Stem Cell Differentiation with Ribosome Biogenesis during Drosophila Oogenesis.” Developmental Cell, vol. 57, no. 7, Elsevier, 2022, p. 883–900.e10, doi:10.1016/j.devcel.2022.03.005.","ieee":"E. T. Martin et al., “A translation control module coordinates germline stem cell differentiation with ribosome biogenesis during Drosophila oogenesis,” Developmental Cell, vol. 57, no. 7. Elsevier, p. 883–900.e10, 2022.","chicago":"Martin, Elliot T., Patrick Blatt, Elaine Ngyuen, Roni Lahr, Sangeetha Selvam, Hyun Ah M. Yoon, Tyler Pocchiari, et al. “A Translation Control Module Coordinates Germline Stem Cell Differentiation with Ribosome Biogenesis during Drosophila Oogenesis.” Developmental Cell. Elsevier, 2022. https://doi.org/10.1016/j.devcel.2022.03.005.","apa":"Martin, E. T., Blatt, P., Ngyuen, E., Lahr, R., Selvam, S., Yoon, H. A. M., … Rangan, P. (2022). A translation control module coordinates germline stem cell differentiation with ribosome biogenesis during Drosophila oogenesis. Developmental Cell. Elsevier. https://doi.org/10.1016/j.devcel.2022.03.005","ama":"Martin ET, Blatt P, Ngyuen E, et al. A translation control module coordinates germline stem cell differentiation with ribosome biogenesis during Drosophila oogenesis. Developmental Cell. 2022;57(7):883-900.e10. doi:10.1016/j.devcel.2022.03.005","short":"E.T. Martin, P. Blatt, E. Ngyuen, R. Lahr, S. Selvam, H.A.M. Yoon, T. Pocchiari, S. Emtenani, D.E. Siekhaus, A. Berman, G. Fuchs, P. Rangan, Developmental Cell 57 (2022) 883–900.e10."},"month":"04","intvolume":" 57","scopus_import":"1","oa_version":"Preprint","language":[{"iso":"eng"}],"year":"2022","day":"11","status":"public","article_type":"original","author":[{"first_name":"Elliot T.","full_name":"Martin, Elliot T.","last_name":"Martin"},{"last_name":"Blatt","full_name":"Blatt, Patrick","first_name":"Patrick"},{"last_name":"Ngyuen","full_name":"Ngyuen, Elaine","first_name":"Elaine"},{"first_name":"Roni","full_name":"Lahr, Roni","last_name":"Lahr"},{"last_name":"Selvam","first_name":"Sangeetha","full_name":"Selvam, Sangeetha"},{"first_name":"Hyun Ah M.","full_name":"Yoon, Hyun Ah M.","last_name":"Yoon"},{"last_name":"Pocchiari","full_name":"Pocchiari, Tyler","first_name":"Tyler"},{"id":"49D32318-F248-11E8-B48F-1D18A9856A87","last_name":"Emtenani","first_name":"Shamsi","full_name":"Emtenani, Shamsi","orcid":"0000-0001-6981-6938"},{"last_name":"Siekhaus","id":"3D224B9E-F248-11E8-B48F-1D18A9856A87","full_name":"Siekhaus, Daria E","first_name":"Daria E","orcid":"0000-0001-8323-8353"},{"last_name":"Berman","full_name":"Berman, Andrea","first_name":"Andrea"},{"last_name":"Fuchs","full_name":"Fuchs, Gabriele","first_name":"Gabriele"},{"last_name":"Rangan","full_name":"Rangan, Prashanth","first_name":"Prashanth"}],"volume":57,"department":[{"_id":"DaSi"}],"issue":"7","project":[{"name":"Investigating the role of transporters in invasive migration through junctions","grant_number":"334077","_id":"2536F660-B435-11E9-9278-68D0E5697425","call_identifier":"FP7"},{"name":"Drosophila TNFa´s Funktion in Immunzellen","grant_number":"P29638","_id":"253B6E48-B435-11E9-9278-68D0E5697425","call_identifier":"FWF"}],"oa":1,"abstract":[{"text":"Ribosomal defects perturb stem cell differentiation, causing diseases called ribosomopathies. How ribosome levels control stem cell differentiation is not fully known. Here, we discovered three RNA helicases are required for ribosome biogenesis and for Drosophila oogenesis. Loss of these helicases, which we named Aramis, Athos and Porthos, lead to aberrant stabilization of p53, cell cycle arrest and stalled GSC differentiation. Unexpectedly, Aramis is required for efficient translation of a cohort of mRNAs containing a 5’-Terminal-Oligo-Pyrimidine (TOP)-motif, including mRNAs that encode ribosomal proteins and a conserved p53 inhibitor, Novel Nucleolar protein 1 (Non1). The TOP-motif co-regulates the translation of growth-related mRNAs in mammals. As in mammals, the La-related protein co-regulates the translation of TOP-motif containing RNAs during Drosophila oogenesis. Thus, a previously unappreciated TOP-motif in Drosophila responds to reduced ribosome biogenesis to co-regulate the translation of ribosomal proteins and a p53 repressor, thus coupling ribosome biogenesis to GSC differentiation.","lang":"eng"}],"ec_funded":1,"publication_identifier":{"eissn":["1878-1551"],"issn":["1534-5807"]},"main_file_link":[{"url":"https://doi.org/10.1101/2021.04.04.438367","open_access":"1"}],"acknowledgement":"We are grateful to all members of the Rangan and Fuchs labs for their discussion and comments on the manuscript. We also thanks Dr. Sammons, Dr. Marlow, Life Science Editors, for their thoughts and comments the manuscript Additionally, we thank the Bloomington Stock Center, the Vienna Drosophila Resource Center, the BDGP Gene Disruption Project, and Flybase for fly stocks, reagents, and other resources. P.R. is funded by the NIH/NIGMS (R01GM111779-06 and RO1GM135628-01), G.F. is funded by NSF MCB-2047629 and NIH RO3 AI144839, D.E.S. was funded by Marie Curie CIG 334077/IRTIM and the Austrian Science Fund (FWF) grant ASI_FWF01_P29638S, and A.B is funded by NIH R01GM116889 and American Cancer Society RSG-17-197-01-RMC.","external_id":{"isi":["000789021800005"]},"date_updated":"2023-08-02T14:07:13Z","publisher":"Elsevier","date_created":"2022-02-01T13:15:05Z","_id":"10714","quality_controlled":"1","title":"A translation control module coordinates germline stem cell differentiation with ribosome biogenesis during Drosophila oogenesis","user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","isi":1},{"_id":"10713","quality_controlled":"1","title":"Cell division in tissues enables macrophage infiltration","user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","isi":1,"issue":"6591","oa":1,"project":[{"name":"Modeling epithelial tissue mechanics during cell invasion","grant_number":"M02379","_id":"264CBBAC-B435-11E9-9278-68D0E5697425","call_identifier":"FWF"}],"abstract":[{"lang":"eng","text":"Cells migrate through crowded microenvironments within tissues during normal development, immune response, and cancer metastasis. Although migration through pores and tracks in the extracellular matrix (ECM) has been well studied, little is known about cellular traversal into confining cell-dense tissues. We find that embryonic tissue invasion by Drosophila macrophages requires division of an epithelial ectodermal cell at the site of entry. Dividing ectodermal cells disassemble ECM attachment formed by integrin-mediated focal adhesions next to mesodermal cells, allowing macrophages to move their nuclei ahead and invade between two immediately adjacent tissues. Invasion efficiency depends on division frequency, but reduction of adhesion strength allows macrophage entry independently of division. This work demonstrates that tissue dynamics can regulate cellular infiltration."}],"publication_identifier":{"issn":["0036-8075"]},"acknowledgement":"We thank J. Friml, C. Guet, T. Hurd, M. Fendrych and members of the laboratory for comments on the manuscript; the Bioimaging Facility of IST Austria for excellent support and T. Lecuit, E. Hafen, R. Levayer and A. Martin for fly strains. This work was supported by a grant from the Austrian Science Fund FWF: Lise Meitner Fellowship M2379-B28 to M.A and D.S., and internal funding from IST Austria to D.S. and EMBL to S.D.R.","main_file_link":[{"url":"https://doi.org/10.1101/2021.04.19.438995","open_access":"1"}],"date_updated":"2023-08-02T14:06:15Z","external_id":{"isi":["000788553700039"],"pmid":["35446632"]},"date_created":"2022-02-01T11:23:18Z","publisher":"American Association for the Advancement of Science","status":"public","day":"22","language":[{"iso":"eng"}],"year":"2022","article_type":"original","author":[{"id":"3425EC26-F248-11E8-B48F-1D18A9856A87","last_name":"Akhmanova","first_name":"Maria","full_name":"Akhmanova, Maria","orcid":"0000-0003-1522-3162"},{"last_name":"Emtenani","id":"49D32318-F248-11E8-B48F-1D18A9856A87","full_name":"Emtenani, Shamsi","first_name":"Shamsi","orcid":"0000-0001-6981-6938"},{"full_name":"Krueger, Daniel","first_name":"Daniel","last_name":"Krueger"},{"id":"3BCEDBE0-F248-11E8-B48F-1D18A9856A87","last_name":"György","orcid":"0000-0002-1819-198X","first_name":"Attila","full_name":"György, Attila"},{"id":"6de81d9d-e2f2-11eb-945a-af8bc2a60b26","last_name":"Pereira Guarda","first_name":"Mariana","full_name":"Pereira Guarda, Mariana"},{"first_name":"Mikhail","full_name":"Vlasov, Mikhail","last_name":"Vlasov"},{"first_name":"Fedor","full_name":"Vlasov, Fedor","last_name":"Vlasov"},{"last_name":"Akopian","first_name":"Andrei","full_name":"Akopian, Andrei"},{"id":"2F064CFE-F248-11E8-B48F-1D18A9856A87","last_name":"Ratheesh","first_name":"Aparna","full_name":"Ratheesh, Aparna"},{"first_name":"Stefano","full_name":"De Renzis, Stefano","last_name":"De Renzis"},{"full_name":"Siekhaus, Daria E","first_name":"Daria E","orcid":"0000-0001-8323-8353","last_name":"Siekhaus","id":"3D224B9E-F248-11E8-B48F-1D18A9856A87"}],"volume":376,"department":[{"_id":"DaSi"}],"pmid":1,"publication_status":"published","tmp":{"image":"/images/cc_by_nc_nd.png","short":"CC BY-NC-ND (4.0)","name":"Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0)","legal_code_url":"https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode"},"page":"394-396","acknowledged_ssus":[{"_id":"Bio"}],"doi":"10.1126/science.abj0425","type":"journal_article","article_processing_charge":"No","citation":{"chicago":"Akhmanova, Maria, Shamsi Emtenani, Daniel Krueger, Attila György, Mariana Pereira Guarda, Mikhail Vlasov, Fedor Vlasov, et al. “Cell Division in Tissues Enables Macrophage Infiltration.” Science. American Association for the Advancement of Science, 2022. https://doi.org/10.1126/science.abj0425.","short":"M. Akhmanova, S. Emtenani, D. Krueger, A. György, M. Pereira Guarda, M. Vlasov, F. Vlasov, A. Akopian, A. Ratheesh, S. De Renzis, D.E. Siekhaus, Science 376 (2022) 394–396.","apa":"Akhmanova, M., Emtenani, S., Krueger, D., György, A., Pereira Guarda, M., Vlasov, M., … Siekhaus, D. E. (2022). Cell division in tissues enables macrophage infiltration. Science. American Association for the Advancement of Science. https://doi.org/10.1126/science.abj0425","ama":"Akhmanova M, Emtenani S, Krueger D, et al. Cell division in tissues enables macrophage infiltration. Science. 2022;376(6591):394-396. doi:10.1126/science.abj0425","ieee":"M. Akhmanova et al., “Cell division in tissues enables macrophage infiltration,” Science, vol. 376, no. 6591. American Association for the Advancement of Science, pp. 394–396, 2022.","mla":"Akhmanova, Maria, et al. “Cell Division in Tissues Enables Macrophage Infiltration.” Science, vol. 376, no. 6591, American Association for the Advancement of Science, 2022, pp. 394–96, doi:10.1126/science.abj0425.","ista":"Akhmanova M, Emtenani S, Krueger D, György A, Pereira Guarda M, Vlasov M, Vlasov F, Akopian A, Ratheesh A, De Renzis S, Siekhaus DE. 2022. Cell division in tissues enables macrophage infiltration. Science. 376(6591), 394–396."},"date_published":"2022-04-22T00:00:00Z","publication":"Science","oa_version":"Preprint","intvolume":" 376","month":"04"},{"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_updated":"2023-08-03T06:13:14Z","external_id":{"isi":["000771957000001"]},"date_created":"2022-03-24T13:23:09Z","publisher":"Embo Press","project":[{"grant_number":"334077","name":"Investigating the role of transporters in invasive migration through junctions","_id":"2536F660-B435-11E9-9278-68D0E5697425","call_identifier":"FP7"},{"grant_number":"M02379","name":"Modeling epithelial tissue mechanics during cell invasion","_id":"264CBBAC-B435-11E9-9278-68D0E5697425","call_identifier":"FWF"},{"call_identifier":"FWF","_id":"253B6E48-B435-11E9-9278-68D0E5697425","name":"Drosophila TNFa´s Funktion in Immunzellen","grant_number":"P29638"}],"oa":1,"ec_funded":1,"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."}],"ddc":["570"],"publication_identifier":{"eissn":["1460-2075"]},"title":"Macrophage mitochondrial bioenergetics and tissue invasion are boosted by an Atossa-Porthos axis in Drosophila","user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","isi":1,"file":[{"file_name":"Macrophage mitochondrial bioenergetics and tissue invasion are boosted by an Atossa-Porthos axis in Drosopila.pdf","content_type":"application/pdf","access_level":"open_access","checksum":"dba48580fe0fefaa4c63078d1d2a35df","date_created":"2022-03-24T13:22:41Z","file_size":4344585,"creator":"siekhaus","file_id":"10919","date_updated":"2022-03-24T13:22:41Z","relation":"main_file"}],"_id":"10918","quality_controlled":"1","citation":{"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.","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.","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).","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","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"},"date_published":"2022-03-23T00:00:00Z","publication":"The Embo Journal","scopus_import":"1","oa_version":"Published Version","month":"03","intvolume":" 41","file_date_updated":"2022-03-24T13:22:41Z","publication_status":"published","acknowledged_ssus":[{"_id":"Bio"}],"tmp":{"image":"/images/cc_by.png","legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","short":"CC BY (4.0)","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)"},"doi":"10.15252/embj.2021109049","type":"journal_article","article_processing_charge":"Yes (via OA deal)","article_number":"e109049","author":[{"orcid":"0000-0001-6981-6938","full_name":"Emtenani, Shamsi","first_name":"Shamsi","last_name":"Emtenani","id":"49D32318-F248-11E8-B48F-1D18A9856A87"},{"last_name":"Martin","full_name":"Martin, Elliot T","first_name":"Elliot T"},{"id":"3BCEDBE0-F248-11E8-B48F-1D18A9856A87","last_name":"György","first_name":"Attila","full_name":"György, Attila","orcid":"0000-0002-1819-198X"},{"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"},{"last_name":"Köcher","first_name":"Thomas","full_name":"Köcher, Thomas"},{"full_name":"Akhmanova, Maria","first_name":"Maria","orcid":"0000-0003-1522-3162","last_name":"Akhmanova","id":"3425EC26-F248-11E8-B48F-1D18A9856A87"},{"id":"6de81d9d-e2f2-11eb-945a-af8bc2a60b26","last_name":"Pereira Guarda","first_name":"Mariana","full_name":"Pereira Guarda, Mariana"},{"orcid":"0000-0001-9588-1389","first_name":"Marko","full_name":"Roblek, Marko","id":"3047D808-F248-11E8-B48F-1D18A9856A87","last_name":"Roblek"},{"last_name":"Bergthaler","first_name":"Andreas","full_name":"Bergthaler, Andreas"},{"full_name":"Hurd, Thomas R","first_name":"Thomas R","last_name":"Hurd"},{"first_name":"Prashanth","full_name":"Rangan, Prashanth","last_name":"Rangan"},{"id":"3D224B9E-F248-11E8-B48F-1D18A9856A87","last_name":"Siekhaus","first_name":"Daria E","full_name":"Siekhaus, Daria E","orcid":"0000-0001-8323-8353"}],"volume":41,"department":[{"_id":"DaSi"},{"_id":"LoSw"}],"status":"public","year":"2022","day":"23","language":[{"iso":"eng"}],"article_type":"original","has_accepted_license":"1"},{"date_updated":"2023-08-03T13:49:07Z","external_id":{"isi":["000932770500001"],"pmid":["35984332"]},"acknowledgement":"This work was supported by JSPS KAKENHI GRANT #18K062291, and the Takeda Science Foundation to J.Y. Toshima, as well as JSPS KAKENHI GRANT #19K065710, the Uehara Memorial Foundation, and Life Science Foundation of JAPAN to J. Toshima.","date_created":"2022-09-11T22:01:54Z","publisher":"Rockefeller University Press","oa":1,"issue":"10","publication_identifier":{"eissn":["1540-8140"],"issn":["0021-9525"]},"abstract":[{"lang":"eng","text":"Endocytosis is a multistep process involving the sequential recruitment and action of numerous proteins. This process can be divided into two phases: an early phase, in which sites of endocytosis are formed, and a late phase in which clathrin-coated vesicles are formed and internalized into the cytosol, but how these phases link to each other remains unclear. In this study, we demonstrate that anchoring the yeast Eps15-like protein Pan1p to the peroxisome triggers most of the events occurring during the late phase at the peroxisome. At this ectopic location, Pan1p recruits most proteins that function in the late phases—including actin nucleation promoting factors—and then initiates actin polymerization. Pan1p also recruited Prk1 kinase and actin depolymerizing factors, thereby triggering disassembly immediately after actin assembly and inducing dissociation of endocytic proteins from the peroxisome. These observations suggest that Pan1p is a key regulator for initiating, processing, and completing the late phase of endocytosis."}],"ddc":["570"],"user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","title":"Eps15/Pan1p is a master regulator of the late stages of the endocytic pathway","isi":1,"file":[{"date_created":"2023-01-20T09:32:53Z","checksum":"f2e581e66b5cdab9df81b56e850b3eaa","file_size":7816875,"relation":"main_file","date_updated":"2023-02-21T23:30:39Z","creator":"dernst","file_id":"12321","embargo":"2023-02-20","file_name":"2022_JCB_Enshoji.pdf","access_level":"open_access","content_type":"application/pdf"}],"_id":"12080","quality_controlled":"1","scopus_import":"1","oa_version":"Published Version","file_date_updated":"2023-02-21T23:30:39Z","intvolume":" 221","month":"08","citation":{"ieee":"M. Enshoji et al., “Eps15/Pan1p is a master regulator of the late stages of the endocytic pathway,” Journal of Cell Biology, vol. 221, no. 10. Rockefeller University Press, 2022.","ista":"Enshoji M, Miyano Y, Yoshida N, Nagano M, Watanabe M, Kunihiro M, Siekhaus DE, Toshima JY, Toshima J. 2022. Eps15/Pan1p is a master regulator of the late stages of the endocytic pathway. Journal of Cell Biology. 221(10), e202112138.","mla":"Enshoji, Mariko, et al. “Eps15/Pan1p Is a Master Regulator of the Late Stages of the Endocytic Pathway.” Journal of Cell Biology, vol. 221, no. 10, e202112138, Rockefeller University Press, 2022, doi:10.1083/jcb.202112138.","apa":"Enshoji, M., Miyano, Y., Yoshida, N., Nagano, M., Watanabe, M., Kunihiro, M., … Toshima, J. (2022). Eps15/Pan1p is a master regulator of the late stages of the endocytic pathway. Journal of Cell Biology. Rockefeller University Press. https://doi.org/10.1083/jcb.202112138","ama":"Enshoji M, Miyano Y, Yoshida N, et al. Eps15/Pan1p is a master regulator of the late stages of the endocytic pathway. Journal of Cell Biology. 2022;221(10). doi:10.1083/jcb.202112138","short":"M. Enshoji, Y. Miyano, N. Yoshida, M. Nagano, M. Watanabe, M. Kunihiro, D.E. Siekhaus, J.Y. Toshima, J. Toshima, Journal of Cell Biology 221 (2022).","chicago":"Enshoji, Mariko, Yoshiko Miyano, Nao Yoshida, Makoto Nagano, Minami Watanabe, Mayumi Kunihiro, Daria E Siekhaus, Junko Y. Toshima, and Jiro Toshima. “Eps15/Pan1p Is a Master Regulator of the Late Stages of the Endocytic Pathway.” Journal of Cell Biology. Rockefeller University Press, 2022. https://doi.org/10.1083/jcb.202112138."},"date_published":"2022-08-19T00:00:00Z","publication":"Journal of Cell Biology","publication_status":"published","tmp":{"image":"/images/cc_by_nc_sa.png","short":"CC BY-NC-SA (4.0)","name":"Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC BY-NC-SA 4.0)","legal_code_url":"https://creativecommons.org/licenses/by-nc-sa/4.0/legalcode"},"license":"https://creativecommons.org/licenses/by-nc-sa/4.0/","article_processing_charge":"No","doi":"10.1083/jcb.202112138","type":"journal_article","author":[{"last_name":"Enshoji","full_name":"Enshoji, Mariko","first_name":"Mariko"},{"last_name":"Miyano","full_name":"Miyano, Yoshiko","first_name":"Yoshiko"},{"last_name":"Yoshida","full_name":"Yoshida, Nao","first_name":"Nao"},{"last_name":"Nagano","full_name":"Nagano, Makoto","first_name":"Makoto"},{"last_name":"Watanabe","first_name":"Minami","full_name":"Watanabe, Minami"},{"full_name":"Kunihiro, Mayumi","first_name":"Mayumi","last_name":"Kunihiro"},{"orcid":"0000-0001-8323-8353","first_name":"Daria E","full_name":"Siekhaus, Daria E","id":"3D224B9E-F248-11E8-B48F-1D18A9856A87","last_name":"Siekhaus"},{"last_name":"Toshima","first_name":"Junko Y.","full_name":"Toshima, Junko Y."},{"last_name":"Toshima","first_name":"Jiro","full_name":"Toshima, Jiro"}],"article_number":"e202112138","department":[{"_id":"DaSi"}],"pmid":1,"volume":221,"status":"public","day":"19","year":"2022","language":[{"iso":"eng"}],"has_accepted_license":"1","article_type":"original"},{"author":[{"full_name":"Belyaeva, Vera","first_name":"Vera","last_name":"Belyaeva","id":"47F080FE-F248-11E8-B48F-1D18A9856A87"},{"first_name":"Stephanie","full_name":"Wachner, Stephanie","id":"2A95E7B0-F248-11E8-B48F-1D18A9856A87","last_name":"Wachner"},{"orcid":"0000-0002-1819-198X","first_name":"Attila","full_name":"György, Attila","id":"3BCEDBE0-F248-11E8-B48F-1D18A9856A87","last_name":"György"},{"full_name":"Emtenani, Shamsi","first_name":"Shamsi","orcid":"0000-0001-6981-6938","last_name":"Emtenani","id":"49D32318-F248-11E8-B48F-1D18A9856A87"},{"id":"4B60654C-F248-11E8-B48F-1D18A9856A87","last_name":"Gridchyn","first_name":"Igor","full_name":"Gridchyn, Igor","orcid":"0000-0002-1807-1929"},{"full_name":"Akhmanova, Maria","first_name":"Maria","orcid":"0000-0003-1522-3162","last_name":"Akhmanova","id":"3425EC26-F248-11E8-B48F-1D18A9856A87"},{"full_name":"Linder, M","first_name":"M","last_name":"Linder"},{"id":"3047D808-F248-11E8-B48F-1D18A9856A87","last_name":"Roblek","orcid":"0000-0001-9588-1389","first_name":"Marko","full_name":"Roblek, Marko"},{"full_name":"Sibilia, M","first_name":"M","last_name":"Sibilia"},{"id":"3D224B9E-F248-11E8-B48F-1D18A9856A87","last_name":"Siekhaus","orcid":"0000-0001-8323-8353","first_name":"Daria E","full_name":"Siekhaus, Daria E"}],"volume":20,"department":[{"_id":"DaSi"},{"_id":"JoCs"}],"pmid":1,"day":"06","language":[{"iso":"eng"}],"year":"2022","status":"public","article_type":"original","has_accepted_license":"1","publication":"PLoS Biology","date_published":"2022-01-06T00:00:00Z","citation":{"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","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.","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.","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.","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.","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."},"intvolume":" 20","month":"01","file_date_updated":"2022-01-12T13:50:04Z","oa_version":"Published Version","scopus_import":"1","page":"e3001494","tmp":{"image":"/images/cc_by.png","legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","short":"CC BY (4.0)","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)"},"acknowledged_ssus":[{"_id":"LifeSc"}],"publication_status":"published","doi":"10.1371/journal.pbio.3001494","type":"journal_article","article_processing_charge":"No","title":"Fos regulates macrophage infiltration against surrounding tissue resistance by a cortical actin-based mechanism in Drosophila","user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","file":[{"file_size":5426932,"checksum":"f454212a5522a7818ba4b2892315c478","date_created":"2022-01-12T13:50:04Z","file_id":"10615","creator":"cchlebak","relation":"main_file","date_updated":"2022-01-12T13:50:04Z","file_name":"2022_PLOSBio_Belyaeva.pdf","content_type":"application/pdf","access_level":"open_access","success":1}],"isi":1,"_id":"10614","quality_controlled":"1","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.","external_id":{"pmid":["34990456"],"isi":["000971223700001"]},"date_updated":"2024-03-29T23:30:28Z","publisher":"Public Library of Science","date_created":"2022-01-12T10:18:17Z","issue":"1","related_material":{"link":[{"relation":"earlier_version","url":"https://www.biorxiv.org/content/10.1101/2020.09.18.301481"},{"description":"News on the ISTA Website","relation":"press_release","url":"https://ista.ac.at/en/news/resisting-the-pressure/"}],"record":[{"id":"8557","relation":"earlier_version","status":"public"},{"id":"11193","status":"public","relation":"dissertation_contains"}]},"oa":1,"project":[{"name":"Drosophila TNFa´s Funktion in Immunzellen","grant_number":"P29638","call_identifier":"FWF","_id":"253B6E48-B435-11E9-9278-68D0E5697425"},{"_id":"26199CA4-B435-11E9-9278-68D0E5697425","name":"Tissue barrier penetration is crucial for immunity and metastasis","grant_number":"24800"},{"name":"Investigating the role of transporters in invasive migration through junctions","grant_number":"334077","call_identifier":"FP7","_id":"2536F660-B435-11E9-9278-68D0E5697425"}],"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. "}],"ddc":["570"],"ec_funded":1,"publication_identifier":{"eissn":["1545-7885"],"issn":["1544-9173"]}},{"file":[{"file_size":8820951,"date_created":"2022-04-20T09:03:57Z","checksum":"999ab16884c4522486136ebc5ae8dbff","file_id":"11195","creator":"cchlebak","date_updated":"2023-04-21T22:30:03Z","relation":"main_file","file_name":"Thesis_Stephanie_Wachner_20200414_formatted.pdf","embargo":"2023-04-20","content_type":"application/pdf","access_level":"open_access"},{"date_updated":"2023-04-21T22:30:03Z","relation":"source_file","creator":"cchlebak","embargo_to":"open_access","file_id":"11329","date_created":"2022-04-22T12:41:00Z","checksum":"fd92b1e38d53bdf8b458213882d41383","file_size":65864612,"access_level":"closed","content_type":"application/x-zip-compressed","file_name":"Thesis_Stephanie_Wachner_20200414.zip"}],"title":"Transcriptional regulation by Dfos and BMP-signaling support tissue invasion of Drosophila immune cells","user_id":"8b945eb4-e2f2-11eb-945a-df72226e66a9","degree_awarded":"PhD","_id":"11193","alternative_title":["ISTA Thesis"],"publisher":"Institute of Science and Technology Austria","date_created":"2022-04-20T08:59:07Z","date_updated":"2023-09-19T10:15:54Z","abstract":[{"lang":"eng","text":"The infiltration of immune cells into tissues underlies the establishment of tissue-resident\r\nmacrophages and responses to infections and tumors. However, the mechanisms immune\r\ncells utilize to collectively migrate through tissue barriers in vivo are not yet well understood.\r\nIn this thesis, I describe two mechanisms that Drosophila immune cells (hemocytes) use to\r\novercome the tissue barrier of the germband in the embryo. One strategy is the strengthening\r\nof the actin cortex through developmentally controlled transcriptional regulation induced by\r\nthe Drosophila proto-oncogene family member Dfos, which I show in Chapter 2. Dfos induces\r\nexpression of the tetraspanin TM4SF and the filamin Cher leading to higher levels of the\r\nactivated formin Dia at the cortex and increased cortical F-actin. This enhanced cortical\r\nstrength allows hemocytes to overcome the physical resistance of the surrounding tissue and\r\ntranslocate their nucleus to move forward. This mechanism affects the speed of migration\r\nwhen hemocytes face a confined environment in vivo.\r\nAnother aspect of the invasion process is the initial step of the leading hemocytes entering\r\nthe tissue, which potentially guides the follower cells. In Chapter 3, I describe a novel\r\nsubpopulation of hemocytes activated by BMP signaling prior to tissue invasion that leads\r\npenetration into the germband. Hemocytes that are deficient in BMP signaling activation\r\nshow impaired persistence at the tissue entry, while their migration speed remains\r\nunaffected.\r\nThis suggests that there might be different mechanisms controlling immune cell migration\r\nwithin the confined environment in vivo, one of these being the general ability to overcome\r\nthe resistance of the surrounding tissue and another affecting the order of hemocytes that\r\ncollectively invade the tissue in a stream of individual cells.\r\nTogether, my findings provide deeper insights into transcriptional changes in immune\r\ncells that enable efficient tissue invasion and pave the way for future studies investigating the\r\nearly colonization of tissues by macrophages in higher organisms. Moreover, they extend the\r\ncurrent view of Drosophila immune cell heterogeneity and point toward a potentially\r\nconserved role for canonical BMP signaling in specifying immune cells that lead the migration\r\nof tissue resident macrophages during embryogenesis."}],"ddc":["570"],"publication_identifier":{"issn":["2663-337X"]},"related_material":{"record":[{"id":"10614","relation":"part_of_dissertation","status":"public"},{"id":"544","status":"public","relation":"part_of_dissertation"}]},"oa":1,"project":[{"_id":"26199CA4-B435-11E9-9278-68D0E5697425","name":"Tissue barrier penetration is crucial for immunity and metastasis","grant_number":"24800"}],"supervisor":[{"last_name":"Siekhaus","id":"3D224B9E-F248-11E8-B48F-1D18A9856A87","full_name":"Siekhaus, Daria E","first_name":"Daria E","orcid":"0000-0001-8323-8353"}],"department":[{"_id":"GradSch"},{"_id":"DaSi"}],"author":[{"full_name":"Wachner, Stephanie","first_name":"Stephanie","last_name":"Wachner","id":"2A95E7B0-F248-11E8-B48F-1D18A9856A87"}],"has_accepted_license":"1","day":"20","year":"2022","language":[{"iso":"eng"}],"status":"public","date_published":"2022-04-20T00:00:00Z","citation":{"apa":"Wachner, S. (2022). Transcriptional regulation by Dfos and BMP-signaling support tissue invasion of Drosophila immune cells. Institute of Science and Technology Austria. https://doi.org/10.15479/at:ista:11193","ama":"Wachner S. Transcriptional regulation by Dfos and BMP-signaling support tissue invasion of Drosophila immune cells. 2022. doi:10.15479/at:ista:11193","short":"S. Wachner, Transcriptional Regulation by Dfos and BMP-Signaling Support Tissue Invasion of Drosophila Immune Cells, Institute of Science and Technology Austria, 2022.","chicago":"Wachner, Stephanie. “Transcriptional Regulation by Dfos and BMP-Signaling Support Tissue Invasion of Drosophila Immune Cells.” Institute of Science and Technology Austria, 2022. https://doi.org/10.15479/at:ista:11193.","ista":"Wachner S. 2022. Transcriptional regulation by Dfos and BMP-signaling support tissue invasion of Drosophila immune cells. Institute of Science and Technology Austria.","ieee":"S. Wachner, “Transcriptional regulation by Dfos and BMP-signaling support tissue invasion of Drosophila immune cells,” Institute of Science and Technology Austria, 2022.","mla":"Wachner, Stephanie. Transcriptional Regulation by Dfos and BMP-Signaling Support Tissue Invasion of Drosophila Immune Cells. Institute of Science and Technology Austria, 2022, doi:10.15479/at:ista:11193."},"month":"04","file_date_updated":"2023-04-21T22:30:03Z","oa_version":"Published Version","doi":"10.15479/at:ista:11193","type":"dissertation","article_processing_charge":"No","tmp":{"image":"/images/cc_by.png","legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","short":"CC BY (4.0)","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)"},"acknowledged_ssus":[{"_id":"LifeSc"}],"page":"170","publication_status":"published"},{"quality_controlled":"1","_id":"9363","isi":1,"file":[{"creator":"kschuh","file_id":"9369","relation":"main_file","date_updated":"2021-05-04T09:05:27Z","date_created":"2021-05-04T09:05:27Z","checksum":"82a74668f863e8dfb22fdd4f845c92ce","file_size":3072764,"content_type":"application/pdf","access_level":"open_access","success":1,"file_name":"2021_PLOS_Ingles-Prieto.pdf"}],"title":"Optogenetic delivery of trophic signals in a genetic model of Parkinson's disease","user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","abstract":[{"lang":"eng","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."}],"ddc":["570"],"publication_identifier":{"eissn":["15537404"]},"issue":"4","oa":1,"date_created":"2021-05-02T22:01:29Z","publisher":"Public Library of Science","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.","date_updated":"2023-08-08T13:17:47Z","external_id":{"isi":["000640606700001"]},"has_accepted_license":"1","status":"public","day":"01","language":[{"iso":"eng"}],"year":"2021","volume":17,"department":[{"_id":"EM-Fac"},{"_id":"LoSw"},{"_id":"DaSi"}],"author":[{"last_name":"Inglés Prieto","id":"2A9DB292-F248-11E8-B48F-1D18A9856A87","full_name":"Inglés Prieto, Álvaro","first_name":"Álvaro","orcid":"0000-0002-5409-8571"},{"full_name":"Furthmann, Nikolas","first_name":"Nikolas","last_name":"Furthmann"},{"first_name":"Samuel H.","full_name":"Crossman, Samuel H.","last_name":"Crossman"},{"last_name":"Tichy","first_name":"Alexandra Madelaine","full_name":"Tichy, Alexandra Madelaine"},{"last_name":"Hoyer","first_name":"Nina","full_name":"Hoyer, Nina"},{"last_name":"Petersen","full_name":"Petersen, Meike","first_name":"Meike"},{"last_name":"Zheden","id":"39C5A68A-F248-11E8-B48F-1D18A9856A87","full_name":"Zheden, Vanessa","first_name":"Vanessa"},{"last_name":"Bicher","id":"3CCBB46E-F248-11E8-B48F-1D18A9856A87","full_name":"Bicher, Julia","first_name":"Julia"},{"orcid":"0000-0002-7218-7738","first_name":"Eva","full_name":"Gschaider-Reichhart, Eva","id":"3FEE232A-F248-11E8-B48F-1D18A9856A87","last_name":"Gschaider-Reichhart"},{"full_name":"György, Attila","first_name":"Attila","orcid":"0000-0002-1819-198X","last_name":"György","id":"3BCEDBE0-F248-11E8-B48F-1D18A9856A87"},{"full_name":"Siekhaus, Daria E","first_name":"Daria E","orcid":"0000-0001-8323-8353","last_name":"Siekhaus","id":"3D224B9E-F248-11E8-B48F-1D18A9856A87"},{"first_name":"Peter","full_name":"Soba, Peter","last_name":"Soba"},{"first_name":"Konstanze F.","full_name":"Winklhofer, Konstanze F.","last_name":"Winklhofer"},{"last_name":"Janovjak","id":"33BA6C30-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-8023-9315","full_name":"Janovjak, Harald L","first_name":"Harald L"}],"doi":"10.1371/journal.pgen.1009479","type":"journal_article","article_processing_charge":"No","publication_status":"published","page":"e1009479","tmp":{"image":"/images/cc_by.png","legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","short":"CC BY (4.0)","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)"},"citation":{"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.","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.","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.","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.","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","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"},"date_published":"2021-04-01T00:00:00Z","publication":"PLoS genetics","scopus_import":"1","oa_version":"Published Version","file_date_updated":"2021-05-04T09:05:27Z","month":"04","intvolume":" 17"},{"oa":1,"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."}],"ddc":["610"],"publication_identifier":{"eissn":["2234-943X"]},"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.","external_id":{"isi":["000726603400001"],"pmid":["34868988"]},"date_updated":"2023-08-17T06:20:32Z","publisher":"Frontiers","date_created":"2021-12-12T23:01:27Z","_id":"10536","quality_controlled":"1","title":"TGFβ signaling in myeloid cells promotes lung and liver metastasis through different mechanisms","user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","file":[{"file_name":"2021_Frontiers_Stefanescu.pdf","content_type":"application/pdf","success":1,"access_level":"open_access","checksum":"56cbac80e6891ce750511a30161b7792","date_created":"2021-12-13T13:32:37Z","file_size":9245199,"creator":"alisjak","file_id":"10539","relation":"main_file","date_updated":"2021-12-13T13:32:37Z"}],"isi":1,"tmp":{"image":"/images/cc_by.png","legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","short":"CC BY (4.0)","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)"},"publication_status":"published","type":"journal_article","doi":"10.3389/fonc.2021.765151","article_processing_charge":"No","date_published":"2021-11-18T00:00:00Z","publication":"Frontiers in Oncology","citation":{"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.","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","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","short":"C. Stefanescu, M. Van Gogh, M. Roblek, M. Heikenwalder, L. Borsig, Frontiers in Oncology 11 (2021).","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."},"intvolume":" 11","month":"11","file_date_updated":"2021-12-13T13:32:37Z","scopus_import":"1","oa_version":"Published Version","year":"2021","language":[{"iso":"eng"}],"day":"18","status":"public","article_type":"original","has_accepted_license":"1","article_number":"765151","author":[{"first_name":"Cristina","full_name":"Stefanescu, Cristina","last_name":"Stefanescu"},{"full_name":"Van Gogh, Merel","first_name":"Merel","last_name":"Van Gogh"},{"last_name":"Roblek","id":"3047D808-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0001-9588-1389","full_name":"Roblek, Marko","first_name":"Marko"},{"full_name":"Heikenwalder, Mathias","first_name":"Mathias","last_name":"Heikenwalder"},{"last_name":"Borsig","full_name":"Borsig, Lubor","first_name":"Lubor"}],"volume":11,"pmid":1,"department":[{"_id":"DaSi"}]},{"citation":{"chicago":"Kierdorf, Katrin, Fabian Hersperger, Jessica Sharrock, Crystal M. Vincent, Pinar Ustaoglu, Jiawen Dou, Attila György, Olaf Groß, Daria E Siekhaus, and Marc S. Dionne. “Muscle Function and Homeostasis Require Cytokine Inhibition of AKT Activity in Drosophila.” ELife. eLife Sciences Publications, 2020. https://doi.org/10.7554/eLife.51595.","apa":"Kierdorf, K., Hersperger, F., Sharrock, J., Vincent, C. M., Ustaoglu, P., Dou, J., … Dionne, M. S. (2020). Muscle function and homeostasis require cytokine inhibition of AKT activity in Drosophila. ELife. eLife Sciences Publications. https://doi.org/10.7554/eLife.51595","ama":"Kierdorf K, Hersperger F, Sharrock J, et al. Muscle function and homeostasis require cytokine inhibition of AKT activity in Drosophila. eLife. 2020;9. doi:10.7554/eLife.51595","short":"K. Kierdorf, F. Hersperger, J. Sharrock, C.M. Vincent, P. Ustaoglu, J. Dou, A. György, O. Groß, D.E. Siekhaus, M.S. Dionne, ELife 9 (2020).","ista":"Kierdorf K, Hersperger F, Sharrock J, Vincent CM, Ustaoglu P, Dou J, György A, Groß O, Siekhaus DE, Dionne MS. 2020. Muscle function and homeostasis require cytokine inhibition of AKT activity in Drosophila. eLife. 9, e51595.","mla":"Kierdorf, Katrin, et al. “Muscle Function and Homeostasis Require Cytokine Inhibition of AKT Activity in Drosophila.” ELife, vol. 9, e51595, eLife Sciences Publications, 2020, doi:10.7554/eLife.51595.","ieee":"K. Kierdorf et al., “Muscle function and homeostasis require cytokine inhibition of AKT activity in Drosophila,” eLife, vol. 9. eLife Sciences Publications, 2020."},"publication":"eLife","date_published":"2020-01-20T00:00:00Z","scopus_import":"1","oa_version":"Published Version","file_date_updated":"2020-07-14T12:47:59Z","month":"01","intvolume":" 9","publication_status":"published","tmp":{"image":"/images/cc_by.png","legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","short":"CC BY (4.0)","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)"},"type":"journal_article","doi":"10.7554/eLife.51595","article_processing_charge":"No","article_number":"e51595","author":[{"last_name":"Kierdorf","first_name":"Katrin","full_name":"Kierdorf, Katrin"},{"last_name":"Hersperger","full_name":"Hersperger, Fabian","first_name":"Fabian"},{"last_name":"Sharrock","first_name":"Jessica","full_name":"Sharrock, Jessica"},{"full_name":"Vincent, Crystal M.","first_name":"Crystal M.","last_name":"Vincent"},{"last_name":"Ustaoglu","first_name":"Pinar","full_name":"Ustaoglu, Pinar"},{"first_name":"Jiawen","full_name":"Dou, Jiawen","last_name":"Dou"},{"id":"3BCEDBE0-F248-11E8-B48F-1D18A9856A87","last_name":"György","orcid":"0000-0002-1819-198X","first_name":"Attila","full_name":"György, Attila"},{"full_name":"Groß, Olaf","first_name":"Olaf","last_name":"Groß"},{"full_name":"Siekhaus, Daria E","first_name":"Daria E","orcid":"0000-0001-8323-8353","last_name":"Siekhaus","id":"3D224B9E-F248-11E8-B48F-1D18A9856A87"},{"last_name":"Dionne","full_name":"Dionne, Marc S.","first_name":"Marc S."}],"volume":9,"department":[{"_id":"DaSi"}],"status":"public","year":"2020","day":"20","language":[{"iso":"eng"}],"article_type":"original","has_accepted_license":"1","date_updated":"2023-08-17T14:36:39Z","external_id":{"isi":["000512304800001"]},"date_created":"2020-02-09T23:00:51Z","publisher":"eLife Sciences Publications","oa":1,"project":[{"call_identifier":"FWF","_id":"253B6E48-B435-11E9-9278-68D0E5697425","name":"Drosophila TNFa´s Funktion in Immunzellen","grant_number":"P29638"}],"ddc":["570"],"abstract":[{"lang":"eng","text":"Unpaired ligands are secreted signals that act via a GP130-like receptor, domeless, to activate JAK/STAT signalling in Drosophila. Like many mammalian cytokines, unpaireds can be activated by infection and other stresses and can promote insulin resistance in target tissues. However, the importance of this effect in non-inflammatory physiology is unknown. Here, we identify a requirement for unpaired-JAK signalling as a metabolic regulator in healthy adult Drosophila muscle. Adult muscles show basal JAK-STAT signalling activity in the absence of any immune challenge. Plasmatocytes (Drosophila macrophages) are an important source of this tonic signal. Loss of the dome receptor on adult muscles significantly reduces lifespan and causes local and systemic metabolic pathology. These pathologies result from hyperactivation of AKT and consequent deregulation of metabolism. Thus, we identify a cytokine signal that must be received in muscle to control AKT activity and metabolic homeostasis."}],"publication_identifier":{"eissn":["2050084X"]},"title":"Muscle function and homeostasis require cytokine inhibition of AKT activity in Drosophila","user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","isi":1,"file":[{"date_created":"2020-02-10T08:53:16Z","checksum":"3a072be843f416c7a7d532a51dc0addb","file_size":4959933,"creator":"dernst","file_id":"7470","relation":"main_file","date_updated":"2020-07-14T12:47:59Z","file_name":"2020_eLife_Kierdorf.pdf","content_type":"application/pdf","access_level":"open_access"}],"_id":"7466","quality_controlled":"1"},{"acknowledgement":"Also, I would like to express my appreciation and thanks to the Bioimaging facility, LSF, GSO, library, and IT people at IST Austria.","date_updated":"2023-09-07T13:24:17Z","publisher":"Institute of Science and Technology Austria","date_created":"2020-12-30T15:41:26Z","related_material":{"record":[{"id":"8557","relation":"part_of_dissertation","status":"public"},{"status":"public","relation":"part_of_dissertation","id":"6187"}]},"oa":1,"ddc":["570"],"abstract":[{"text":"Metabolic adaptation is a critical feature of migrating cells. It tunes the metabolic programs of migrating cells to allow them to efficiently exert their crucial roles in development, inflammatory responses and tumor metastasis. Cell migration through physically challenging contexts requires energy. However, how the metabolic reprogramming that underlies in vivo cell invasion is controlled is still unanswered. In my PhD project, I identify a novel conserved metabolic shift in Drosophila melanogaster immune cells that by modulating their bioenergetic potential controls developmentally programmed tissue invasion. We show that this regulation requires a novel conserved nuclear protein, named Atossa. Atossa enhances the transcription of a set of proteins, including an RNA helicase Porthos and two metabolic enzymes, each of which increases the tissue invasion of leading Drosophila macrophages and can rescue the atossa mutant phenotype. Porthos selectively regulates the translational efficiency of a subset of mRNAs containing a 5’-UTR cis-regulatory TOP-like sequence. These 5’TOPL mRNA targets encode mitochondrial-related proteins, including subunits of mitochondrial oxidative phosphorylation (OXPHOS) components III and V and other metabolic-related proteins. Porthos powers up mitochondrial OXPHOS to engender a sufficient ATP supply, which is required for tissue invasion of leading macrophages. Atossa’s two vertebrate orthologs rescue the invasion defect. In my PhD project, I elucidate that Atossa displays a conserved developmental metabolic control to modulate metabolic capacities and the cellular energy state, through altered transcription and translation, to aid the tissue infiltration of leading cells into energy demanding barriers.","lang":"eng"}],"publication_identifier":{"issn":["2663-337X"]},"title":"Metabolic regulation of Drosophila macrophage tissue invasion","user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","file":[{"date_updated":"2021-12-31T23:30:04Z","relation":"main_file","creator":"semtenan","file_id":"8984","date_created":"2020-12-30T15:34:01Z","checksum":"ec2797ab7a6f253b35df0572b36d1b43","file_size":10848175,"access_level":"open_access","content_type":"application/pdf","embargo":"2021-12-30","file_name":"Thesis_Shamsi_Emtenani_pdfA.pdf"},{"checksum":"cc30e6608a9815414024cf548dff3b3a","date_created":"2020-12-30T15:37:36Z","file_size":10073648,"relation":"source_file","date_updated":"2021-12-31T23:30:04Z","creator":"semtenan","embargo_to":"open_access","file_id":"8985","file_name":"Thesis_Shamsi_Emtenani_source file.pdf","access_level":"closed","content_type":"application/pdf"}],"_id":"8983","alternative_title":["ISTA Thesis"],"degree_awarded":"PhD","date_published":"2020-12-30T00:00:00Z","citation":{"apa":"Emtenani, S. (2020). Metabolic regulation of Drosophila macrophage tissue invasion. Institute of Science and Technology Austria. https://doi.org/10.15479/AT:ISTA:8983","ama":"Emtenani S. Metabolic regulation of Drosophila macrophage tissue invasion. 2020. doi:10.15479/AT:ISTA:8983","short":"S. Emtenani, Metabolic Regulation of Drosophila Macrophage Tissue Invasion, Institute of Science and Technology Austria, 2020.","chicago":"Emtenani, Shamsi. “Metabolic Regulation of Drosophila Macrophage Tissue Invasion.” Institute of Science and Technology Austria, 2020. https://doi.org/10.15479/AT:ISTA:8983.","mla":"Emtenani, Shamsi. Metabolic Regulation of Drosophila Macrophage Tissue Invasion. Institute of Science and Technology Austria, 2020, doi:10.15479/AT:ISTA:8983.","ieee":"S. Emtenani, “Metabolic regulation of Drosophila macrophage tissue invasion,” Institute of Science and Technology Austria, 2020.","ista":"Emtenani S. 2020. Metabolic regulation of Drosophila macrophage tissue invasion. Institute of Science and Technology Austria."},"month":"12","file_date_updated":"2021-12-31T23:30:04Z","oa_version":"Published Version","acknowledged_ssus":[{"_id":"Bio"},{"_id":"LifeSc"},{"_id":"E-Lib"},{"_id":"CampIT"}],"page":"141","publication_status":"published","doi":"10.15479/AT:ISTA:8983","type":"dissertation","article_processing_charge":"No","author":[{"id":"49D32318-F248-11E8-B48F-1D18A9856A87","last_name":"Emtenani","first_name":"Shamsi","full_name":"Emtenani, Shamsi","orcid":"0000-0001-6981-6938"}],"supervisor":[{"orcid":"0000-0001-8323-8353","full_name":"Siekhaus, Daria E","first_name":"Daria E","last_name":"Siekhaus","id":"3D224B9E-F248-11E8-B48F-1D18A9856A87"}],"department":[{"_id":"DaSi"}],"year":"2020","language":[{"iso":"eng"}],"day":"30","status":"public","has_accepted_license":"1"},{"month":"09","date_created":"2020-09-23T09:36:47Z","oa_version":"Preprint","date_published":"2020-09-18T00:00:00Z","publication":"bioRxiv","citation":{"mla":"Belyaeva, Vera, et al. “Cortical Actin Properties Controlled by Drosophila Fos Aid Macrophage Infiltration against Surrounding Tissue Resistance.” BioRxiv, doi:10.1101/2020.09.18.301481.","ieee":"V. Belyaeva et al., “Cortical actin properties controlled by Drosophila Fos aid macrophage infiltration against surrounding tissue resistance,” bioRxiv. .","ista":"Belyaeva V, Wachner S, Gridchyn I, Linder M, Emtenani S, György A, Sibilia M, Siekhaus DE. Cortical actin properties controlled by Drosophila Fos aid macrophage infiltration against surrounding tissue resistance. bioRxiv, 10.1101/2020.09.18.301481.","chicago":"Belyaeva, Vera, Stephanie Wachner, Igor Gridchyn, Markus Linder, Shamsi Emtenani, Attila György, Maria Sibilia, and Daria E Siekhaus. “Cortical Actin Properties Controlled by Drosophila Fos Aid Macrophage Infiltration against Surrounding Tissue Resistance.” BioRxiv, n.d. https://doi.org/10.1101/2020.09.18.301481.","ama":"Belyaeva V, Wachner S, Gridchyn I, et al. Cortical actin properties controlled by Drosophila Fos aid macrophage infiltration against surrounding tissue resistance. bioRxiv. doi:10.1101/2020.09.18.301481","apa":"Belyaeva, V., Wachner, S., Gridchyn, I., Linder, M., Emtenani, S., György, A., … Siekhaus, D. E. (n.d.). Cortical actin properties controlled by Drosophila Fos aid macrophage infiltration against surrounding tissue resistance. bioRxiv. https://doi.org/10.1101/2020.09.18.301481","short":"V. Belyaeva, S. Wachner, I. Gridchyn, M. Linder, S. Emtenani, A. György, M. Sibilia, D.E. Siekhaus, BioRxiv (n.d.)."},"date_updated":"2024-03-29T23:30:24Z","main_file_link":[{"open_access":"1","url":"https://doi.org/10.1101/2020.09.18.301481"}],"acknowledgement":"We thank the following for their contributions: The Drosophila Genomics Resource Center supported by NIH grant 2P40OD010949-10A1 for plasmids, K. Brueckner. B. Stramer, M. Uhlirova, O. Schuldiner, the Bloomington Drosophila Stock Center supported by NIH grant P40OD018537 and the Vienna Drosophila Resource Center for fly stocks, FlyBase (Thurmond et al., 2019) for essential genomic information, and the BDGP in situ database for data (Tomancak et al., 2002, 2007). 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. A.G. was supported by the Austrian Science Fund (FWF) grant DASI_FWF01_P29638S, D.E.S. by Marie Curie CIG 334077/IRTIM. M.S. is supported by the FWF, PhD program W1212 915 and the European Research Council (ERC) Advanced grant (ERC-2015-AdG TNT-Tumors 694883). S.W. is supported by an OEAW, DOC fellowship.","article_processing_charge":"No","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. Cortical F-actin levels are critical as expressing a dominant active form of Diaphanous, a actin polymerizing Formin, can rescue the Dfos Dominant Negative macrophage invasion defect. In vivo imaging shows that Dfos is required to enhance 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 mechanical properties of the macrophage nucleus from affecting tissue entry. We thus identify tuning the cortical actin cytoskeleton through Dfos as a key process allowing efficient forward movement of an immune cell into surrounding tissues."}],"doi":"10.1101/2020.09.18.301481","ec_funded":1,"type":"preprint","project":[{"_id":"253B6E48-B435-11E9-9278-68D0E5697425","call_identifier":"FWF","grant_number":"P29638","name":"Drosophila TNFa´s Funktion in Immunzellen"},{"grant_number":"334077","name":"Investigating the role of transporters in invasive migration through junctions","_id":"2536F660-B435-11E9-9278-68D0E5697425","call_identifier":"FP7"},{"grant_number":"24800","name":"Tissue barrier penetration is crucial for immunity and metastasis","_id":"26199CA4-B435-11E9-9278-68D0E5697425"}],"oa":1,"acknowledged_ssus":[{"_id":"LifeSc"}],"publication_status":"submitted","related_material":{"record":[{"id":"10614","relation":"later_version","status":"public"},{"status":"public","relation":"dissertation_contains","id":"8983"}]},"department":[{"_id":"DaSi"},{"_id":"JoCs"}],"author":[{"first_name":"Vera","full_name":"Belyaeva, Vera","id":"47F080FE-F248-11E8-B48F-1D18A9856A87","last_name":"Belyaeva"},{"first_name":"Stephanie","full_name":"Wachner, Stephanie","id":"2A95E7B0-F248-11E8-B48F-1D18A9856A87","last_name":"Wachner"},{"id":"4B60654C-F248-11E8-B48F-1D18A9856A87","last_name":"Gridchyn","first_name":"Igor","full_name":"Gridchyn, Igor","orcid":"0000-0002-1807-1929"},{"first_name":"Markus","full_name":"Linder, Markus","last_name":"Linder"},{"orcid":"0000-0001-6981-6938","full_name":"Emtenani, Shamsi","first_name":"Shamsi","last_name":"Emtenani","id":"49D32318-F248-11E8-B48F-1D18A9856A87"},{"last_name":"György","id":"3BCEDBE0-F248-11E8-B48F-1D18A9856A87","full_name":"György, Attila","first_name":"Attila","orcid":"0000-0002-1819-198X"},{"last_name":"Sibilia","first_name":"Maria","full_name":"Sibilia, Maria"},{"orcid":"0000-0001-8323-8353","first_name":"Daria E","full_name":"Siekhaus, Daria E","id":"3D224B9E-F248-11E8-B48F-1D18A9856A87","last_name":"Siekhaus"}],"user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","title":"Cortical actin properties controlled by Drosophila Fos aid macrophage infiltration against surrounding tissue resistance","_id":"8557","year":"2020","day":"18","language":[{"iso":"eng"}],"status":"public"},{"scopus_import":"1","oa_version":"Published Version","intvolume":" 17","month":"03","citation":{"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","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","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.","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.","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.","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.","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."},"date_published":"2019-03-01T00:00:00Z","publication":"Molecular Cancer Research","publication_status":"published","page":"783-793","article_processing_charge":"No","type":"journal_article","doi":"10.1158/1541-7786.MCR-18-0530","author":[{"id":"3047D808-F248-11E8-B48F-1D18A9856A87","last_name":"Roblek","first_name":"Marko","full_name":"Roblek, Marko","orcid":"0000-0001-9588-1389"},{"last_name":"Protsyuk","full_name":"Protsyuk, Darya","first_name":"Darya"},{"first_name":"Paul F.","full_name":"Becker, Paul F.","last_name":"Becker"},{"last_name":"Stefanescu","first_name":"Cristina","full_name":"Stefanescu, Cristina"},{"last_name":"Gorzelanny","full_name":"Gorzelanny, Christian","first_name":"Christian"},{"last_name":"Glaus Garzon","full_name":"Glaus Garzon, Jesus F.","first_name":"Jesus F."},{"last_name":"Knopfova","first_name":"Lucia","full_name":"Knopfova, Lucia"},{"full_name":"Heikenwalder, Mathias","first_name":"Mathias","last_name":"Heikenwalder"},{"last_name":"Luckow","first_name":"Bruno","full_name":"Luckow, Bruno"},{"full_name":"Schneider, Stefan W.","first_name":"Stefan W.","last_name":"Schneider"},{"first_name":"Lubor","full_name":"Borsig, Lubor","last_name":"Borsig"}],"department":[{"_id":"DaSi"}],"pmid":1,"volume":17,"status":"public","year":"2019","day":"01","language":[{"iso":"eng"}],"article_type":"original","date_updated":"2023-08-25T08:57:01Z","external_id":{"isi":["000460099800012"],"pmid":["30552233"]},"main_file_link":[{"url":"https://doi.org/10.1158/1541-7786.MCR-18-0530","open_access":"1"}],"date_created":"2019-03-31T21:59:12Z","publisher":"AACR","oa":1,"issue":"3","publication_identifier":{"eissn":["15573125"],"issn":["15417786"]},"abstract":[{"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.","lang":"eng"}],"user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","title":"CCL2 is a vascular permeability factor inducing CCR2-dependent endothelial retraction during lung metastasis","isi":1,"_id":"6190","quality_controlled":"1"},{"volume":2,"department":[{"_id":"DaSi"}],"article_number":"419","author":[{"full_name":"Nagano, Makoto","first_name":"Makoto","last_name":"Nagano"},{"full_name":"Toshima, Junko Y.","first_name":"Junko Y.","last_name":"Toshima"},{"id":"3D224B9E-F248-11E8-B48F-1D18A9856A87","last_name":"Siekhaus","first_name":"Daria E","full_name":"Siekhaus, Daria E","orcid":"0000-0001-8323-8353"},{"last_name":"Toshima","full_name":"Toshima, Jiro","first_name":"Jiro"}],"article_type":"original","has_accepted_license":"1","day":"15","language":[{"iso":"eng"}],"year":"2019","status":"public","publication":"Communications Biology","date_published":"2019-11-15T00:00:00Z","citation":{"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.","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","short":"M. Nagano, J.Y. Toshima, D.E. Siekhaus, J. Toshima, Communications Biology 2 (2019).","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.","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.","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."},"file_date_updated":"2020-07-14T12:47:49Z","month":"11","intvolume":" 2","scopus_import":"1","oa_version":"Published Version","doi":"10.1038/s42003-019-0670-5","type":"journal_article","article_processing_charge":"No","tmp":{"image":"/images/cc_by.png","legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","short":"CC BY (4.0)","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)"},"publication_status":"published","file":[{"content_type":"application/pdf","access_level":"open_access","file_name":"2019_CommunicBiology_Nagano.pdf","creator":"dernst","file_id":"7098","date_updated":"2020-07-14T12:47:49Z","relation":"main_file","date_created":"2019-11-25T07:58:05Z","checksum":"c63c69a264fc8a0e52f2b0d482f3bdae","file_size":2626069}],"isi":1,"title":"Rab5-mediated endosome formation is regulated at the trans-Golgi network","user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","quality_controlled":"1","_id":"7097","publisher":"Springer Nature","date_created":"2019-11-25T07:55:01Z","external_id":{"isi":["000496767800005"]},"date_updated":"2023-08-30T07:27:55Z","ddc":["570"],"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"}],"publication_identifier":{"issn":["2399-3642"]},"issue":"1","oa":1},{"isi":1,"file":[{"access_level":"open_access","content_type":"application/pdf","file_name":"2019_NatureComm_Retzer.pdf","date_updated":"2020-07-14T12:47:52Z","relation":"main_file","file_id":"7184","creator":"dernst","file_size":5156533,"checksum":"77e8720a8e0f3091b98159f85be40893","date_created":"2019-12-16T07:37:50Z"}],"title":"Brassinosteroid signaling delimits root gravitropism via sorting of the Arabidopsis PIN2 auxin transporter","user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","quality_controlled":"1","_id":"7180","date_created":"2019-12-15T23:00:43Z","publisher":"Springer Nature","date_updated":"2023-09-06T14:08:21Z","external_id":{"pmid":["31797871"],"isi":["000500508100001"]},"ddc":["570"],"abstract":[{"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.","lang":"eng"}],"publication_identifier":{"eissn":["20411723"]},"oa":1,"project":[{"name":"Modeling epithelial tissue mechanics during cell invasion","grant_number":"M02379","_id":"264CBBAC-B435-11E9-9278-68D0E5697425","call_identifier":"FWF"}],"volume":10,"pmid":1,"department":[{"_id":"DaSi"}],"article_number":"5516","author":[{"last_name":"Retzer","first_name":"Katarzyna","full_name":"Retzer, Katarzyna"},{"id":"3425EC26-F248-11E8-B48F-1D18A9856A87","last_name":"Akhmanova","first_name":"Maria","full_name":"Akhmanova, Maria","orcid":"0000-0003-1522-3162"},{"last_name":"Konstantinova","full_name":"Konstantinova, Nataliia","first_name":"Nataliia"},{"first_name":"Kateřina","full_name":"Malínská, Kateřina","last_name":"Malínská"},{"last_name":"Leitner","first_name":"Johannes","full_name":"Leitner, Johannes"},{"first_name":"Jan","full_name":"Petrášek, Jan","last_name":"Petrášek"},{"first_name":"Christian","full_name":"Luschnig, Christian","last_name":"Luschnig"}],"article_type":"original","has_accepted_license":"1","status":"public","day":"01","year":"2019","language":[{"iso":"eng"}],"citation":{"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.","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.","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.","short":"K. Retzer, M. Akhmanova, N. Konstantinova, K. Malínská, J. Leitner, J. Petrášek, C. Luschnig, Nature Communications 10 (2019).","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"},"publication":"Nature Communications","date_published":"2019-12-01T00:00:00Z","oa_version":"Published Version","scopus_import":"1","month":"12","intvolume":" 10","file_date_updated":"2020-07-14T12:47:52Z","doi":"10.1038/s41467-019-13543-1","type":"journal_article","article_processing_charge":"No","publication_status":"published","tmp":{"image":"/images/cc_by.png","legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","short":"CC BY (4.0)","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)"}},{"article_processing_charge":"No","doi":"10.1523/JNEUROSCI.1059-18.2018","type":"journal_article","publication_status":"published","page":"238-255","oa_version":"Published Version","scopus_import":"1","intvolume":" 39","file_date_updated":"2020-10-02T09:33:28Z","month":"01","citation":{"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.","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","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.","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.","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."},"date_published":"2019-01-09T00:00:00Z","publication":"Journal of Neuroscience","has_accepted_license":"1","article_type":"original","status":"public","year":"2019","language":[{"iso":"eng"}],"day":"09","pmid":1,"department":[{"_id":"DaSi"}],"volume":39,"author":[{"last_name":"Trébuchet","first_name":"Guillaume","full_name":"Trébuchet, Guillaume"},{"last_name":"Cattenoz","full_name":"Cattenoz, Pierre B","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","id":"3D224B9E-F248-11E8-B48F-1D18A9856A87","full_name":"Siekhaus, Daria E","first_name":"Daria E","orcid":"0000-0001-8323-8353"},{"full_name":"Fanto, Manolis","first_name":"Manolis","last_name":"Fanto"},{"last_name":"Giangrande","first_name":"Angela","full_name":"Giangrande, Angela"}],"ec_funded":1,"abstract":[{"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.","lang":"eng"}],"ddc":["570"],"project":[{"name":"Investigating the role of transporters in invasive migration through junctions","grant_number":"334077","_id":"2536F660-B435-11E9-9278-68D0E5697425","call_identifier":"FP7"}],"oa":1,"issue":"2","date_created":"2018-12-11T11:44:07Z","publisher":"Society for Neuroscience","publist_id":"8048","date_updated":"2023-09-19T10:10:55Z","external_id":{"pmid":["30504274"],"isi":["000455189900006"]},"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.","quality_controlled":"1","_id":"8","isi":1,"file":[{"file_id":"8596","creator":"dernst","date_updated":"2020-10-02T09:33:28Z","relation":"main_file","file_size":9455414,"checksum":"8f6925eb4cd1e8747d8ea25929c68de6","date_created":"2020-10-02T09:33:28Z","content_type":"application/pdf","success":1,"access_level":"open_access","file_name":"2019_JournNeuroscience_Trebuchet.pdf"}],"user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","title":"The Repo homeodomain transcription factor suppresses hematopoiesis in Drosophila and preserves the glial fate"},{"user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","title":"A conserved major facilitator superfamily member orchestrates a subset of O-glycosylation to aid macrophage tissue invasion","file":[{"date_updated":"2020-07-14T12:47:23Z","relation":"main_file","creator":"dernst","file_id":"6188","checksum":"cc0d1a512559d52e7e7cb0e9b9854b40","date_created":"2019-03-28T14:00:41Z","file_size":4496017,"access_level":"open_access","content_type":"application/pdf","file_name":"2019_eLife_Valoskova.pdf"}],"isi":1,"_id":"6187","quality_controlled":"1","external_id":{"isi":["000462530200001"]},"date_updated":"2024-03-29T23:30:29Z","publisher":"eLife Sciences Publications","date_created":"2019-03-28T13:37:45Z","oa":1,"project":[{"_id":"253CDE40-B435-11E9-9278-68D0E5697425","grant_number":"24283","name":"Examination of the role of a MFS transporter in the migration of Drosophila immune cells"},{"call_identifier":"FWF","_id":"253B6E48-B435-11E9-9278-68D0E5697425","grant_number":"P29638","name":"The role of Drosophila TNF alpha in immune cell invasion"},{"_id":"2536F660-B435-11E9-9278-68D0E5697425","call_identifier":"FP7","name":"Investigating the role of transporters in invasive migration through junctions","grant_number":"334077"},{"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"},{"name":"International IST Doctoral Program","grant_number":"665385","call_identifier":"H2020","_id":"2564DBCA-B435-11E9-9278-68D0E5697425"}],"related_material":{"record":[{"id":"6530","relation":"dissertation_contains"},{"relation":"dissertation_contains","status":"public","id":"8983"},{"id":"6546","relation":"dissertation_contains","status":"public"}],"link":[{"url":"https://ist.ac.at/en/news/new-gene-potentially-involved-in-metastasis-identified/","description":"News on IST Homepage","relation":"press_release"}]},"publication_identifier":{"issn":["2050-084X"]},"ddc":["570"],"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."}],"ec_funded":1,"author":[{"full_name":"Valosková, Katarina","first_name":"Katarina","last_name":"Valosková","id":"46F146FC-F248-11E8-B48F-1D18A9856A87"},{"full_name":"Biebl, Julia","first_name":"Julia","last_name":"Biebl","id":"3CCBB46E-F248-11E8-B48F-1D18A9856A87"},{"full_name":"Roblek, Marko","first_name":"Marko","orcid":"0000-0001-9588-1389","last_name":"Roblek","id":"3047D808-F248-11E8-B48F-1D18A9856A87"},{"id":"49D32318-F248-11E8-B48F-1D18A9856A87","last_name":"Emtenani","orcid":"0000-0001-6981-6938","first_name":"Shamsi","full_name":"Emtenani, Shamsi"},{"last_name":"György","id":"3BCEDBE0-F248-11E8-B48F-1D18A9856A87","full_name":"György, Attila","first_name":"Attila","orcid":"0000-0002-1819-198X"},{"first_name":"Michaela","full_name":"Misova, Michaela","orcid":"0000-0003-2427-6856","id":"495A3C32-F248-11E8-B48F-1D18A9856A87","last_name":"Misova"},{"full_name":"Ratheesh, Aparna","first_name":"Aparna","orcid":"0000-0001-7190-0776","last_name":"Ratheesh","id":"2F064CFE-F248-11E8-B48F-1D18A9856A87"},{"first_name":"Patricia","full_name":"Rodrigues, Patricia","id":"2CE4065A-F248-11E8-B48F-1D18A9856A87","last_name":"Rodrigues"},{"last_name":"Shkarina","full_name":"Shkarina, Katerina","first_name":"Katerina"},{"first_name":"Ida Signe Bohse","full_name":"Larsen, Ida Signe Bohse","last_name":"Larsen"},{"full_name":"Vakhrushev, Sergey Y","first_name":"Sergey Y","last_name":"Vakhrushev"},{"last_name":"Clausen","full_name":"Clausen, Henrik","first_name":"Henrik"},{"last_name":"Siekhaus","id":"3D224B9E-F248-11E8-B48F-1D18A9856A87","full_name":"Siekhaus, Daria E","first_name":"Daria E","orcid":"0000-0001-8323-8353"}],"article_number":"e41801","department":[{"_id":"DaSi"}],"volume":8,"day":"26","year":"2019","language":[{"iso":"eng"}],"status":"public","has_accepted_license":"1","file_date_updated":"2020-07-14T12:47:23Z","month":"03","intvolume":" 8","scopus_import":"1","oa_version":"Published Version","date_published":"2019-03-26T00:00:00Z","publication":"eLife","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.","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.","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","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."},"acknowledged_ssus":[{"_id":"LifeSc"}],"tmp":{"image":"/images/cc_by.png","legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","short":"CC BY (4.0)","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)"},"publication_status":"published","article_processing_charge":"No","doi":"10.7554/elife.41801","type":"journal_article"},{"author":[{"last_name":"Valosková","id":"46F146FC-F248-11E8-B48F-1D18A9856A87","full_name":"Valosková, Katarina","first_name":"Katarina"}],"supervisor":[{"full_name":"Siekhaus, Daria E","first_name":"Daria E","orcid":"0000-0001-8323-8353","last_name":"Siekhaus","id":"3D224B9E-F248-11E8-B48F-1D18A9856A87"}],"department":[{"_id":"DaSi"}],"status":"public","year":"2019","language":[{"iso":"eng"}],"day":"07","has_accepted_license":"1","citation":{"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.","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","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.","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."},"date_published":"2019-06-07T00:00:00Z","oa_version":"Published Version","file_date_updated":"2021-02-11T11:17:14Z","month":"06","publication_status":"published","page":"141","acknowledged_ssus":[{"_id":"Bio"}],"doi":"10.15479/AT:ISTA:6546","type":"dissertation","article_processing_charge":"No","title":"The role of a highly conserved major facilitator superfamily member in Drosophila embryonic macrophage migration","user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","file":[{"access_level":"closed","content_type":"application/vnd.openxmlformats-officedocument.wordprocessingml.document","file_name":"Katarina Valoskova_PhD thesis_final version.docx","relation":"source_file","date_updated":"2020-07-14T12:47:33Z","creator":"khribikova","file_id":"6549","embargo_to":"open_access","date_created":"2019-06-07T13:00:04Z","checksum":"68949c2d96210b45b981a23e9c9cd93c","file_size":14110626},{"checksum":"555329cd76e196c96f5278c480ee2e6e","date_created":"2019-06-07T13:00:08Z","file_size":10054156,"creator":"khribikova","file_id":"6550","date_updated":"2021-02-11T11:17:14Z","relation":"main_file","embargo":"2020-06-07","file_name":"Katarina Valoskova_PhD thesis_final version.pdf","content_type":"application/pdf","access_level":"open_access"}],"_id":"6546","degree_awarded":"PhD","alternative_title":["ISTA Thesis"],"date_updated":"2023-09-19T10:15:54Z","date_created":"2019-06-07T12:49:19Z","publisher":"Institute of Science and Technology Austria","related_material":{"record":[{"id":"6187","status":"public","relation":"part_of_dissertation"},{"id":"544","relation":"part_of_dissertation","status":"public"}]},"oa":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"}],"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"}],"ddc":["570"],"publication_identifier":{"issn":["2663-337X"]}},{"volume":45,"pmid":1,"department":[{"_id":"DaSi"},{"_id":"CaHe"},{"_id":"Bio"},{"_id":"EM-Fac"},{"_id":"MiSi"}],"author":[{"id":"2F064CFE-F248-11E8-B48F-1D18A9856A87","last_name":"Ratheesh","orcid":"0000-0001-7190-0776","first_name":"Aparna","full_name":"Ratheesh, Aparna"},{"full_name":"Biebl, Julia","first_name":"Julia","last_name":"Biebl","id":"3CCBB46E-F248-11E8-B48F-1D18A9856A87"},{"first_name":"Michael","full_name":"Smutny, Michael","last_name":"Smutny"},{"id":"433253EE-F248-11E8-B48F-1D18A9856A87","last_name":"Veselá","first_name":"Jana","full_name":"Veselá, Jana"},{"last_name":"Papusheva","id":"41DB591E-F248-11E8-B48F-1D18A9856A87","full_name":"Papusheva, Ekaterina","first_name":"Ekaterina"},{"orcid":"0000-0003-4761-5996","full_name":"Krens, Gabriel","first_name":"Gabriel","last_name":"Krens","id":"2B819732-F248-11E8-B48F-1D18A9856A87"},{"id":"3F99E422-F248-11E8-B48F-1D18A9856A87","last_name":"Kaufmann","orcid":"0000-0001-9735-5315","first_name":"Walter","full_name":"Kaufmann, Walter"},{"orcid":"0000-0002-1819-198X","first_name":"Attila","full_name":"György, Attila","id":"3BCEDBE0-F248-11E8-B48F-1D18A9856A87","last_name":"György"},{"first_name":"Alessandra M","full_name":"Casano, Alessandra M","orcid":"0000-0002-6009-6804","id":"3DBA3F4E-F248-11E8-B48F-1D18A9856A87","last_name":"Casano"},{"last_name":"Siekhaus","id":"3D224B9E-F248-11E8-B48F-1D18A9856A87","full_name":"Siekhaus, Daria E","first_name":"Daria E","orcid":"0000-0001-8323-8353"}],"article_type":"original","year":"2018","language":[{"iso":"eng"}],"day":"07","status":"public","date_published":"2018-05-07T00:00:00Z","publication":"Developmental Cell","citation":{"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.","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.","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.","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","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","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."},"intvolume":" 45","month":"05","oa_version":"Published Version","scopus_import":"1","doi":"10.1016/j.devcel.2018.04.002","type":"journal_article","article_processing_charge":"No","page":"331 - 346","acknowledged_ssus":[{"_id":"SSU"}],"publication_status":"published","isi":1,"title":"Drosophila TNF modulates tissue tension in the embryo to facilitate macrophage invasive migration","user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","quality_controlled":"1","_id":"308","publisher":"Elsevier","date_created":"2018-12-11T11:45:44Z","main_file_link":[{"url":"https://doi.org/10.1016/j.devcel.2018.04.002","open_access":"1"}],"external_id":{"isi":["000432461400009"],"pmid":["29738712"]},"date_updated":"2023-09-11T13:22:13Z","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"}],"ec_funded":1,"issue":"3","related_material":{"link":[{"relation":"press_release","description":"News on IST Homepage","url":"https://ist.ac.at/en/news/cells-change-tension-to-make-tissue-barriers-easier-to-get-through/"}]},"oa":1,"project":[{"_id":"253B6E48-B435-11E9-9278-68D0E5697425","call_identifier":"FWF","grant_number":"P29638","name":"Drosophila TNFa´s Funktion in Immunzellen"},{"call_identifier":"FP7","_id":"2536F660-B435-11E9-9278-68D0E5697425","name":"Investigating the role of transporters in invasive migration through junctions","grant_number":"334077"}]},{"article_number":"jcs207696","author":[{"first_name":"Wataru","full_name":"Yamamoto, Wataru","last_name":"Yamamoto"},{"last_name":"Wada","first_name":"Suguru","full_name":"Wada, Suguru"},{"last_name":"Nagano","first_name":"Makoto","full_name":"Nagano, Makoto"},{"last_name":"Aoshima","first_name":"Kaito","full_name":"Aoshima, Kaito"},{"first_name":"Daria E","full_name":"Siekhaus, Daria E","orcid":"0000-0001-8323-8353","id":"3D224B9E-F248-11E8-B48F-1D18A9856A87","last_name":"Siekhaus"},{"last_name":"Toshima","full_name":"Toshima, Junko","first_name":"Junko"},{"last_name":"Toshima","full_name":"Toshima, Jiro","first_name":"Jiro"}],"volume":131,"department":[{"_id":"DaSi"}],"pmid":1,"status":"public","language":[{"iso":"eng"}],"year":"2018","day":"04","citation":{"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.","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.","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.","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.","short":"W. Yamamoto, S. Wada, M. Nagano, K. Aoshima, D.E. Siekhaus, J. Toshima, J. Toshima, Journal of Cell Science 131 (2018).","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","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"},"date_published":"2018-01-04T00:00:00Z","publication":"Journal of Cell Science","scopus_import":"1","oa_version":"Published Version","intvolume":" 131","month":"01","publication_status":"published","type":"journal_article","doi":"10.1242/jcs.207696","article_processing_charge":"No","title":"Distinct roles for plasma membrane PtdIns 4 P and PtdIns 4 5 P2 during yeast receptor mediated endocytosis","user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","isi":1,"_id":"620","quality_controlled":"1","main_file_link":[{"url":"https://www.ncbi.nlm.nih.gov/pubmed/29192062","open_access":"1"}],"date_updated":"2023-09-11T12:57:13Z","external_id":{"isi":["000424786900012"],"pmid":["29192062"]},"publist_id":"7184","date_created":"2018-12-11T11:47:32Z","publisher":"Company of Biologists","issue":"1","oa":1,"abstract":[{"lang":"eng","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."}]},{"user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","title":"Rapid and reversible root growth inhibition by TIR1 auxin signalling","isi":1,"_id":"192","quality_controlled":"1","external_id":{"pmid":["29942048"],"isi":["000443221200017"]},"date_updated":"2023-09-15T12:11:03Z","main_file_link":[{"open_access":"1","url":"https://www.ncbi.nlm.nih.gov/pubmed/29942048"}],"publisher":"Springer Nature","date_created":"2018-12-11T11:45:07Z","publist_id":"7728","oa":1,"issue":"7","related_material":{"link":[{"description":"News on IST Homepage","relation":"press_release","url":"https://ist.ac.at/en/news/new-mechanism-for-the-plant-hormone-auxin-discovered/"}]},"abstract":[{"lang":"eng","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."}],"author":[{"orcid":"0000-0002-9767-8699","full_name":"Fendrych, Matyas","first_name":"Matyas","last_name":"Fendrych","id":"43905548-F248-11E8-B48F-1D18A9856A87"},{"id":"3425EC26-F248-11E8-B48F-1D18A9856A87","last_name":"Akhmanova","first_name":"Maria","full_name":"Akhmanova, Maria","orcid":"0000-0003-1522-3162"},{"id":"4515C308-F248-11E8-B48F-1D18A9856A87","last_name":"Merrin","orcid":"0000-0001-5145-4609","first_name":"Jack","full_name":"Merrin, Jack"},{"last_name":"Glanc","first_name":"Matous","full_name":"Glanc, Matous"},{"full_name":"Hagihara, Shinya","first_name":"Shinya","last_name":"Hagihara"},{"last_name":"Takahashi","first_name":"Koji","full_name":"Takahashi, Koji"},{"full_name":"Uchida, Naoyuki","first_name":"Naoyuki","last_name":"Uchida"},{"last_name":"Torii","full_name":"Torii, Keiko U","first_name":"Keiko U"},{"full_name":"Friml, Jirí","first_name":"Jirí","orcid":"0000-0002-8302-7596","last_name":"Friml","id":"4159519E-F248-11E8-B48F-1D18A9856A87"}],"department":[{"_id":"JiFr"},{"_id":"DaSi"},{"_id":"NanoFab"}],"pmid":1,"volume":4,"year":"2018","language":[{"iso":"eng"}],"day":"25","status":"public","article_type":"original","intvolume":" 4","month":"06","scopus_import":"1","oa_version":"Submitted Version","publication":"Nature Plants","date_published":"2018-06-25T00:00:00Z","citation":{"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.","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.","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.","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.","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.","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","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"},"page":"453 - 459","publication_status":"published","article_processing_charge":"No","type":"journal_article","doi":"10.1038/s41477-018-0190-1"},{"doi":"10.3390/ijms19113566","type":"journal_article","article_processing_charge":"No","tmp":{"image":"/images/cc_by.png","legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","short":"CC BY (4.0)","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)"},"publication_status":"published","date_published":"2018-11-12T00:00:00Z","publication":"International Journal of Molecular Sciences","citation":{"short":"S. Hille, M. Akhmanova, M. Glanc, A.J. Johnson, J. Friml, International Journal of Molecular Sciences 19 (2018).","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","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.","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.","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.","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)."},"month":"11","intvolume":" 19","file_date_updated":"2020-07-14T12:44:50Z","scopus_import":"1","oa_version":"Published Version","article_type":"original","has_accepted_license":"1","language":[{"iso":"eng"}],"year":"2018","day":"12","status":"public","volume":19,"department":[{"_id":"DaSi"},{"_id":"JiFr"}],"author":[{"first_name":"Sander","full_name":"Hille, Sander","last_name":"Hille"},{"orcid":"0000-0003-1522-3162","first_name":"Maria","full_name":"Akhmanova, Maria","id":"3425EC26-F248-11E8-B48F-1D18A9856A87","last_name":"Akhmanova"},{"id":"1AE1EA24-02D0-11E9-9BAA-DAF4881429F2","last_name":"Glanc","orcid":"0000-0003-0619-7783","first_name":"Matous","full_name":"Glanc, Matous"},{"id":"46A62C3A-F248-11E8-B48F-1D18A9856A87","last_name":"Johnson","orcid":"0000-0002-2739-8843","first_name":"Alexander J","full_name":"Johnson, Alexander J"},{"id":"4159519E-F248-11E8-B48F-1D18A9856A87","last_name":"Friml","orcid":"0000-0002-8302-7596","first_name":"Jirí","full_name":"Friml, Jirí"}],"abstract":[{"lang":"eng","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."}],"ddc":["580"],"ec_funded":1,"publication_identifier":{"eissn":["1422-0067"]},"issue":"11","oa":1,"project":[{"grant_number":"742985","name":"Tracing Evolution of Auxin Transport and Polarity in Plants","call_identifier":"H2020","_id":"261099A6-B435-11E9-9278-68D0E5697425"},{"call_identifier":"FWF","_id":"26538374-B435-11E9-9278-68D0E5697425","name":"Molecular mechanisms of endocytic cargo recognition in plants","grant_number":"I03630"}],"publist_id":"8042","publisher":"MDPI","date_created":"2018-12-11T11:44:09Z","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.","external_id":{"isi":["000451528500282"]},"date_updated":"2023-09-18T08:09:32Z","quality_controlled":"1","_id":"14","file":[{"relation":"main_file","date_updated":"2020-07-14T12:44:50Z","file_id":"5719","creator":"dernst","file_size":2200593,"date_created":"2018-12-17T16:04:11Z","checksum":"e4b59c2599b0ca26ebf5b8434bcde94a","access_level":"open_access","content_type":"application/pdf","file_name":"2018_IJMS_Hille.pdf"}],"isi":1,"title":"Relative contribution of PIN-containing secretory vesicles and plasma membrane PINs to the directed auxin transport: Theoretical estimation","user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1"},{"date_updated":"2023-09-07T12:43:10Z","publist_id":"8047","date_created":"2018-12-11T11:44:08Z","publisher":"Institute of Science and Technology Austria","oa":1,"ddc":["570"],"abstract":[{"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.","lang":"eng"}],"publication_identifier":{"issn":["2663-337X"]},"title":"Transcriptional regulation of macrophage migration in the Drosophila melanogaster embryo ","user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","file":[{"file_name":"2018_Thesis_Belyaeva_source.docx","content_type":"application/vnd.openxmlformats-officedocument.wordprocessingml.document","access_level":"closed","checksum":"d27b2465cb70d0c9678a0381b9b6ced1","date_created":"2019-04-08T14:13:12Z","file_size":102737483,"creator":"dernst","file_id":"6243","embargo_to":"open_access","relation":"source_file","date_updated":"2020-07-14T12:48:14Z"},{"checksum":"a2939b61bde2de7b8ced77bbae0eaaed","date_created":"2019-04-08T14:14:08Z","file_size":88077843,"creator":"dernst","file_id":"6244","relation":"main_file","date_updated":"2021-02-11T11:17:16Z","embargo":"2019-11-19","file_name":"2018_Thesis_Belyaeva.pdf","content_type":"application/pdf","access_level":"open_access"}],"alternative_title":["ISTA Thesis"],"_id":"9","degree_awarded":"PhD","citation":{"ieee":"V. Belyaeva, “Transcriptional regulation of macrophage migration in the Drosophila melanogaster embryo ,” Institute of Science and Technology Austria, 2018.","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.","ista":"Belyaeva V. 2018. Transcriptional regulation of macrophage migration in the Drosophila melanogaster embryo . Institute of Science and Technology Austria.","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.","ama":"Belyaeva V. Transcriptional regulation of macrophage migration in the Drosophila melanogaster embryo . 2018. doi:10.15479/AT:ISTA:th1064","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","short":"V. Belyaeva, Transcriptional Regulation of Macrophage Migration in the Drosophila Melanogaster Embryo , Institute of Science and Technology Austria, 2018."},"date_published":"2018-07-01T00:00:00Z","oa_version":"Published Version","file_date_updated":"2021-02-11T11:17:16Z","month":"07","publication_status":"published","page":"96","type":"dissertation","doi":"10.15479/AT:ISTA:th1064","article_processing_charge":"No","author":[{"id":"47F080FE-F248-11E8-B48F-1D18A9856A87","last_name":"Belyaeva","first_name":"Vera","full_name":"Belyaeva, Vera"}],"supervisor":[{"full_name":"Siekhaus, Daria E","first_name":"Daria E","orcid":"0000-0001-8323-8353","last_name":"Siekhaus","id":"3D224B9E-F248-11E8-B48F-1D18A9856A87"}],"department":[{"_id":"DaSi"}],"status":"public","year":"2018","language":[{"iso":"eng"}],"day":"01","pubrep_id":"1064","has_accepted_license":"1"},{"tmp":{"image":"/images/cc_by.png","legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","short":"CC BY (4.0)","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)"},"acknowledged_ssus":[{"_id":"LifeSc"}],"page":"845 - 857","publication_status":"published","doi":"10.1534/g3.117.300452","type":"journal_article","article_processing_charge":"No","date_published":"2018-03-01T00:00:00Z","publication":"G3: Genes, Genomes, Genetics","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.","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","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.","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.","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.","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."},"file_date_updated":"2020-07-14T12:46:56Z","month":"03","intvolume":" 8","oa_version":"Published Version","scopus_import":"1","language":[{"iso":"eng"}],"year":"2018","day":"01","status":"public","has_accepted_license":"1","pubrep_id":"990","author":[{"orcid":"0000-0002-1819-198X","full_name":"György, Attila","first_name":"Attila","last_name":"György","id":"3BCEDBE0-F248-11E8-B48F-1D18A9856A87"},{"first_name":"Marko","full_name":"Roblek, Marko","orcid":"0000-0001-9588-1389","id":"3047D808-F248-11E8-B48F-1D18A9856A87","last_name":"Roblek"},{"last_name":"Ratheesh","id":"2F064CFE-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0001-7190-0776","full_name":"Ratheesh, Aparna","first_name":"Aparna"},{"full_name":"Valosková, Katarina","first_name":"Katarina","last_name":"Valosková","id":"46F146FC-F248-11E8-B48F-1D18A9856A87"},{"first_name":"Vera","full_name":"Belyaeva, Vera","id":"47F080FE-F248-11E8-B48F-1D18A9856A87","last_name":"Belyaeva"},{"full_name":"Wachner, Stephanie","first_name":"Stephanie","last_name":"Wachner","id":"2A95E7B0-F248-11E8-B48F-1D18A9856A87"},{"last_name":"Matsubayashi","first_name":"Yutaka","full_name":"Matsubayashi, Yutaka"},{"first_name":"Besaiz","full_name":"Sanchez Sanchez, Besaiz","last_name":"Sanchez Sanchez"},{"last_name":"Stramer","first_name":"Brian","full_name":"Stramer, Brian"},{"id":"3D224B9E-F248-11E8-B48F-1D18A9856A87","last_name":"Siekhaus","orcid":"0000-0001-8323-8353","first_name":"Daria E","full_name":"Siekhaus, Daria E"}],"volume":8,"department":[{"_id":"DaSi"}],"issue":"3","related_material":{"record":[{"relation":"research_paper","id":"6530"},{"id":"6543","relation":"research_paper"},{"id":"11193","relation":"dissertation_contains","status":"public"},{"relation":"dissertation_contains","status":"public","id":"6546"}]},"oa":1,"project":[{"name":"Drosophila TNFa´s Funktion in Immunzellen","grant_number":"P29638","call_identifier":"FWF","_id":"253B6E48-B435-11E9-9278-68D0E5697425"},{"grant_number":"P29638","name":"The role of Drosophila TNF alpha in immune cell invasion","call_identifier":"FWF","_id":"253B6E48-B435-11E9-9278-68D0E5697425"},{"_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 "},{"call_identifier":"FP7","_id":"2536F660-B435-11E9-9278-68D0E5697425","name":"Investigating the role of transporters in invasive migration through junctions","grant_number":"334077"}],"abstract":[{"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.","lang":"eng"}],"ddc":["570"],"ec_funded":1,"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, ","external_id":{"isi":["000426693300011"]},"date_updated":"2024-03-29T23:30:29Z","publist_id":"7271","publisher":"Genetics Society of America","date_created":"2018-12-11T11:47:05Z","_id":"544","quality_controlled":"1","title":"Tools allowing independent visualization and genetic manipulation of Drosophila melanogaster macrophages and surrounding tissues","user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","file":[{"date_created":"2018-12-12T10:11:48Z","checksum":"7d9d28b915159078a4ca7add568010e8","file_size":2251222,"creator":"system","file_id":"4905","relation":"main_file","date_updated":"2020-07-14T12:46:56Z","file_name":"IST-2018-990-v1+1_2018_Gyoergy_Tools_allowing.pdf","content_type":"application/pdf","access_level":"open_access"}],"isi":1},{"has_accepted_license":"1","pubrep_id":"875","status":"public","year":"2017","language":[{"iso":"eng"}],"day":"09","volume":27,"department":[{"_id":"DaSi"}],"author":[{"last_name":"Matsubayashi","first_name":"Yutaka","full_name":"Matsubayashi, Yutaka"},{"first_name":"Adam","full_name":"Louani, Adam","last_name":"Louani"},{"full_name":"Dragu, Anca","first_name":"Anca","last_name":"Dragu"},{"full_name":"Sanchez Sanchez, Besaiz","first_name":"Besaiz","last_name":"Sanchez Sanchez"},{"first_name":"Eduardo","full_name":"Serna Morales, Eduardo","last_name":"Serna Morales"},{"last_name":"Yolland","full_name":"Yolland, Lawrence","first_name":"Lawrence"},{"id":"3BCEDBE0-F248-11E8-B48F-1D18A9856A87","last_name":"György","first_name":"Attila","full_name":"György, Attila","orcid":"0000-0002-1819-198X"},{"first_name":"Gema","full_name":"Vizcay, Gema","last_name":"Vizcay"},{"last_name":"Fleck","first_name":"Roland","full_name":"Fleck, Roland"},{"last_name":"Heddleston","first_name":"John","full_name":"Heddleston, John"},{"full_name":"Chew, Teng","first_name":"Teng","last_name":"Chew"},{"id":"3D224B9E-F248-11E8-B48F-1D18A9856A87","last_name":"Siekhaus","orcid":"0000-0001-8323-8353","first_name":"Daria E","full_name":"Siekhaus, Daria E"},{"first_name":"Brian","full_name":"Stramer, Brian","last_name":"Stramer"}],"doi":"10.1016/j.cub.2017.10.001","type":"journal_article","article_processing_charge":"No","publication_status":"published","tmp":{"image":"/images/cc_by.png","legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","short":"CC BY (4.0)","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)"},"page":"3526 - 3534e.4","citation":{"ieee":"Y. Matsubayashi et al., “A moving source of matrix components is essential for De Novo basement membrane formation,” Current Biology, vol. 27, no. 22. Cell Press, p. 3526–3534e.4, 2017.","ista":"Matsubayashi Y, Louani A, Dragu A, Sanchez Sanchez B, Serna Morales E, Yolland L, György A, Vizcay G, Fleck R, Heddleston J, Chew T, Siekhaus DE, Stramer B. 2017. A moving source of matrix components is essential for De Novo basement membrane formation. Current Biology. 27(22), 3526–3534e.4.","mla":"Matsubayashi, Yutaka, et al. “A Moving Source of Matrix Components Is Essential for De Novo Basement Membrane Formation.” Current Biology, vol. 27, no. 22, Cell Press, 2017, p. 3526–3534e.4, doi:10.1016/j.cub.2017.10.001.","apa":"Matsubayashi, Y., Louani, A., Dragu, A., Sanchez Sanchez, B., Serna Morales, E., Yolland, L., … Stramer, B. (2017). A moving source of matrix components is essential for De Novo basement membrane formation. Current Biology. Cell Press. https://doi.org/10.1016/j.cub.2017.10.001","ama":"Matsubayashi Y, Louani A, Dragu A, et al. A moving source of matrix components is essential for De Novo basement membrane formation. Current Biology. 2017;27(22):3526-3534e.4. doi:10.1016/j.cub.2017.10.001","short":"Y. Matsubayashi, A. Louani, A. Dragu, B. Sanchez Sanchez, E. Serna Morales, L. Yolland, A. György, G. Vizcay, R. Fleck, J. Heddleston, T. Chew, D.E. Siekhaus, B. Stramer, Current Biology 27 (2017) 3526–3534e.4.","chicago":"Matsubayashi, Yutaka, Adam Louani, Anca Dragu, Besaiz Sanchez Sanchez, Eduardo Serna Morales, Lawrence Yolland, Attila György, et al. “A Moving Source of Matrix Components Is Essential for De Novo Basement Membrane Formation.” Current Biology. Cell Press, 2017. https://doi.org/10.1016/j.cub.2017.10.001."},"date_published":"2017-11-09T00:00:00Z","publication":"Current Biology","oa_version":"Published Version","scopus_import":"1","intvolume":" 27","month":"11","file_date_updated":"2020-07-14T12:47:59Z","quality_controlled":"1","_id":"751","isi":1,"file":[{"access_level":"open_access","content_type":"application/pdf","file_name":"IST-2017-875-v1+1_1-s2.0-S0960982217312691-main.pdf","date_updated":"2020-07-14T12:47:59Z","relation":"main_file","file_id":"4770","creator":"system","file_size":4770657,"checksum":"264cf6c6c3551486ba5ea786850e000a","date_created":"2018-12-12T10:09:45Z"}],"title":"A moving source of matrix components is essential for De Novo basement membrane formation","user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","abstract":[{"lang":"eng","text":"The basement membrane (BM) is a thin layer of extracellular matrix (ECM) beneath nearly all epithelial cell types that is critical for cellular and tissue function. It is composed of numerous components conserved among all bilaterians [1]; however, it is unknown how all of these components are generated and subsequently constructed to form a fully mature BM in the living animal. Although BM formation is thought to simply involve a process of self-assembly [2], this concept suffers from a number of logistical issues when considering its construction in vivo. First, incorporation of BM components appears to be hierarchical [3-5], yet it is unclear whether their production during embryogenesis must also be regulated in a temporal fashion. Second, many BM proteins are produced not only by the cells residing on the BM but also by surrounding cell types [6-9], and it is unclear how large, possibly insoluble protein complexes [10] are delivered into the matrix. Here we exploit our ability to live image and genetically dissect de novo BM formation during Drosophila development. This reveals that there is a temporal hierarchy of BM protein production that is essential for proper component incorporation. Furthermore, we show that BM components require secretion by migrating macrophages (hemocytes) during their developmental dispersal, which is critical for embryogenesis. Indeed, hemocyte migration is essential to deliver a subset of ECM components evenly throughout the embryo. This reveals that de novo BM construction requires a combination of both production and distribution logistics allowing for the timely delivery of core components."}],"ddc":["570","576"],"publication_identifier":{"issn":["09609822"]},"issue":"22","oa":1,"publist_id":"6905","date_created":"2018-12-11T11:48:18Z","publisher":"Cell Press","date_updated":"2023-09-27T12:25:31Z","external_id":{"isi":["000415815800031"]}},{"publication_status":"published","page":"367 - 379","doi":"10.1242/jcs.176651","type":"journal_article","oa_version":"Published Version","scopus_import":1,"file_date_updated":"2020-07-14T12:44:56Z","month":"01","intvolume":" 129","citation":{"ista":"Toshima J, Horikomi C, Okada A, Hatori M, Nagano M, Masuda A, Yamamoto W, Siekhaus DE, Toshima J. 2016. Srv2/CAP is required for polarized actin cable assembly and patch internalization during clathrin-mediated endocytosis. Journal of Cell Science. 129(2), 367–379.","ieee":"J. Toshima et al., “Srv2/CAP is required for polarized actin cable assembly and patch internalization during clathrin-mediated endocytosis,” Journal of Cell Science, vol. 129, no. 2. Company of Biologists, pp. 367–379, 2016.","mla":"Toshima, Junko, et al. “Srv2/CAP Is Required for Polarized Actin Cable Assembly and Patch Internalization during Clathrin-Mediated Endocytosis.” Journal of Cell Science, vol. 129, no. 2, Company of Biologists, 2016, pp. 367–79, doi:10.1242/jcs.176651.","apa":"Toshima, J., Horikomi, C., Okada, A., Hatori, M., Nagano, M., Masuda, A., … Toshima, J. (2016). Srv2/CAP is required for polarized actin cable assembly and patch internalization during clathrin-mediated endocytosis. Journal of Cell Science. Company of Biologists. https://doi.org/10.1242/jcs.176651","ama":"Toshima J, Horikomi C, Okada A, et al. Srv2/CAP is required for polarized actin cable assembly and patch internalization during clathrin-mediated endocytosis. Journal of Cell Science. 2016;129(2):367-379. doi:10.1242/jcs.176651","short":"J. Toshima, C. Horikomi, A. Okada, M. Hatori, M. Nagano, A. Masuda, W. Yamamoto, D.E. Siekhaus, J. Toshima, Journal of Cell Science 129 (2016) 367–379.","chicago":"Toshima, Junko, Chika Horikomi, Asuka Okada, Makiko Hatori, Makoto Nagano, Atsushi Masuda, Wataru Yamamoto, Daria E Siekhaus, and Jiro Toshima. “Srv2/CAP Is Required for Polarized Actin Cable Assembly and Patch Internalization during Clathrin-Mediated Endocytosis.” Journal of Cell Science. Company of Biologists, 2016. https://doi.org/10.1242/jcs.176651."},"publication":"Journal of Cell Science","date_published":"2016-01-15T00:00:00Z","status":"public","year":"2016","language":[{"iso":"eng"}],"day":"15","pubrep_id":"767","has_accepted_license":"1","author":[{"last_name":"Toshima","first_name":"Junko","full_name":"Toshima, Junko"},{"full_name":"Horikomi, Chika","first_name":"Chika","last_name":"Horikomi"},{"last_name":"Okada","full_name":"Okada, Asuka","first_name":"Asuka"},{"first_name":"Makiko","full_name":"Hatori, Makiko","last_name":"Hatori"},{"last_name":"Nagano","first_name":"Makoto","full_name":"Nagano, Makoto"},{"full_name":"Masuda, Atsushi","first_name":"Atsushi","last_name":"Masuda"},{"full_name":"Yamamoto, Wataru","first_name":"Wataru","last_name":"Yamamoto"},{"full_name":"Siekhaus, Daria E","first_name":"Daria E","orcid":"0000-0001-8323-8353","last_name":"Siekhaus","id":"3D224B9E-F248-11E8-B48F-1D18A9856A87"},{"first_name":"Jiro","full_name":"Toshima, Jiro","last_name":"Toshima"}],"department":[{"_id":"DaSi"}],"volume":129,"oa":1,"project":[{"name":"Investigating the role of transporters in invasive migration through junctions","grant_number":"334077","call_identifier":"FP7","_id":"2536F660-B435-11E9-9278-68D0E5697425"}],"issue":"2","ec_funded":1,"ddc":["570","576"],"abstract":[{"lang":"eng","text":"The dynamic assembly and disassembly of actin filaments is essential for the formation and transport of vesicles during endocytosis. In yeast, two types of actin structures, namely cortical patches and cytoplasmic cables, play a direct role in endocytosis, but how their interaction is regulated remains unclear. Here, we show that Srv2/CAP, an evolutionarily conserved actin regulator, is required for efficient endocytosis owing to its role in the formation of the actin patches that aid initial vesicle invagination and of the actin cables that these move along. Deletion of the SRV2 gene resulted in the appearance of aberrant fragmented actin cables that frequently moved past actin patches, the sites of endocytosis. We find that the C-terminal CARP domain of Srv2p is vitally important for the proper assembly of actin patches and cables; we also demonstrate that the N-terminal helical folded domain of Srv2 is required for its localization to actin patches, specifically to the ADP-actin rich region through an interaction with cofilin. These results demonstrate the in vivo roles of Srv2p in the regulation of the actin cytoskeleton during clathrin-mediated endocytosis"}],"date_updated":"2021-01-12T06:51:00Z","acknowledgement":"We are grateful to Anthony Bretscher (Cornell University, NY) for providing the bni1-12 bnr1Δ (Y4135) strain. J.Y.T. was supported by a Japan Society for the Promotion of Science (JSPS) KAKENHI grant [grant number 26440067]; the Takeda Science Foundation; and the Novartis Foundation (Japan). J.T. was supported by a JSPS KAKENHI grant [grant number 25440054]; the Takeda Science Foundation; and the Kurata Memorial Hitachi Science and Technology Foundation. D.E.S. was supported by the European Union [grant number PCIG12-GA-2012-334077].","date_created":"2018-12-11T11:52:14Z","publisher":"Company of Biologists","publist_id":"5720","_id":"1476","quality_controlled":"1","user_id":"3E5EF7F0-F248-11E8-B48F-1D18A9856A87","title":"Srv2/CAP is required for polarized actin cable assembly and patch internalization during clathrin-mediated endocytosis","file":[{"file_name":"IST-2017-767-v1+1_367.full.pdf","access_level":"open_access","content_type":"application/pdf","checksum":"2da0a09149a9ed956cdf79a95c17f08a","date_created":"2018-12-12T10:11:08Z","file_size":7176912,"relation":"main_file","date_updated":"2020-07-14T12:44:56Z","creator":"system","file_id":"4861"}]},{"oa":1,"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":"February 2016","ec_funded":1,"abstract":[{"lang":"eng","text":"The actin cytoskeleton plays important roles in the formation and internalization of endocytic vesicles. In yeast, endocytic vesicles move towards early endosomes along actin cables, however, the molecular machinery regulating interaction between endocytic vesicles and actin cables is poorly understood. The Eps15-like protein Pan1p plays a key role in actin-mediated endocytosis and is negatively regulated by Ark1 and Prk1 kinases. Here we show that pan1 mutated to prevent phosphorylation at all 18 threonines, pan1-18TA, displayed almost the same endocytic defect as ark1Δ prk1Δ cells, and contained abnormal actin concentrations including several endocytic compartments. Early endosomes were highly localized in the actin concentrations and displayed movement along actin cables. The dephosphorylated form of Pan1p also caused stable associations between endocytic vesicles and actin cables, and between endocytic vesicles and endosomes. Thus Pan1 phosphorylation is part of a novel mechanism that regulates endocytic compartment interactions with each other and with actin cables."}],"ddc":["570"],"date_updated":"2021-01-12T06:50:59Z","date_created":"2018-12-11T11:52:14Z","publisher":"eLife Sciences Publications","publist_id":"5721","_id":"1475","quality_controlled":"1","user_id":"3E5EF7F0-F248-11E8-B48F-1D18A9856A87","title":"Yeast Eps15-like endocytic protein Pan1p regulates the interaction between endocytic vesicles, endosomes and the actin cytoskeleton","file":[{"date_updated":"2020-07-14T12:44:56Z","relation":"main_file","file_id":"4793","creator":"system","file_size":5198001,"checksum":"d1cc44870580756ba8badd8e41adfdb5","date_created":"2018-12-12T10:10:08Z","access_level":"open_access","content_type":"application/pdf","file_name":"IST-2016-529-v1+1_elife-10276-v1.pdf"}],"publication_status":"published","tmp":{"image":"/images/cc_by.png","legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","short":"CC BY (4.0)","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)"},"type":"journal_article","doi":"10.7554/eLife.10276","scopus_import":1,"oa_version":"Published Version","intvolume":" 5","month":"02","file_date_updated":"2020-07-14T12:44:56Z","citation":{"chicago":"Toshima, Junko, Eri Furuya, Makoto Nagano, Chisa Kanno, Yuta Sakamoto, Masashi Ebihara, Daria E Siekhaus, and Jiro Toshima. “Yeast Eps15-like Endocytic Protein Pan1p Regulates the Interaction between Endocytic Vesicles, Endosomes and the Actin Cytoskeleton.” ELife. eLife Sciences Publications, 2016. https://doi.org/10.7554/eLife.10276.","short":"J. Toshima, E. Furuya, M. Nagano, C. Kanno, Y. Sakamoto, M. Ebihara, D.E. Siekhaus, J. Toshima, ELife 5 (2016).","apa":"Toshima, J., Furuya, E., Nagano, M., Kanno, C., Sakamoto, Y., Ebihara, M., … Toshima, J. (2016). Yeast Eps15-like endocytic protein Pan1p regulates the interaction between endocytic vesicles, endosomes and the actin cytoskeleton. ELife. eLife Sciences Publications. https://doi.org/10.7554/eLife.10276","ama":"Toshima J, Furuya E, Nagano M, et al. Yeast Eps15-like endocytic protein Pan1p regulates the interaction between endocytic vesicles, endosomes and the actin cytoskeleton. eLife. 2016;5(February 2016). doi:10.7554/eLife.10276","mla":"Toshima, Junko, et al. “Yeast Eps15-like Endocytic Protein Pan1p Regulates the Interaction between Endocytic Vesicles, Endosomes and the Actin Cytoskeleton.” ELife, vol. 5, no. February 2016, e10276, eLife Sciences Publications, 2016, doi:10.7554/eLife.10276.","ista":"Toshima J, Furuya E, Nagano M, Kanno C, Sakamoto Y, Ebihara M, Siekhaus DE, Toshima J. 2016. Yeast Eps15-like endocytic protein Pan1p regulates the interaction between endocytic vesicles, endosomes and the actin cytoskeleton. eLife. 5(February 2016), e10276.","ieee":"J. Toshima et al., “Yeast Eps15-like endocytic protein Pan1p regulates the interaction between endocytic vesicles, endosomes and the actin cytoskeleton,” eLife, vol. 5, no. February 2016. eLife Sciences Publications, 2016."},"publication":"eLife","date_published":"2016-02-25T00:00:00Z","status":"public","language":[{"iso":"eng"}],"day":"25","year":"2016","pubrep_id":"529","has_accepted_license":"1","author":[{"last_name":"Toshima","full_name":"Toshima, Junko","first_name":"Junko"},{"first_name":"Eri","full_name":"Furuya, Eri","last_name":"Furuya"},{"last_name":"Nagano","first_name":"Makoto","full_name":"Nagano, Makoto"},{"first_name":"Chisa","full_name":"Kanno, Chisa","last_name":"Kanno"},{"full_name":"Sakamoto, Yuta","first_name":"Yuta","last_name":"Sakamoto"},{"full_name":"Ebihara, Masashi","first_name":"Masashi","last_name":"Ebihara"},{"first_name":"Daria E","full_name":"Siekhaus, Daria E","orcid":"0000-0001-8323-8353","id":"3D224B9E-F248-11E8-B48F-1D18A9856A87","last_name":"Siekhaus"},{"last_name":"Toshima","first_name":"Jiro","full_name":"Toshima, Jiro"}],"article_number":"e10276","department":[{"_id":"DaSi"}],"volume":5},{"_id":"1712","quality_controlled":"1","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","title":"Drosophila immune cell migration and adhesion during embryonic development and larval immune responses","file":[{"file_name":"IST-2015-346-v1+1_Current_Opinion_Review_Ratheesh_et_al_2015.pdf","content_type":"application/pdf","access_level":"open_access","date_created":"2018-12-12T10:14:44Z","checksum":"bbb1ee39ca52929aefe4f48752b166ee","file_size":1023680,"creator":"system","file_id":"5098","date_updated":"2020-07-14T12:45:13Z","relation":"main_file"}],"project":[{"_id":"2536F660-B435-11E9-9278-68D0E5697425","call_identifier":"FP7","name":"Investigating the role of transporters in invasive migration through junctions","grant_number":"334077"}],"oa":1,"issue":"10","ec_funded":1,"ddc":["573"],"abstract":[{"lang":"eng","text":"The majority of immune cells in Drosophila melanogaster are plasmatocytes; they carry out similar functions to vertebrate macrophages, influencing development as well as protecting against infection and cancer. Plasmatocytes, sometimes referred to with the broader term of hemocytes, migrate widely during embryonic development and cycle in the larvae between sessile and circulating positions. Here we discuss the similarities of plasmatocyte developmental migration and its functions to that of vertebrate macrophages, considering the recent controversy regarding the functions of Drosophila PDGF/VEGF related ligands. We also examine recent findings on the significance of adhesion for plasmatocyte migration in the embryo, as well as proliferation, trans-differentiation, and tumor responses in the larva. We spotlight parallels throughout to vertebrate immune responses."}],"date_updated":"2021-01-12T06:52:41Z","date_created":"2018-12-11T11:53:36Z","publisher":"Elsevier","publist_id":"5421","status":"public","year":"2015","day":"01","language":[{"iso":"eng"}],"pubrep_id":"346","has_accepted_license":"1","author":[{"last_name":"Ratheesh","id":"2F064CFE-F248-11E8-B48F-1D18A9856A87","full_name":"Ratheesh, Aparna","first_name":"Aparna"},{"first_name":"Vera","full_name":"Belyaeva, Vera","id":"47F080FE-F248-11E8-B48F-1D18A9856A87","last_name":"Belyaeva"},{"full_name":"Siekhaus, Daria E","first_name":"Daria E","orcid":"0000-0001-8323-8353","last_name":"Siekhaus","id":"3D224B9E-F248-11E8-B48F-1D18A9856A87"}],"department":[{"_id":"DaSi"}],"volume":36,"publication_status":"published","page":"71 - 79","tmp":{"image":"/images/cc_by_nc_nd.png","short":"CC BY-NC-ND (4.0)","name":"Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0)","legal_code_url":"https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode"},"doi":"10.1016/j.ceb.2015.07.003","type":"journal_article","scopus_import":1,"oa_version":"Published Version","file_date_updated":"2020-07-14T12:45:13Z","intvolume":" 36","month":"10","citation":{"ista":"Ratheesh A, Belyaeva V, Siekhaus DE. 2015. Drosophila immune cell migration and adhesion during embryonic development and larval immune responses. Current Opinion in Cell Biology. 36(10), 71–79.","mla":"Ratheesh, Aparna, et al. “Drosophila Immune Cell Migration and Adhesion during Embryonic Development and Larval Immune Responses.” Current Opinion in Cell Biology, vol. 36, no. 10, Elsevier, 2015, pp. 71–79, doi:10.1016/j.ceb.2015.07.003.","ieee":"A. Ratheesh, V. Belyaeva, and D. E. Siekhaus, “Drosophila immune cell migration and adhesion during embryonic development and larval immune responses,” Current Opinion in Cell Biology, vol. 36, no. 10. Elsevier, pp. 71–79, 2015.","chicago":"Ratheesh, Aparna, Vera Belyaeva, and Daria E Siekhaus. “Drosophila Immune Cell Migration and Adhesion during Embryonic Development and Larval Immune Responses.” Current Opinion in Cell Biology. Elsevier, 2015. https://doi.org/10.1016/j.ceb.2015.07.003.","ama":"Ratheesh A, Belyaeva V, Siekhaus DE. Drosophila immune cell migration and adhesion during embryonic development and larval immune responses. Current Opinion in Cell Biology. 2015;36(10):71-79. doi:10.1016/j.ceb.2015.07.003","apa":"Ratheesh, A., Belyaeva, V., & Siekhaus, D. E. (2015). Drosophila immune cell migration and adhesion during embryonic development and larval immune responses. Current Opinion in Cell Biology. Elsevier. https://doi.org/10.1016/j.ceb.2015.07.003","short":"A. Ratheesh, V. Belyaeva, D.E. Siekhaus, Current Opinion in Cell Biology 36 (2015) 71–79."},"publication":"Current Opinion in Cell Biology","date_published":"2015-10-01T00:00:00Z"},{"author":[{"last_name":"Kawada","first_name":"Daiki","full_name":"Kawada, Daiki"},{"first_name":"Hiromu","full_name":"Kobayashi, Hiromu","last_name":"Kobayashi"},{"last_name":"Tomita","full_name":"Tomita, Tsuyoshi","first_name":"Tsuyoshi"},{"full_name":"Nakata, Eisuke","first_name":"Eisuke","last_name":"Nakata"},{"last_name":"Nagano","first_name":"Makoto","full_name":"Nagano, Makoto"},{"first_name":"Daria E","full_name":"Siekhaus, Daria E","orcid":"0000-0001-8323-8353","id":"3D224B9E-F248-11E8-B48F-1D18A9856A87","last_name":"Siekhaus"},{"first_name":"Junko","full_name":"Toshima, Junko","last_name":"Toshima"},{"last_name":"Toshimaa","full_name":"Toshimaa, Jiro","first_name":"Jiro"}],"volume":1853,"department":[{"_id":"DaSi"}],"status":"public","day":"01","language":[{"iso":"eng"}],"year":"2015","has_accepted_license":"1","pubrep_id":"615","citation":{"mla":"Kawada, Daiki, et al. “The Yeast Arf-GAP Glo3p Is Required for the Endocytic Recycling of Cell Surface Proteins.” Biochimica et Biophysica Acta - Molecular Cell Research, vol. 1853, no. 1, Elsevier, 2015, pp. 144–56, doi:10.1016/j.bbamcr.2014.10.009.","ieee":"D. Kawada et al., “The yeast Arf-GAP Glo3p is required for the endocytic recycling of cell surface proteins,” Biochimica et Biophysica Acta - Molecular Cell Research, vol. 1853, no. 1. Elsevier, pp. 144–156, 2015.","ista":"Kawada D, Kobayashi H, Tomita T, Nakata E, Nagano M, Siekhaus DE, Toshima J, Toshimaa J. 2015. The yeast Arf-GAP Glo3p is required for the endocytic recycling of cell surface proteins. Biochimica et Biophysica Acta - Molecular Cell Research. 1853(1), 144–156.","short":"D. Kawada, H. Kobayashi, T. Tomita, E. Nakata, M. Nagano, D.E. Siekhaus, J. Toshima, J. Toshimaa, Biochimica et Biophysica Acta - Molecular Cell Research 1853 (2015) 144–156.","ama":"Kawada D, Kobayashi H, Tomita T, et al. The yeast Arf-GAP Glo3p is required for the endocytic recycling of cell surface proteins. Biochimica et Biophysica Acta - Molecular Cell Research. 2015;1853(1):144-156. doi:10.1016/j.bbamcr.2014.10.009","apa":"Kawada, D., Kobayashi, H., Tomita, T., Nakata, E., Nagano, M., Siekhaus, D. E., … Toshimaa, J. (2015). The yeast Arf-GAP Glo3p is required for the endocytic recycling of cell surface proteins. Biochimica et Biophysica Acta - Molecular Cell Research. Elsevier. https://doi.org/10.1016/j.bbamcr.2014.10.009","chicago":"Kawada, Daiki, Hiromu Kobayashi, Tsuyoshi Tomita, Eisuke Nakata, Makoto Nagano, Daria E Siekhaus, Junko Toshima, and Jiro Toshimaa. “The Yeast Arf-GAP Glo3p Is Required for the Endocytic Recycling of Cell Surface Proteins.” Biochimica et Biophysica Acta - Molecular Cell Research. Elsevier, 2015. https://doi.org/10.1016/j.bbamcr.2014.10.009."},"publication":"Biochimica et Biophysica Acta - Molecular Cell Research","date_published":"2015-01-01T00:00:00Z","oa_version":"Submitted Version","scopus_import":1,"month":"01","file_date_updated":"2020-07-14T12:45:25Z","intvolume":" 1853","publication_status":"published","page":"144 - 156","tmp":{"image":"/images/cc_by_nc_nd.png","short":"CC BY-NC-ND (4.0)","name":"Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0)","legal_code_url":"https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode"},"type":"journal_article","doi":"10.1016/j.bbamcr.2014.10.009","title":"The yeast Arf-GAP Glo3p is required for the endocytic recycling of cell surface proteins","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","file":[{"file_name":"IST-2016-615-v1+1_BBAMCR.pdf","content_type":"application/pdf","access_level":"open_access","file_size":926685,"date_created":"2018-12-12T10:12:18Z","checksum":"5bb328edebb6a91337cadd7d63f961b7","file_id":"4936","creator":"system","relation":"main_file","date_updated":"2020-07-14T12:45:25Z"}],"_id":"2025","quality_controlled":"1","date_updated":"2021-01-12T06:54:48Z","publist_id":"5047","date_created":"2018-12-11T11:55:17Z","publisher":"Elsevier","issue":"1","oa":1,"abstract":[{"text":"Small GTP-binding proteins of the Ras superfamily play diverse roles in intracellular trafficking. Among them, the Rab, Arf, and Rho families function in successive steps of vesicle transport, in forming vesicles from donor membranes, directing vesicle trafficking toward target membranes and docking vesicles onto target membranes. These proteins act as molecular switches that are controlled by a cycle of GTP binding and hydrolysis regulated by guanine nucleotide exchange factors (GEFs) and GTPase-activating proteins (GAPs). In this study we explored the role of GAPs in the regulation of the endocytic pathway using fluorescently labeled yeast mating pheromone α-factor. Among 25 non-essential GAP mutants, we found that deletion of the GLO3 gene, encoding Arf-GAP protein, caused defective internalization of fluorescently labeled α-factor. Quantitative analysis revealed that glo3Δ cells show defective α-factor binding to the cell surface. Interestingly, Ste2p, the α-factor receptor, was mis-localized from the plasma membrane to the vacuole in glo3Δ cells. Domain deletion mutants of Glo3p revealed that a GAP-independent function, as well as the GAP activity, of Glo3p is important for both α-factor binding and Ste2p localization at the cell surface. Additionally, we found that deletion of the GLO3 gene affects the size and number of Arf1p-residing Golgi compartments and causes a defect in transport from the TGN to the plasma membrane. Furthermore, we demonstrated that glo3Δ cells were defective in the late endosome-to-TGN transport pathway, but not in the early endosome-to-TGN transport pathway. These findings suggest novel roles for Arf-GAP Glo3p in endocytic recycling of cell surface proteins.","lang":"eng"}],"ddc":["570"]},{"language":[{"iso":"eng"}],"day":"25","year":"2014","status":"public","has_accepted_license":"1","pubrep_id":"616","author":[{"last_name":"Toshima","full_name":"Toshima, Junko","first_name":"Junko"},{"full_name":"Nishinoaki, Show","first_name":"Show","last_name":"Nishinoaki"},{"last_name":"Sato","full_name":"Sato, Yoshifumi","first_name":"Yoshifumi"},{"full_name":"Yamamoto, Wataru","first_name":"Wataru","last_name":"Yamamoto"},{"first_name":"Daiki","full_name":"Furukawa, Daiki","last_name":"Furukawa"},{"last_name":"Siekhaus","id":"3D224B9E-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0001-8323-8353","full_name":"Siekhaus, Daria E","first_name":"Daria E"},{"last_name":"Sawaguchi","first_name":"Akira","full_name":"Sawaguchi, Akira"},{"full_name":"Toshima, Jiro","first_name":"Jiro","last_name":"Toshima"}],"article_number":"3498","department":[{"_id":"DaSi"}],"volume":5,"publication_status":"published","type":"journal_article","doi":"10.1038/ncomms4498","month":"03","file_date_updated":"2020-07-14T12:45:25Z","intvolume":" 5","scopus_import":1,"oa_version":"Submitted Version","date_published":"2014-03-25T00:00:00Z","publication":"Nature Communications","citation":{"ama":"Toshima J, Nishinoaki S, Sato Y, et al. Bifurcation of the endocytic pathway into Rab5-dependent and -independent transport to the vacuole. Nature Communications. 2014;5. doi:10.1038/ncomms4498","apa":"Toshima, J., Nishinoaki, S., Sato, Y., Yamamoto, W., Furukawa, D., Siekhaus, D. E., … Toshima, J. (2014). Bifurcation of the endocytic pathway into Rab5-dependent and -independent transport to the vacuole. Nature Communications. Nature Publishing Group. https://doi.org/10.1038/ncomms4498","short":"J. Toshima, S. Nishinoaki, Y. Sato, W. Yamamoto, D. Furukawa, D.E. Siekhaus, A. Sawaguchi, J. Toshima, Nature Communications 5 (2014).","chicago":"Toshima, Junko, Show Nishinoaki, Yoshifumi Sato, Wataru Yamamoto, Daiki Furukawa, Daria E Siekhaus, Akira Sawaguchi, and Jiro Toshima. “Bifurcation of the Endocytic Pathway into Rab5-Dependent and -Independent Transport to the Vacuole.” Nature Communications. Nature Publishing Group, 2014. https://doi.org/10.1038/ncomms4498.","ista":"Toshima J, Nishinoaki S, Sato Y, Yamamoto W, Furukawa D, Siekhaus DE, Sawaguchi A, Toshima J. 2014. Bifurcation of the endocytic pathway into Rab5-dependent and -independent transport to the vacuole. Nature Communications. 5, 3498.","ieee":"J. Toshima et al., “Bifurcation of the endocytic pathway into Rab5-dependent and -independent transport to the vacuole,” Nature Communications, vol. 5. Nature Publishing Group, 2014.","mla":"Toshima, Junko, et al. “Bifurcation of the Endocytic Pathway into Rab5-Dependent and -Independent Transport to the Vacuole.” Nature Communications, vol. 5, 3498, Nature Publishing Group, 2014, doi:10.1038/ncomms4498."},"_id":"2024","quality_controlled":"1","user_id":"4435EBFC-F248-11E8-B48F-1D18A9856A87","title":"Bifurcation of the endocytic pathway into Rab5-dependent and -independent transport to the vacuole","file":[{"file_name":"IST-2016-616-v1+1_DaSi_Bifurcation_Postprint.pdf","access_level":"open_access","content_type":"application/pdf","checksum":"614fb6579c86d1f95bdd95eeb9ab01b0","date_created":"2018-12-12T10:11:11Z","file_size":4803515,"relation":"main_file","date_updated":"2020-07-14T12:45:25Z","creator":"system","file_id":"4864"}],"oa":1,"abstract":[{"text":"The yeast Rab5 homologue, Vps21p, is known to be involved both in the vacuolar protein sorting (VPS) pathway from the trans-Golgi network to the vacuole, and in the endocytic pathway from the plasma membrane to the vacuole. However, the intracellular location at which these two pathways converge remains unclear. In addition, the endocytic pathway is not completely blocked in yeast cells lacking all Rab5 genes, suggesting the existence of an unidentified route that bypasses the Rab5-dependent endocytic pathway. Here we show that convergence of the endocytic and VPS pathways occurs upstream of the requirement for Vps21p in these pathways. We also identify a previously unidentified endocytic pathway mediated by the AP-3 complex. Importantly, the AP-3-mediated pathway appears mostly intact in Rab5-disrupted cells, and thus works as an alternative route to the vacuole/lysosome. We propose that the endocytic traffic branches into two routes to reach the vacuole: a Rab5-dependent VPS pathway and a Rab5-independent AP-3-mediated pathway.","lang":"eng"}],"ddc":["570"],"date_updated":"2021-01-12T06:54:48Z","publisher":"Nature Publishing Group","date_created":"2018-12-11T11:55:16Z","publist_id":"5048"}]