[{"acknowledgement":"We thank the members of the Matsuda Laboratory for their helpful discussion and encouragement, and we thank K. Hirano and K. Takakura for their technical assistance. This work was supported by the Kyoto University Live Imaging Center. Financial support was provided in the form of JSPS KAKENHI grants (nos. 17J02107 and 20K22653 to N.H., and 20H05898 and 19H00993 to M.M.), a JST CREST grant (no. JPMJCR1654 to M.M.), a Moonshot R&D grant (no. JPMJPS2022-11 to M.M.), Generalitat de Catalunya and the CERCA Programme (no. SGR-2017-01602 to X.T.), MICCINN/FEDER (no. PGC2018-099645-B-I00 to X.T.), and European Research Council (no. Adv-883739 to X.T.). IBEC is a recipient of a Severo Ochoa Award of Excellence from the MINECO. This work was partly supported by an Extramural Collaborative Research Grant of Cancer Research Institute, Kanazawa University.","pmid":1,"language":[{"iso":"eng"}],"keyword":["Developmental Biology","Cell Biology","General Biochemistry","Genetics and Molecular Biology","Molecular Biology"],"doi":"10.1016/j.devcel.2022.09.003","citation":{"apa":"Hino, N., Matsuda, K., Jikko, Y., Maryu, G., Sakai, K., Imamura, R., … Matsuda, M. (2022). A feedback loop between lamellipodial extension and HGF-ERK signaling specifies leader cells during collective cell migration. <i>Developmental Cell</i>. Elsevier. <a href=\"https://doi.org/10.1016/j.devcel.2022.09.003\">https://doi.org/10.1016/j.devcel.2022.09.003</a>","ama":"Hino N, Matsuda K, Jikko Y, et al. A feedback loop between lamellipodial extension and HGF-ERK signaling specifies leader cells during collective cell migration. <i>Developmental Cell</i>. 2022;57(19):2290-2304.e7. doi:<a href=\"https://doi.org/10.1016/j.devcel.2022.09.003\">10.1016/j.devcel.2022.09.003</a>","short":"N. Hino, K. Matsuda, Y. Jikko, G. Maryu, K. Sakai, R. Imamura, S. Tsukiji, K. Aoki, K. Terai, T. Hirashima, X. Trepat, M. Matsuda, Developmental Cell 57 (2022) 2290–2304.e7.","mla":"Hino, Naoya, et al. “A Feedback Loop between Lamellipodial Extension and HGF-ERK Signaling Specifies Leader Cells during Collective Cell Migration.” <i>Developmental Cell</i>, vol. 57, no. 19, Elsevier, 2022, p. 2290–2304.e7, doi:<a href=\"https://doi.org/10.1016/j.devcel.2022.09.003\">10.1016/j.devcel.2022.09.003</a>.","ista":"Hino N, Matsuda K, Jikko Y, Maryu G, Sakai K, Imamura R, Tsukiji S, Aoki K, Terai K, Hirashima T, Trepat X, Matsuda M. 2022. A feedback loop between lamellipodial extension and HGF-ERK signaling specifies leader cells during collective cell migration. Developmental Cell. 57(19), 2290–2304.e7.","ieee":"N. Hino <i>et al.</i>, “A feedback loop between lamellipodial extension and HGF-ERK signaling specifies leader cells during collective cell migration,” <i>Developmental Cell</i>, vol. 57, no. 19. Elsevier, p. 2290–2304.e7, 2022.","chicago":"Hino, Naoya, Kimiya Matsuda, Yuya Jikko, Gembu Maryu, Katsuya Sakai, Ryu Imamura, Shinya Tsukiji, et al. “A Feedback Loop between Lamellipodial Extension and HGF-ERK Signaling Specifies Leader Cells during Collective Cell Migration.” <i>Developmental Cell</i>. Elsevier, 2022. <a href=\"https://doi.org/10.1016/j.devcel.2022.09.003\">https://doi.org/10.1016/j.devcel.2022.09.003</a>."},"title":"A feedback loop between lamellipodial extension and HGF-ERK signaling specifies leader cells during collective cell migration","day":"01","type":"journal_article","author":[{"id":"5299a9ce-7679-11eb-a7bc-d1e62b936307","first_name":"Naoya","full_name":"Hino, Naoya","last_name":"Hino"},{"full_name":"Matsuda, Kimiya","first_name":"Kimiya","last_name":"Matsuda"},{"first_name":"Yuya","full_name":"Jikko, Yuya","last_name":"Jikko"},{"last_name":"Maryu","full_name":"Maryu, Gembu","first_name":"Gembu"},{"last_name":"Sakai","full_name":"Sakai, Katsuya","first_name":"Katsuya"},{"last_name":"Imamura","first_name":"Ryu","full_name":"Imamura, Ryu"},{"last_name":"Tsukiji","full_name":"Tsukiji, Shinya","first_name":"Shinya"},{"last_name":"Aoki","first_name":"Kazuhiro","full_name":"Aoki, Kazuhiro"},{"last_name":"Terai","full_name":"Terai, Kenta","first_name":"Kenta"},{"last_name":"Hirashima","first_name":"Tsuyoshi","full_name":"Hirashima, Tsuyoshi"},{"full_name":"Trepat, Xavier","first_name":"Xavier","last_name":"Trepat"},{"first_name":"Michiyuki","full_name":"Matsuda, Michiyuki","last_name":"Matsuda"}],"publisher":"Elsevier","isi":1,"department":[{"_id":"CaHe"}],"quality_controlled":"1","publication":"Developmental Cell","intvolume":"        57","status":"public","page":"2290-2304.e7","month":"10","date_created":"2023-01-16T09:51:39Z","date_updated":"2023-08-04T09:38:53Z","user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","scopus_import":"1","external_id":{"pmid":["36174555"],"isi":["000898428700006"]},"publication_identifier":{"issn":["1534-5807"]},"article_type":"original","oa_version":"None","year":"2022","publication_status":"published","volume":57,"issue":"19","article_processing_charge":"No","_id":"12238","date_published":"2022-10-01T00:00:00Z","abstract":[{"text":"Upon the initiation of collective cell migration, the cells at the free edge are specified as leader cells; however, the mechanism underlying the leader cell specification remains elusive. Here, we show that lamellipodial extension after the release from mechanical confinement causes sustained extracellular signal-regulated kinase (ERK) activation and underlies the leader cell specification. Live-imaging of Madin-Darby canine kidney (MDCK) cells and mouse epidermis through the use of Förster resonance energy transfer (FRET)-based biosensors showed that leader cells exhibit sustained ERK activation in a hepatocyte growth factor (HGF)-dependent manner. Meanwhile, follower cells exhibit oscillatory ERK activation waves in an epidermal growth factor (EGF) signaling-dependent manner. Lamellipodial extension at the free edge increases the cellular sensitivity to HGF. The HGF-dependent ERK activation, in turn, promotes lamellipodial extension, thereby forming a positive feedback loop between cell extension and ERK activation and specifying the cells at the free edge as the leader cells. Our findings show that the integration of physical and biochemical cues underlies the leader cell specification during collective cell migration.","lang":"eng"}]},{"publication_status":"published","license":"https://creativecommons.org/licenses/by-nc-sa/4.0/","oa":1,"file_date_updated":"2023-01-30T10:39:34Z","volume":221,"tmp":{"legal_code_url":"https://creativecommons.org/licenses/by-nc-sa/4.0/legalcode","image":"/images/cc_by_nc_sa.png","name":"Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC BY-NC-SA 4.0)","short":"CC BY-NC-SA (4.0)"},"issue":"8","article_processing_charge":"No","article_number":"e202206127","file":[{"date_created":"2023-01-30T10:39:34Z","success":1,"content_type":"application/pdf","file_id":"12451","relation":"main_file","checksum":"6b1620743669679b48b9389bb40f5a11","date_updated":"2023-01-30T10:39:34Z","access_level":"open_access","file_name":"2022_JourCellBiology_Stopp.pdf","file_size":969969,"creator":"dernst"}],"date_published":"2022-07-20T00:00:00Z","_id":"12272","abstract":[{"text":"Reading, interpreting and crawling along gradients of chemotactic cues is one of the most complex questions in cell biology. In this issue, Georgantzoglou et al. (2022. J. Cell. Biol.https://doi.org/10.1083/jcb.202103207) use in vivo models to map the temporal sequence of how neutrophils respond to an acutely arising gradient of chemoattractant.","lang":"eng"}],"date_updated":"2023-12-21T14:30:01Z","user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","external_id":{"pmid":["35856919"],"isi":["000874717200001"]},"scopus_import":"1","publication_identifier":{"issn":["0021-9525"],"eissn":["1540-8140"]},"article_type":"original","year":"2022","oa_version":"Published Version","has_accepted_license":"1","publisher":"Rockefeller University Press","isi":1,"department":[{"_id":"MiSi"}],"quality_controlled":"1","publication":"Journal of Cell Biology","intvolume":"       221","status":"public","month":"07","date_created":"2023-01-16T10:01:08Z","related_material":{"record":[{"status":"public","relation":"dissertation_contains","id":"14697"}]},"pmid":1,"language":[{"iso":"eng"}],"keyword":["Cell Biology"],"ddc":["570"],"doi":"10.1083/jcb.202206127","citation":{"short":"J.A. Stopp, M.K. Sixt, Journal of Cell Biology 221 (2022).","apa":"Stopp, J. A., &#38; Sixt, M. K. (2022). Plan your trip before you leave: The neutrophils’ search-and-run journey. <i>Journal of Cell Biology</i>. Rockefeller University Press. <a href=\"https://doi.org/10.1083/jcb.202206127\">https://doi.org/10.1083/jcb.202206127</a>","ama":"Stopp JA, Sixt MK. Plan your trip before you leave: The neutrophils’ search-and-run journey. <i>Journal of Cell Biology</i>. 2022;221(8). doi:<a href=\"https://doi.org/10.1083/jcb.202206127\">10.1083/jcb.202206127</a>","ista":"Stopp JA, Sixt MK. 2022. Plan your trip before you leave: The neutrophils’ search-and-run journey. Journal of Cell Biology. 221(8), e202206127.","ieee":"J. A. Stopp and M. K. Sixt, “Plan your trip before you leave: The neutrophils’ search-and-run journey,” <i>Journal of Cell Biology</i>, vol. 221, no. 8. Rockefeller University Press, 2022.","chicago":"Stopp, Julian A, and Michael K Sixt. “Plan Your Trip before You Leave: The Neutrophils’ Search-and-Run Journey.” <i>Journal of Cell Biology</i>. Rockefeller University Press, 2022. <a href=\"https://doi.org/10.1083/jcb.202206127\">https://doi.org/10.1083/jcb.202206127</a>.","mla":"Stopp, Julian A., and Michael K. Sixt. “Plan Your Trip before You Leave: The Neutrophils’ Search-and-Run Journey.” <i>Journal of Cell Biology</i>, vol. 221, no. 8, e202206127, Rockefeller University Press, 2022, doi:<a href=\"https://doi.org/10.1083/jcb.202206127\">10.1083/jcb.202206127</a>."},"title":"Plan your trip before you leave: The neutrophils’ search-and-run journey","day":"20","type":"journal_article","author":[{"id":"489E3F00-F248-11E8-B48F-1D18A9856A87","last_name":"Stopp","first_name":"Julian A","full_name":"Stopp, Julian A"},{"orcid":"0000-0002-6620-9179","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","last_name":"Sixt","full_name":"Sixt, Michael K","first_name":"Michael K"}]},{"date_created":"2023-01-16T10:03:24Z","month":"04","status":"public","intvolume":"       135","quality_controlled":"1","department":[{"_id":"SiHi"}],"publication":"Journal of Cell Science","isi":1,"publisher":"The Company of Biologists","author":[{"full_name":"Atherton, Joseph","first_name":"Joseph","last_name":"Atherton"},{"id":"4C9372C4-F248-11E8-B48F-1D18A9856A87","full_name":"Stouffer, Melissa A","first_name":"Melissa A","last_name":"Stouffer"},{"first_name":"Fiona","full_name":"Francis, Fiona","last_name":"Francis"},{"last_name":"Moores","first_name":"Carolyn A.","full_name":"Moores, Carolyn A."}],"type":"journal_article","day":"01","title":"Visualising the cytoskeletal machinery in neuronal growth cones using cryo-electron tomography","citation":{"ama":"Atherton J, Stouffer MA, Francis F, Moores CA. Visualising the cytoskeletal machinery in neuronal growth cones using cryo-electron tomography. <i>Journal of Cell Science</i>. 2022;135(7). doi:<a href=\"https://doi.org/10.1242/jcs.259234\">10.1242/jcs.259234</a>","apa":"Atherton, J., Stouffer, M. A., Francis, F., &#38; Moores, C. A. (2022). Visualising the cytoskeletal machinery in neuronal growth cones using cryo-electron tomography. <i>Journal of Cell Science</i>. The Company of Biologists. <a href=\"https://doi.org/10.1242/jcs.259234\">https://doi.org/10.1242/jcs.259234</a>","short":"J. Atherton, M.A. Stouffer, F. Francis, C.A. Moores, Journal of Cell Science 135 (2022).","mla":"Atherton, Joseph, et al. “Visualising the Cytoskeletal Machinery in Neuronal Growth Cones Using Cryo-Electron Tomography.” <i>Journal of Cell Science</i>, vol. 135, no. 7, 259234, The Company of Biologists, 2022, doi:<a href=\"https://doi.org/10.1242/jcs.259234\">10.1242/jcs.259234</a>.","chicago":"Atherton, Joseph, Melissa A Stouffer, Fiona Francis, and Carolyn A. Moores. “Visualising the Cytoskeletal Machinery in Neuronal Growth Cones Using Cryo-Electron Tomography.” <i>Journal of Cell Science</i>. The Company of Biologists, 2022. <a href=\"https://doi.org/10.1242/jcs.259234\">https://doi.org/10.1242/jcs.259234</a>.","ista":"Atherton J, Stouffer MA, Francis F, Moores CA. 2022. Visualising the cytoskeletal machinery in neuronal growth cones using cryo-electron tomography. Journal of Cell Science. 135(7), 259234.","ieee":"J. Atherton, M. A. Stouffer, F. Francis, and C. A. Moores, “Visualising the cytoskeletal machinery in neuronal growth cones using cryo-electron tomography,” <i>Journal of Cell Science</i>, vol. 135, no. 7. The Company of Biologists, 2022."},"ddc":["570"],"doi":"10.1242/jcs.259234","language":[{"iso":"eng"}],"keyword":["Cell Biology"],"acknowledgement":"J.A. was supported by a grant from the Medical Research Council (MRC), UK (MR/R000352/1) to C.A.M. Cryo-EM data were collected on equipment funded by the Wellcome Trust, UK (079605/Z/06/Z) and the Biotechnology and Biological Sciences Research Council (BBSRC) UK (BB/L014211/1). F.F.’s salary and institute were supported by Inserm (Institut National de la Santé et de la Recherche Médicale), CNRS (Centre National de la Recherche Scientifique) and Sorbonne Université. F.F.’s group was particularly supported by Agence Nationale de la\r\nRecherche (ANR-16-CE16-0011-03) and Seventh Framework Programme (EUHEALTH-\r\n2013, DESIRE, N° 60253; also funding M.S.’s salary) and the European Cooperation in Science and Technology (COST Action CA16118). Open Access funding provided by Birkbeck College: Birkbeck University of London. Deposited in PMC for immediate release.","pmid":1,"date_published":"2022-04-01T00:00:00Z","_id":"12283","abstract":[{"lang":"eng","text":"Neurons extend axons to form the complex circuitry of the mature brain. This depends on the coordinated response and continuous remodelling of the microtubule and F-actin networks in the axonal growth cone. Growth cone architecture remains poorly understood at nanoscales. We therefore investigated mouse hippocampal neuron growth cones using cryo-electron tomography to directly visualise their three-dimensional subcellular architecture with molecular detail. Our data showed that the hexagonal arrays of actin bundles that form filopodia penetrate and terminate deep within the growth cone interior. We directly observed the modulation of these and other growth cone actin bundles by alteration of individual F-actin helical structures. Microtubules with blunt, slightly flared or gently curved ends predominated in the growth cone, frequently contained lumenal particles and exhibited lattice defects. Investigation of the effect of absence of doublecortin, a neurodevelopmental cytoskeleton regulator, on growth cone cytoskeleton showed no major anomalies in overall growth cone organisation or in F-actin subpopulations. However, our data suggested that microtubules sustained more structural defects, highlighting the importance of microtubule integrity during growth cone migration."}],"article_number":"259234","file":[{"file_name":"2022_JourCellBiology_Atherton.pdf","file_size":13868733,"creator":"dernst","date_updated":"2023-01-30T11:41:01Z","access_level":"open_access","checksum":"4346ed32cb7c89a8ca051c7da68a9a1c","content_type":"application/pdf","file_id":"12461","relation":"main_file","success":1,"date_created":"2023-01-30T11:41:01Z"}],"issue":"7","article_processing_charge":"No","volume":135,"tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","image":"/images/cc_by.png","short":"CC BY (4.0)"},"file_date_updated":"2023-01-30T11:41:01Z","oa":1,"publication_status":"published","has_accepted_license":"1","year":"2022","oa_version":"Published Version","article_type":"original","publication_identifier":{"issn":["0021-9533"],"eissn":["1477-9137"]},"user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","date_updated":"2023-08-04T10:28:34Z","external_id":{"pmid":["35383828"],"isi":["000783840400010"]},"scopus_import":"1"},{"citation":{"ieee":"S. Krishna, R. Arrojo e Drigo, J. S. Capitanio, R. Ramachandra, M. Ellisman, and M. Hetzer, “Identification of long-lived proteins in the mitochondria reveals increased stability of the electron transport chain,” <i>Developmental Cell</i>, vol. 56, no. 21. Elsevier, p. P2952–2965.e9, 2021.","ista":"Krishna S, Arrojo e Drigo R, Capitanio JS, Ramachandra R, Ellisman M, Hetzer M. 2021. Identification of long-lived proteins in the mitochondria reveals increased stability of the electron transport chain. Developmental Cell. 56(21), P2952–2965.e9.","chicago":"Krishna, Shefali, Rafael Arrojo e Drigo, Juliana S. Capitanio, Ranjan Ramachandra, Mark Ellisman, and Martin Hetzer. “Identification of Long-Lived Proteins in the Mitochondria Reveals Increased Stability of the Electron Transport Chain.” <i>Developmental Cell</i>. Elsevier, 2021. <a href=\"https://doi.org/10.1016/j.devcel.2021.10.008\">https://doi.org/10.1016/j.devcel.2021.10.008</a>.","mla":"Krishna, Shefali, et al. “Identification of Long-Lived Proteins in the Mitochondria Reveals Increased Stability of the Electron Transport Chain.” <i>Developmental Cell</i>, vol. 56, no. 21, Elsevier, 2021, p. P2952–2965.e9, doi:<a href=\"https://doi.org/10.1016/j.devcel.2021.10.008\">10.1016/j.devcel.2021.10.008</a>.","short":"S. Krishna, R. Arrojo e Drigo, J.S. Capitanio, R. Ramachandra, M. Ellisman, M. Hetzer, Developmental Cell 56 (2021) P2952–2965.e9.","apa":"Krishna, S., Arrojo e Drigo, R., Capitanio, J. S., Ramachandra, R., Ellisman, M., &#38; Hetzer, M. (2021). Identification of long-lived proteins in the mitochondria reveals increased stability of the electron transport chain. <i>Developmental Cell</i>. Elsevier. <a href=\"https://doi.org/10.1016/j.devcel.2021.10.008\">https://doi.org/10.1016/j.devcel.2021.10.008</a>","ama":"Krishna S, Arrojo e Drigo R, Capitanio JS, Ramachandra R, Ellisman M, Hetzer M. Identification of long-lived proteins in the mitochondria reveals increased stability of the electron transport chain. <i>Developmental Cell</i>. 2021;56(21):P2952-2965.e9. doi:<a href=\"https://doi.org/10.1016/j.devcel.2021.10.008\">10.1016/j.devcel.2021.10.008</a>"},"title":"Identification of long-lived proteins in the mitochondria reveals increased stability of the electron transport chain","day":"08","type":"journal_article","author":[{"first_name":"Shefali","full_name":"Krishna, Shefali","last_name":"Krishna"},{"first_name":"Rafael","full_name":"Arrojo e Drigo, Rafael","last_name":"Arrojo e Drigo"},{"full_name":"Capitanio, Juliana S.","first_name":"Juliana S.","last_name":"Capitanio"},{"last_name":"Ramachandra","full_name":"Ramachandra, Ranjan","first_name":"Ranjan"},{"last_name":"Ellisman","full_name":"Ellisman, Mark","first_name":"Mark"},{"id":"86c0d31b-b4eb-11ec-ac5a-eae7b2e135ed","orcid":"0000-0002-2111-992X","last_name":"HETZER","first_name":"Martin W","full_name":"HETZER, Martin W"}],"pmid":1,"keyword":["Developmental Biology","Cell Biology","General Biochemistry","Genetics and Molecular Biology","Molecular Biology"],"language":[{"iso":"eng"}],"doi":"10.1016/j.devcel.2021.10.008","page":"P2952-2965.e9","month":"11","extern":"1","date_created":"2022-04-07T07:43:14Z","publisher":"Elsevier","publication":"Developmental Cell","quality_controlled":"1","status":"public","intvolume":"        56","article_type":"original","year":"2021","oa_version":"None","external_id":{"pmid":["34715012"]},"scopus_import":"1","date_updated":"2022-07-18T08:26:38Z","user_id":"72615eeb-f1f3-11ec-aa25-d4573ddc34fd","publication_identifier":{"issn":["1534-5807"]},"article_processing_charge":"No","issue":"21","date_published":"2021-11-08T00:00:00Z","_id":"11052","abstract":[{"lang":"eng","text":"In order to combat molecular damage, most cellular proteins undergo rapid turnover. We have previously identified large nuclear protein assemblies that can persist for years in post-mitotic tissues and are subject to age-related decline. Here, we report that mitochondria can be long lived in the mouse brain and reveal that specific mitochondrial proteins have half-lives longer than the average proteome. These mitochondrial long-lived proteins (mitoLLPs) are core components of the electron transport chain (ETC) and display increased longevity in respiratory supercomplexes. We find that COX7C, a mitoLLP that forms a stable contact site between complexes I and IV, is required for complex IV and supercomplex assembly. Remarkably, even upon depletion of COX7C transcripts, ETC function is maintained for days, effectively uncoupling mitochondrial function from ongoing transcription of its mitoLLPs. Our results suggest that modulating protein longevity within the ETC is critical for mitochondrial proteome maintenance and the robustness of mitochondrial function."}],"publication_status":"published","volume":56},{"publication_status":"published","oa":1,"file_date_updated":"2021-08-11T10:28:06Z","tmp":{"name":"Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0)","image":"/images/cc_by_nc_nd.png","legal_code_url":"https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode","short":"CC BY-NC-ND (4.0)"},"volume":474,"article_processing_charge":"Yes (via OA deal)","file":[{"date_updated":"2021-08-11T10:28:06Z","access_level":"open_access","checksum":"fa2a5731fd16ab171b029f32f031c440","file_name":"2021_DevBiology_Schauer.pdf","creator":"kschuh","file_size":1440321,"success":1,"date_created":"2021-08-11T10:28:06Z","content_type":"application/pdf","relation":"main_file","file_id":"9880"}],"_id":"8966","abstract":[{"text":"During development, a single cell is transformed into a highly complex organism through progressive cell division, specification and rearrangement. An important prerequisite for the emergence of patterns within the developing organism is to establish asymmetries at various scales, ranging from individual cells to the entire embryo, eventually giving rise to the different body structures. This becomes especially apparent during gastrulation, when the earliest major lineage restriction events lead to the formation of the different germ layers. Traditionally, the unfolding of the developmental program from symmetry breaking to germ layer formation has been studied by dissecting the contributions of different signaling pathways and cellular rearrangements in the in vivo context of intact embryos. Recent efforts, using the intrinsic capacity of embryonic stem cells to self-assemble and generate embryo-like structures de novo, have opened new avenues for understanding the many ways by which an embryo can be built and the influence of extrinsic factors therein. Here, we discuss and compare divergent and conserved strategies leading to germ layer formation in embryos as compared to in vitro systems, their upstream molecular cascades and the role of extrinsic factors in this process.","lang":"eng"}],"date_published":"2021-06-01T00:00:00Z","scopus_import":"1","external_id":{"isi":["000639461800008"]},"user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","date_updated":"2023-08-07T13:30:01Z","publication_identifier":{"issn":["0012-1606"]},"article_type":"original","year":"2021","oa_version":"Published Version","has_accepted_license":"1","publisher":"Elsevier","isi":1,"publication":"Developmental Biology","department":[{"_id":"CaHe"}],"quality_controlled":"1","status":"public","intvolume":"       474","page":"71-81","month":"06","date_created":"2020-12-22T09:53:34Z","related_material":{"record":[{"id":"12891","relation":"dissertation_contains","status":"public"}]},"project":[{"grant_number":"742573","name":"Interaction and feedback between cell mechanics and fate specification in vertebrate gastrulation","call_identifier":"H2020","_id":"260F1432-B435-11E9-9278-68D0E5697425"},{"name":"Mesendoderm specification in zebrafish: The role of extraembryonic tissues","grant_number":"25239","_id":"26B1E39C-B435-11E9-9278-68D0E5697425"}],"acknowledgement":"We thank Nicoletta Petridou, Diana Pinheiro, Cornelia Schwayer and Stefania Tavano for feedback on the manuscript. Research in the Heisenberg lab is supported by an ERC Advanced Grant (MECSPEC 742573) to C.-P.H. A.S. is a recipient of a DOC Fellowship of the Austrian Academy of Science.","keyword":["Developmental Biology","Cell Biology","Molecular Biology"],"language":[{"iso":"eng"}],"doi":"10.1016/j.ydbio.2020.12.014","ddc":["570"],"citation":{"ista":"Schauer A, Heisenberg C-PJ. 2021. Reassembling gastrulation. Developmental Biology. 474, 71–81.","ieee":"A. Schauer and C.-P. J. Heisenberg, “Reassembling gastrulation,” <i>Developmental Biology</i>, vol. 474. Elsevier, pp. 71–81, 2021.","chicago":"Schauer, Alexandra, and Carl-Philipp J Heisenberg. “Reassembling Gastrulation.” <i>Developmental Biology</i>. Elsevier, 2021. <a href=\"https://doi.org/10.1016/j.ydbio.2020.12.014\">https://doi.org/10.1016/j.ydbio.2020.12.014</a>.","mla":"Schauer, Alexandra, and Carl-Philipp J. Heisenberg. “Reassembling Gastrulation.” <i>Developmental Biology</i>, vol. 474, Elsevier, 2021, pp. 71–81, doi:<a href=\"https://doi.org/10.1016/j.ydbio.2020.12.014\">10.1016/j.ydbio.2020.12.014</a>.","short":"A. Schauer, C.-P.J. Heisenberg, Developmental Biology 474 (2021) 71–81.","apa":"Schauer, A., &#38; Heisenberg, C.-P. J. (2021). Reassembling gastrulation. <i>Developmental Biology</i>. Elsevier. <a href=\"https://doi.org/10.1016/j.ydbio.2020.12.014\">https://doi.org/10.1016/j.ydbio.2020.12.014</a>","ama":"Schauer A, Heisenberg C-PJ. Reassembling gastrulation. <i>Developmental Biology</i>. 2021;474:71-81. doi:<a href=\"https://doi.org/10.1016/j.ydbio.2020.12.014\">10.1016/j.ydbio.2020.12.014</a>"},"ec_funded":1,"title":"Reassembling gastrulation","day":"01","type":"journal_article","author":[{"orcid":"0000-0001-7659-9142","id":"30A536BA-F248-11E8-B48F-1D18A9856A87","last_name":"Schauer","first_name":"Alexandra","full_name":"Schauer, Alexandra"},{"id":"39427864-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-0912-4566","first_name":"Carl-Philipp J","full_name":"Heisenberg, Carl-Philipp J","last_name":"Heisenberg"}]},{"project":[{"_id":"260018B0-B435-11E9-9278-68D0E5697425","call_identifier":"H2020","grant_number":"725780","name":"Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development"},{"name":"Mapping Cell-Type Specificity of the Genomic Imprintome in the Brain","grant_number":"LS13-002","_id":"25D92700-B435-11E9-9278-68D0E5697425"}],"pmid":1,"acknowledgement":"We thank Melissa Stouffer for critically reading the manuscript. This work was supported by IST Austria institutional funds; NÖ Forschung und Bildung n[f + b] life science call grant (C13-002) to S.H. and the European Research Council (ERC) under the European Union's Horizon 2020 research and innovation program (grant agreement 725780 LinPro) to S.H.","ddc":["570"],"doi":"10.1016/j.neuint.2021.104986","keyword":["Cell Biology","Cellular and Molecular Neuroscience"],"language":[{"iso":"eng"}],"title":"Inducible uniparental chromosome disomy to probe genomic imprinting at single-cell level in brain and beyond","citation":{"mla":"Pauler, Florian, et al. “Inducible Uniparental Chromosome Disomy to Probe Genomic Imprinting at Single-Cell Level in Brain and Beyond.” <i>Neurochemistry International</i>, vol. 145, no. 5, 104986, Elsevier, 2021, doi:<a href=\"https://doi.org/10.1016/j.neuint.2021.104986\">10.1016/j.neuint.2021.104986</a>.","ieee":"F. Pauler, Q. Hudson, S. Laukoter, and S. Hippenmeyer, “Inducible uniparental chromosome disomy to probe genomic imprinting at single-cell level in brain and beyond,” <i>Neurochemistry International</i>, vol. 145, no. 5. Elsevier, 2021.","ista":"Pauler F, Hudson Q, Laukoter S, Hippenmeyer S. 2021. Inducible uniparental chromosome disomy to probe genomic imprinting at single-cell level in brain and beyond. Neurochemistry International. 145(5), 104986.","chicago":"Pauler, Florian, Quanah Hudson, Susanne Laukoter, and Simon Hippenmeyer. “Inducible Uniparental Chromosome Disomy to Probe Genomic Imprinting at Single-Cell Level in Brain and Beyond.” <i>Neurochemistry International</i>. Elsevier, 2021. <a href=\"https://doi.org/10.1016/j.neuint.2021.104986\">https://doi.org/10.1016/j.neuint.2021.104986</a>.","apa":"Pauler, F., Hudson, Q., Laukoter, S., &#38; Hippenmeyer, S. (2021). Inducible uniparental chromosome disomy to probe genomic imprinting at single-cell level in brain and beyond. <i>Neurochemistry International</i>. Elsevier. <a href=\"https://doi.org/10.1016/j.neuint.2021.104986\">https://doi.org/10.1016/j.neuint.2021.104986</a>","ama":"Pauler F, Hudson Q, Laukoter S, Hippenmeyer S. Inducible uniparental chromosome disomy to probe genomic imprinting at single-cell level in brain and beyond. <i>Neurochemistry International</i>. 2021;145(5). doi:<a href=\"https://doi.org/10.1016/j.neuint.2021.104986\">10.1016/j.neuint.2021.104986</a>","short":"F. Pauler, Q. Hudson, S. Laukoter, S. Hippenmeyer, Neurochemistry International 145 (2021)."},"ec_funded":1,"type":"journal_article","author":[{"last_name":"Pauler","full_name":"Pauler, Florian","first_name":"Florian","id":"48EA0138-F248-11E8-B48F-1D18A9856A87"},{"first_name":"Quanah","full_name":"Hudson, Quanah","last_name":"Hudson"},{"first_name":"Susanne","full_name":"Laukoter, Susanne","last_name":"Laukoter","id":"2D6B7A9A-F248-11E8-B48F-1D18A9856A87"},{"first_name":"Simon","full_name":"Hippenmeyer, Simon","last_name":"Hippenmeyer","id":"37B36620-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0003-2279-1061"}],"day":"01","isi":1,"publisher":"Elsevier","intvolume":"       145","status":"public","publication":"Neurochemistry International","department":[{"_id":"SiHi"}],"quality_controlled":"1","date_created":"2021-02-23T12:31:43Z","month":"05","publication_identifier":{"issn":["0197-0186"]},"external_id":{"pmid":["33600873"],"isi":["000635575000005"]},"scopus_import":"1","user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","date_updated":"2023-08-07T13:48:26Z","has_accepted_license":"1","year":"2021","oa_version":"Published Version","article_type":"original","oa":1,"publication_status":"published","tmp":{"name":"Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0)","image":"/images/cc_by_nc_nd.png","legal_code_url":"https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode","short":"CC BY-NC-ND (4.0)"},"volume":145,"file_date_updated":"2021-08-11T12:30:38Z","article_processing_charge":"Yes (via OA deal)","issue":"5","_id":"9188","abstract":[{"text":"Genomic imprinting is an epigenetic mechanism that results in parental allele-specific expression of ~1% of all genes in mouse and human. Imprinted genes are key developmental regulators and play pivotal roles in many biological processes such as nutrient transfer from the mother to offspring and neuronal development. Imprinted genes are also involved in human disease, including neurodevelopmental disorders, and often occur in clusters that are regulated by a common imprint control region (ICR). In extra-embryonic tissues ICRs can act over large distances, with the largest surrounding Igf2r spanning over 10 million base-pairs. Besides classical imprinted expression that shows near exclusive maternal or paternal expression, widespread biased imprinted expression has been identified mainly in brain. In this review we discuss recent developments mapping cell type specific imprinted expression in extra-embryonic tissues and neocortex in the mouse. We highlight the advantages of using an inducible uniparental chromosome disomy (UPD) system to generate cells carrying either two maternal or two paternal copies of a specific chromosome to analyze the functional consequences of genomic imprinting. Mosaic Analysis with Double Markers (MADM) allows fluorescent labeling and concomitant induction of UPD sparsely in specific cell types, and thus to over-express or suppress all imprinted genes on that chromosome. To illustrate the utility of this technique, we explain how MADM-induced UPD revealed new insights about the function of the well-studied Cdkn1c imprinted gene, and how MADM-induced UPDs led to identification of highly cell type specific phenotypes related to perturbed imprinted expression in the mouse neocortex. Finally, we give an outlook on how MADM could be used to probe cell type specific imprinted expression in other tissues in mouse, particularly in extra-embryonic tissues.","lang":"eng"}],"date_published":"2021-05-01T00:00:00Z","article_number":"104986","file":[{"content_type":"application/pdf","file_id":"9883","relation":"main_file","success":1,"date_created":"2021-08-11T12:30:38Z","file_name":"2021_NCI_Pauler.pdf","file_size":7083499,"creator":"kschuh","date_updated":"2021-08-11T12:30:38Z","access_level":"open_access","checksum":"c6d7a40089cd29e289f9b22e75768304"}]},{"title":"The Wdr1-LIMK-Cofilin axis controls B cell antigen receptor-induced actin remodeling and signaling at the immune synapse","citation":{"mla":"Bolger-Munro, Madison, et al. “The Wdr1-LIMK-Cofilin Axis Controls B Cell Antigen Receptor-Induced Actin Remodeling and Signaling at the Immune Synapse.” <i>Frontiers in Cell and Developmental Biology</i>, vol. 9, 649433, Frontiers Media, 2021, doi:<a href=\"https://doi.org/10.3389/fcell.2021.649433\">10.3389/fcell.2021.649433</a>.","ista":"Bolger-Munro M, Choi K, Cheung F, Liu YT, Dang-Lawson M, Deretic N, Keane C, Gold MR. 2021. The Wdr1-LIMK-Cofilin axis controls B cell antigen receptor-induced actin remodeling and signaling at the immune synapse. Frontiers in Cell and Developmental Biology. 9, 649433.","ieee":"M. Bolger-Munro <i>et al.</i>, “The Wdr1-LIMK-Cofilin axis controls B cell antigen receptor-induced actin remodeling and signaling at the immune synapse,” <i>Frontiers in Cell and Developmental Biology</i>, vol. 9. Frontiers Media, 2021.","chicago":"Bolger-Munro, Madison, Kate Choi, Faith Cheung, Yi Tian Liu, May Dang-Lawson, Nikola Deretic, Connor Keane, and Michael R. Gold. “The Wdr1-LIMK-Cofilin Axis Controls B Cell Antigen Receptor-Induced Actin Remodeling and Signaling at the Immune Synapse.” <i>Frontiers in Cell and Developmental Biology</i>. Frontiers Media, 2021. <a href=\"https://doi.org/10.3389/fcell.2021.649433\">https://doi.org/10.3389/fcell.2021.649433</a>.","apa":"Bolger-Munro, M., Choi, K., Cheung, F., Liu, Y. T., Dang-Lawson, M., Deretic, N., … Gold, M. R. (2021). The Wdr1-LIMK-Cofilin axis controls B cell antigen receptor-induced actin remodeling and signaling at the immune synapse. <i>Frontiers in Cell and Developmental Biology</i>. Frontiers Media. <a href=\"https://doi.org/10.3389/fcell.2021.649433\">https://doi.org/10.3389/fcell.2021.649433</a>","ama":"Bolger-Munro M, Choi K, Cheung F, et al. The Wdr1-LIMK-Cofilin axis controls B cell antigen receptor-induced actin remodeling and signaling at the immune synapse. <i>Frontiers in Cell and Developmental Biology</i>. 2021;9. doi:<a href=\"https://doi.org/10.3389/fcell.2021.649433\">10.3389/fcell.2021.649433</a>","short":"M. Bolger-Munro, K. Choi, F. Cheung, Y.T. Liu, M. Dang-Lawson, N. Deretic, C. Keane, M.R. Gold, Frontiers in Cell and Developmental Biology 9 (2021)."},"author":[{"id":"516F03FA-93A3-11EA-A7C5-D6BE3DDC885E","orcid":"0000-0002-8176-4824","full_name":"Bolger-Munro, Madison","first_name":"Madison","last_name":"Bolger-Munro"},{"first_name":"Kate","full_name":"Choi, Kate","last_name":"Choi"},{"last_name":"Cheung","full_name":"Cheung, Faith","first_name":"Faith"},{"first_name":"Yi Tian","full_name":"Liu, Yi Tian","last_name":"Liu"},{"last_name":"Dang-Lawson","first_name":"May","full_name":"Dang-Lawson, May"},{"last_name":"Deretic","first_name":"Nikola","full_name":"Deretic, Nikola"},{"last_name":"Keane","first_name":"Connor","full_name":"Keane, Connor"},{"first_name":"Michael R.","full_name":"Gold, Michael R.","last_name":"Gold"}],"type":"journal_article","day":"13","pmid":1,"acknowledgement":"We thank the UBC Life Sciences Institute Imaging Facility andthe UBC Flow Cytometry Facility.","doi":"10.3389/fcell.2021.649433","ddc":["570"],"keyword":["B cell","actin","immune synapse","cell spreading","cofilin","WDR1 (AIP1)","LIM domain kinase","B cell receptor (BCR)"],"language":[{"iso":"eng"}],"date_created":"2021-05-09T22:01:37Z","month":"04","isi":1,"publisher":"Frontiers Media","status":"public","intvolume":"         9","publication":"Frontiers in Cell and Developmental Biology","department":[{"_id":"CaHe"}],"quality_controlled":"1","year":"2021","oa_version":"Published Version","has_accepted_license":"1","article_type":"original","publication_identifier":{"eissn":["2296-634X"]},"external_id":{"pmid":["33928084"],"isi":["000644419500001"]},"scopus_import":"1","date_updated":"2023-10-18T08:19:49Z","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","article_processing_charge":"No","_id":"9379","abstract":[{"lang":"eng","text":"When B cells encounter membrane-bound antigens, the formation and coalescence of B cell antigen receptor (BCR) microclusters amplifies BCR signaling. The ability of B cells to probe the surface of antigen-presenting cells (APCs) and respond to APC-bound antigens requires remodeling of the actin cytoskeleton. Initial BCR signaling stimulates actin-related protein (Arp) 2/3 complex-dependent actin polymerization, which drives B cell spreading as well as the centripetal movement and coalescence of BCR microclusters at the B cell-APC synapse. Sustained actin polymerization depends on concomitant actin filament depolymerization, which enables the recycling of actin monomers and Arp2/3 complexes. Cofilin-mediated severing of actin filaments is a rate-limiting step in the morphological changes that occur during immune synapse formation. Hence, regulators of cofilin activity such as WD repeat-containing protein 1 (Wdr1), LIM domain kinase (LIMK), and coactosin-like 1 (Cotl1) may also be essential for actin-dependent processes in B cells. Wdr1 enhances cofilin-mediated actin disassembly. Conversely, Cotl1 competes with cofilin for binding to actin and LIMK phosphorylates cofilin and prevents it from binding to actin filaments. We now show that Wdr1 and LIMK have distinct roles in BCR-induced assembly of the peripheral actin structures that drive B cell spreading, and that cofilin, Wdr1, and LIMK all contribute to the actin-dependent amplification of BCR signaling at the immune synapse. Depleting Cotl1 had no effect on these processes. Thus, the Wdr1-LIMK-cofilin axis is critical for BCR-induced actin remodeling and for B cell responses to APC-bound antigens."}],"date_published":"2021-04-13T00:00:00Z","article_number":"649433","file":[{"file_size":4076024,"creator":"kschuh","file_name":"2021_Frontiers_Cell_Bolger-Munro.pdf","checksum":"8c8a03575d2f7583f88dc3b658b0976b","access_level":"open_access","date_updated":"2021-05-11T15:09:23Z","relation":"main_file","file_id":"9386","content_type":"application/pdf","date_created":"2021-05-11T15:09:23Z","success":1}],"oa":1,"publication_status":"published","tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","image":"/images/cc_by.png","short":"CC BY (4.0)"},"volume":9,"file_date_updated":"2021-05-11T15:09:23Z"},{"year":"2021","oa_version":"None","article_type":"original","publication_identifier":{"eissn":["1540-8140"],"issn":["0021-9525"]},"external_id":{"pmid":["33929486"]},"scopus_import":"1","date_updated":"2021-11-25T15:33:08Z","user_id":"8b945eb4-e2f2-11eb-945a-df72226e66a9","article_processing_charge":"No","issue":"6","abstract":[{"text":"The T cell receptor (TCR) pathway receives, processes, and amplifies the signal from pathogenic antigens to the activation of T cells. Although major components in this pathway have been identified, the knowledge on how individual components cooperate to effectively transduce signals remains limited. Phase separation emerges as a biophysical principle in organizing signaling molecules into liquid-like condensates. Here, we report that phospholipase Cγ1 (PLCγ1) promotes phase separation of LAT, a key adaptor protein in the TCR pathway. PLCγ1 directly cross-links LAT through its two SH2 domains. PLCγ1 also protects LAT from dephosphorylation by the phosphatase CD45 and promotes LAT-dependent ERK activation and SLP76 phosphorylation. Intriguingly, a nonmonotonic effect of PLCγ1 on LAT clustering was discovered. Computer simulations, based on patchy particles, revealed how the cluster size is regulated by protein compositions. Together, these results define a critical function of PLCγ1 in promoting phase separation of the LAT complex and TCR signal transduction.","lang":"eng"}],"_id":"10337","date_published":"2021-04-30T00:00:00Z","article_number":"e202009154","publication_status":"published","tmp":{"legal_code_url":"https://creativecommons.org/licenses/by-nc-sa/4.0/legalcode","image":"/images/cc_by_nc_sa.png","name":"Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC BY-NC-SA 4.0)","short":"CC BY-NC-SA (4.0)"},"volume":220,"title":"PLCγ1 promotes phase separation of T cell signaling components","citation":{"ista":"Zeng L, Palaia I, Šarić A, Su X. 2021. PLCγ1 promotes phase separation of T cell signaling components. Journal of Cell Biology. 220(6), e202009154.","ieee":"L. Zeng, I. Palaia, A. Šarić, and X. Su, “PLCγ1 promotes phase separation of T cell signaling components,” <i>Journal of Cell Biology</i>, vol. 220, no. 6. Rockefeller University Press, 2021.","chicago":"Zeng, Longhui, Ivan Palaia, Anđela Šarić, and Xiaolei Su. “PLCγ1 Promotes Phase Separation of T Cell Signaling Components.” <i>Journal of Cell Biology</i>. Rockefeller University Press, 2021. <a href=\"https://doi.org/10.1083/jcb.202009154\">https://doi.org/10.1083/jcb.202009154</a>.","mla":"Zeng, Longhui, et al. “PLCγ1 Promotes Phase Separation of T Cell Signaling Components.” <i>Journal of Cell Biology</i>, vol. 220, no. 6, e202009154, Rockefeller University Press, 2021, doi:<a href=\"https://doi.org/10.1083/jcb.202009154\">10.1083/jcb.202009154</a>.","short":"L. Zeng, I. Palaia, A. Šarić, X. Su, Journal of Cell Biology 220 (2021).","apa":"Zeng, L., Palaia, I., Šarić, A., &#38; Su, X. (2021). PLCγ1 promotes phase separation of T cell signaling components. <i>Journal of Cell Biology</i>. Rockefeller University Press. <a href=\"https://doi.org/10.1083/jcb.202009154\">https://doi.org/10.1083/jcb.202009154</a>","ama":"Zeng L, Palaia I, Šarić A, Su X. PLCγ1 promotes phase separation of T cell signaling components. <i>Journal of Cell Biology</i>. 2021;220(6). doi:<a href=\"https://doi.org/10.1083/jcb.202009154\">10.1083/jcb.202009154</a>"},"type":"journal_article","author":[{"full_name":"Zeng, Longhui","first_name":"Longhui","last_name":"Zeng"},{"first_name":"Ivan","full_name":"Palaia, Ivan","last_name":"Palaia"},{"orcid":"0000-0002-7854-2139","id":"bf63d406-f056-11eb-b41d-f263a6566d8b","full_name":"Šarić, Anđela","first_name":"Anđela","last_name":"Šarić"},{"last_name":"Su","first_name":"Xiaolei","full_name":"Su, Xiaolei"}],"day":"30","pmid":1,"acknowledgement":"Charles H. Hood Foundation (NO AWARD) ; Rally Foundation (NO AWARD)","doi":"10.1083/jcb.202009154","keyword":["cell biology"],"language":[{"iso":"eng"}],"date_created":"2021-11-25T15:21:30Z","month":"04","extern":"1","publisher":"Rockefeller University Press","status":"public","intvolume":"       220","publication":"Journal of Cell Biology","quality_controlled":"1"},{"oa_version":"Published Version","has_accepted_license":"1","year":"2021","publication_identifier":{"issn":["2663-337X"]},"date_updated":"2023-09-22T09:58:30Z","user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","article_processing_charge":"No","date_published":"2021-09-02T00:00:00Z","_id":"9962","abstract":[{"text":"The brain is one of the largest and most complex organs and it is composed of billions of neurons that communicate together enabling e.g. consciousness. The cerebral cortex is the largest site of neural integration in the central nervous system. Concerted radial migration of newly born cortical projection neurons, from their birthplace to their final position, is a key step in the assembly of the cerebral cortex. The cellular and molecular mechanisms regulating radial neuronal migration in vivo are however still unclear. Recent evidence suggests that distinct signaling cues act cell-autonomously but differentially at certain steps during the overall migration process. Moreover, functional analysis of genetic mosaics (mutant neurons present in wild-type/heterozygote environment) using the MADM (Mosaic Analysis with Double Markers) analyses in comparison to global knockout also indicate a significant degree of non-cell-autonomous and/or community effects in the control of cortical neuron migration. The interactions of cell-intrinsic (cell-autonomous) and cell-extrinsic (non-cell-autonomous) components are largely unknown. In part of this thesis work we established a MADM-based experimental strategy for the quantitative analysis of cell-autonomous gene function versus non-cell-autonomous and/or community effects. The direct comparison of mutant neurons from the genetic mosaic (cell-autonomous) to mutant neurons in the conditional and/or global knockout (cell-autonomous + non-cell-autonomous) allows to quantitatively analyze non-cell-autonomous effects. Such analysis enable the high-resolution analysis of projection neuron migration dynamics in distinct environments with concomitant isolation of genomic and proteomic profiles. Using these experimental paradigms and in combination with computational modeling we show and characterize the nature of non-cell-autonomous effects to coordinate radial neuron migration. Furthermore, this thesis discusses recent developments in neurodevelopment with focus on neuronal polarization and non-cell-autonomous mechanisms in neuronal migration.","lang":"eng"}],"file":[{"file_id":"9971","relation":"source_file","content_type":"application/vnd.openxmlformats-officedocument.wordprocessingml.document","embargo_to":"open_access","date_created":"2021-08-30T09:17:39Z","creator":"ahansen","file_size":10629190,"file_name":"Thesis_Hansen.docx","checksum":"66b56f5b988b233dc66a4f4b4fb2cdfe","access_level":"closed","date_updated":"2022-09-03T22:30:04Z"},{"content_type":"application/pdf","file_id":"9972","relation":"main_file","date_created":"2021-08-30T09:29:44Z","embargo":"2022-09-02","file_name":"Thesis_Hansen_PDFA-1a.pdf","creator":"ahansen","file_size":13457469,"date_updated":"2022-09-03T22:30:04Z","access_level":"open_access","checksum":"204fa40321a1c6289b68c473634c4bf3"}],"oa":1,"publication_status":"published","tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","image":"/images/cc_by.png","short":"CC BY (4.0)"},"file_date_updated":"2022-09-03T22:30:04Z","title":"Cell-autonomous gene function and non-cell-autonomous effects in radial projection neuron migration","citation":{"ama":"Hansen AH. Cell-autonomous gene function and non-cell-autonomous effects in radial projection neuron migration. 2021. doi:<a href=\"https://doi.org/10.15479/at:ista:9962\">10.15479/at:ista:9962</a>","apa":"Hansen, A. H. (2021). <i>Cell-autonomous gene function and non-cell-autonomous effects in radial projection neuron migration</i>. Institute of Science and Technology Austria. <a href=\"https://doi.org/10.15479/at:ista:9962\">https://doi.org/10.15479/at:ista:9962</a>","short":"A.H. Hansen, Cell-Autonomous Gene Function and Non-Cell-Autonomous Effects in Radial Projection Neuron Migration, Institute of Science and Technology Austria, 2021.","mla":"Hansen, Andi H. <i>Cell-Autonomous Gene Function and Non-Cell-Autonomous Effects in Radial Projection Neuron Migration</i>. Institute of Science and Technology Austria, 2021, doi:<a href=\"https://doi.org/10.15479/at:ista:9962\">10.15479/at:ista:9962</a>.","chicago":"Hansen, Andi H. “Cell-Autonomous Gene Function and Non-Cell-Autonomous Effects in Radial Projection Neuron Migration.” Institute of Science and Technology Austria, 2021. <a href=\"https://doi.org/10.15479/at:ista:9962\">https://doi.org/10.15479/at:ista:9962</a>.","ieee":"A. H. Hansen, “Cell-autonomous gene function and non-cell-autonomous effects in radial projection neuron migration,” Institute of Science and Technology Austria, 2021.","ista":"Hansen AH. 2021. Cell-autonomous gene function and non-cell-autonomous effects in radial projection neuron migration. Institute of Science and Technology Austria."},"type":"dissertation","author":[{"last_name":"Hansen","first_name":"Andi H","full_name":"Hansen, Andi H","id":"38853E16-F248-11E8-B48F-1D18A9856A87"}],"alternative_title":["ISTA Thesis"],"day":"02","project":[{"_id":"2625A13E-B435-11E9-9278-68D0E5697425","grant_number":"24812","name":"Molecular Mechanisms of Radial Neuronal Migration"}],"related_material":{"record":[{"status":"public","relation":"part_of_dissertation","id":"8569"},{"id":"960","relation":"part_of_dissertation","status":"public"}]},"doi":"10.15479/at:ista:9962","ddc":["570"],"keyword":["Neuronal migration","Non-cell-autonomous","Cell-autonomous","Neurodevelopmental disease"],"language":[{"iso":"eng"}],"page":"182","supervisor":[{"id":"37B36620-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0003-2279-1061","first_name":"Simon","full_name":"Hippenmeyer, Simon","last_name":"Hippenmeyer"}],"date_created":"2021-08-29T12:36:50Z","month":"09","degree_awarded":"PhD","publisher":"Institute of Science and Technology Austria","status":"public","department":[{"_id":"GradSch"},{"_id":"SiHi"}]},{"_id":"9986","abstract":[{"text":"Size control is a fundamental question in biology, showing incremental complexity in plants, whose cells possess a rigid cell wall. The phytohormone auxin is a vital growth regulator with central importance for differential growth control. Our results indicate that auxin-reliant growth programs affect the molecular complexity of xyloglucans, the major type of cell wall hemicellulose in eudicots. Auxin-dependent induction and repression of growth coincide with reduced and enhanced molecular complexity of xyloglucans, respectively. In agreement with a proposed function in growth control, genetic interference with xyloglucan side decorations distinctly modulates auxin-dependent differential growth rates. Our work proposes that auxin-dependent growth programs have a spatially defined effect on xyloglucan’s molecular structure, which in turn affects cell wall mechanics and specifies differential, gravitropic hypocotyl growth.","lang":"eng"}],"date_published":"2021-08-26T00:00:00Z","file":[{"date_created":"2021-09-06T12:50:19Z","content_type":"application/pdf","file_id":"9988","relation":"main_file","checksum":"6b7055cf89f1b7ed8594c3fdf56f000b","date_updated":"2021-09-07T09:04:53Z","access_level":"open_access","file_name":"2021_IntJMolecularSciences_Velasquez.pdf","creator":"cchlebak","file_size":2162247}],"article_number":"9222","article_processing_charge":"Yes","issue":"17","tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","image":"/images/cc_by.png","short":"CC BY (4.0)"},"volume":22,"file_date_updated":"2021-09-07T09:04:53Z","oa":1,"publication_status":"published","has_accepted_license":"1","oa_version":"Published Version","year":"2021","article_type":"original","publication_identifier":{"issn":["1661-6596"],"eissn":["1422-0067"]},"external_id":{"pmid":["34502129"],"isi":["000694347100001"]},"scopus_import":"1","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","date_updated":"2023-10-31T19:29:38Z","date_created":"2021-09-05T22:01:24Z","month":"08","status":"public","intvolume":"        22","publication":"International Journal of Molecular Sciences","quality_controlled":"1","department":[{"_id":"EvBe"}],"isi":1,"publisher":"MDPI","author":[{"first_name":"Silvia Melina","full_name":"Velasquez, Silvia Melina","last_name":"Velasquez"},{"last_name":"Guo","first_name":"Xiaoyuan","full_name":"Guo, Xiaoyuan"},{"orcid":"0000-0003-4675-6893","id":"460C6802-F248-11E8-B48F-1D18A9856A87","full_name":"Gallemi, Marçal","first_name":"Marçal","last_name":"Gallemi"},{"last_name":"Aryal","first_name":"Bibek","full_name":"Aryal, Bibek"},{"full_name":"Venhuizen, Peter","first_name":"Peter","last_name":"Venhuizen"},{"last_name":"Barbez","full_name":"Barbez, Elke","first_name":"Elke"},{"full_name":"Dünser, Kai Alexander","first_name":"Kai Alexander","last_name":"Dünser"},{"first_name":"Martin","full_name":"Darino, Martin","last_name":"Darino"},{"full_name":"Pӗnčík, Aleš","first_name":"Aleš","last_name":"Pӗnčík"},{"full_name":"Novák, Ondřej","first_name":"Ondřej","last_name":"Novák"},{"last_name":"Kalyna","first_name":"Maria","full_name":"Kalyna, Maria"},{"first_name":"Gregory","full_name":"Mouille, Gregory","last_name":"Mouille"},{"id":"38F4F166-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-8510-9739","last_name":"Benková","first_name":"Eva","full_name":"Benková, Eva"},{"full_name":"Bhalerao, Rishikesh P.","first_name":"Rishikesh P.","last_name":"Bhalerao"},{"last_name":"Mravec","full_name":"Mravec, Jozef","first_name":"Jozef"},{"last_name":"Kleine-Vehn","full_name":"Kleine-Vehn, Jürgen","first_name":"Jürgen"}],"type":"journal_article","day":"26","title":"Xyloglucan remodeling defines auxin-dependent differential tissue expansion in plants","citation":{"mla":"Velasquez, Silvia Melina, et al. “Xyloglucan Remodeling Defines Auxin-Dependent Differential Tissue Expansion in Plants.” <i>International Journal of Molecular Sciences</i>, vol. 22, no. 17, 9222, MDPI, 2021, doi:<a href=\"https://doi.org/10.3390/ijms22179222\">10.3390/ijms22179222</a>.","chicago":"Velasquez, Silvia Melina, Xiaoyuan Guo, Marçal Gallemi, Bibek Aryal, Peter Venhuizen, Elke Barbez, Kai Alexander Dünser, et al. “Xyloglucan Remodeling Defines Auxin-Dependent Differential Tissue Expansion in Plants.” <i>International Journal of Molecular Sciences</i>. MDPI, 2021. <a href=\"https://doi.org/10.3390/ijms22179222\">https://doi.org/10.3390/ijms22179222</a>.","ieee":"S. M. Velasquez <i>et al.</i>, “Xyloglucan remodeling defines auxin-dependent differential tissue expansion in plants,” <i>International Journal of Molecular Sciences</i>, vol. 22, no. 17. MDPI, 2021.","ista":"Velasquez SM, Guo X, Gallemi M, Aryal B, Venhuizen P, Barbez E, Dünser KA, Darino M, Pӗnčík A, Novák O, Kalyna M, Mouille G, Benková E, Bhalerao RP, Mravec J, Kleine-Vehn J. 2021. Xyloglucan remodeling defines auxin-dependent differential tissue expansion in plants. International Journal of Molecular Sciences. 22(17), 9222.","ama":"Velasquez SM, Guo X, Gallemi M, et al. Xyloglucan remodeling defines auxin-dependent differential tissue expansion in plants. <i>International Journal of Molecular Sciences</i>. 2021;22(17). doi:<a href=\"https://doi.org/10.3390/ijms22179222\">10.3390/ijms22179222</a>","apa":"Velasquez, S. M., Guo, X., Gallemi, M., Aryal, B., Venhuizen, P., Barbez, E., … Kleine-Vehn, J. (2021). Xyloglucan remodeling defines auxin-dependent differential tissue expansion in plants. <i>International Journal of Molecular Sciences</i>. MDPI. <a href=\"https://doi.org/10.3390/ijms22179222\">https://doi.org/10.3390/ijms22179222</a>","short":"S.M. Velasquez, X. Guo, M. Gallemi, B. Aryal, P. Venhuizen, E. Barbez, K.A. Dünser, M. Darino, A. Pӗnčík, O. Novák, M. Kalyna, G. Mouille, E. Benková, R.P. Bhalerao, J. Mravec, J. Kleine-Vehn, International Journal of Molecular Sciences 22 (2021)."},"doi":"10.3390/ijms22179222","ddc":["575"],"keyword":["auxin","growth","cell wall","xyloglucans","hypocotyls","gravitropism"],"language":[{"iso":"eng"}],"pmid":1,"acknowledgement":"We are grateful to Paul Knox, Markus Pauly, Malcom O’Neill, and Ignacio Zarra for providing published material; the BOKU-VIBT Imaging Center for access and M. Debreczeny for expertise; J.I. Thaker and Georg Seifert for critical reading.\r\n"},{"publication":"eLife","quality_controlled":"1","department":[{"_id":"CaHe"}],"intvolume":"        10","status":"public","publisher":"eLife Sciences Publications","isi":1,"month":"08","date_created":"2021-09-12T22:01:23Z","keyword":["cell delamination","apical constriction","dragging","mechanical forces","collective 18 locomotion","dorsal forerunner cells","zebrafish"],"language":[{"iso":"eng"}],"doi":"10.7554/eLife.66483","ddc":["570"],"pmid":1,"project":[{"_id":"260F1432-B435-11E9-9278-68D0E5697425","call_identifier":"H2020","grant_number":"742573","name":"Interaction and feedback between cell mechanics and fate specification in vertebrate gastrulation"}],"day":"27","type":"journal_article","author":[{"first_name":"Eduardo","full_name":"Pulgar, Eduardo","last_name":"Pulgar"},{"id":"3436488C-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0001-5130-2226","full_name":"Schwayer, Cornelia","first_name":"Cornelia","last_name":"Schwayer"},{"last_name":"Guerrero","first_name":"Néstor","full_name":"Guerrero, Néstor"},{"last_name":"López","first_name":"Loreto","full_name":"López, Loreto"},{"first_name":"Susana","full_name":"Márquez, Susana","last_name":"Márquez"},{"last_name":"Härtel","full_name":"Härtel, Steffen","first_name":"Steffen"},{"last_name":"Soto","first_name":"Rodrigo","full_name":"Soto, Rodrigo"},{"full_name":"Heisenberg, Carl Philipp","first_name":"Carl Philipp","last_name":"Heisenberg"},{"last_name":"Concha","full_name":"Concha, Miguel L.","first_name":"Miguel L."}],"citation":{"short":"E. Pulgar, C. Schwayer, N. Guerrero, L. López, S. Márquez, S. Härtel, R. Soto, C.P. Heisenberg, M.L. Concha, ELife 10 (2021).","apa":"Pulgar, E., Schwayer, C., Guerrero, N., López, L., Márquez, S., Härtel, S., … Concha, M. L. (2021). Apical contacts stemming from incomplete delamination guide progenitor cell allocation through a dragging mechanism. <i>ELife</i>. eLife Sciences Publications. <a href=\"https://doi.org/10.7554/eLife.66483\">https://doi.org/10.7554/eLife.66483</a>","ama":"Pulgar E, Schwayer C, Guerrero N, et al. Apical contacts stemming from incomplete delamination guide progenitor cell allocation through a dragging mechanism. <i>eLife</i>. 2021;10. doi:<a href=\"https://doi.org/10.7554/eLife.66483\">10.7554/eLife.66483</a>","ista":"Pulgar E, Schwayer C, Guerrero N, López L, Márquez S, Härtel S, Soto R, Heisenberg CP, Concha ML. 2021. Apical contacts stemming from incomplete delamination guide progenitor cell allocation through a dragging mechanism. eLife. 10, e66483.","ieee":"E. Pulgar <i>et al.</i>, “Apical contacts stemming from incomplete delamination guide progenitor cell allocation through a dragging mechanism,” <i>eLife</i>, vol. 10. eLife Sciences Publications, 2021.","chicago":"Pulgar, Eduardo, Cornelia Schwayer, Néstor Guerrero, Loreto López, Susana Márquez, Steffen Härtel, Rodrigo Soto, Carl Philipp Heisenberg, and Miguel L. Concha. “Apical Contacts Stemming from Incomplete Delamination Guide Progenitor Cell Allocation through a Dragging Mechanism.” <i>ELife</i>. eLife Sciences Publications, 2021. <a href=\"https://doi.org/10.7554/eLife.66483\">https://doi.org/10.7554/eLife.66483</a>.","mla":"Pulgar, Eduardo, et al. “Apical Contacts Stemming from Incomplete Delamination Guide Progenitor Cell Allocation through a Dragging Mechanism.” <i>ELife</i>, vol. 10, e66483, eLife Sciences Publications, 2021, doi:<a href=\"https://doi.org/10.7554/eLife.66483\">10.7554/eLife.66483</a>."},"ec_funded":1,"title":"Apical contacts stemming from incomplete delamination guide progenitor cell allocation through a dragging mechanism","file_date_updated":"2022-05-13T08:03:37Z","tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","image":"/images/cc_by.png","short":"CC BY (4.0)"},"volume":10,"publication_status":"published","oa":1,"file":[{"file_id":"11371","relation":"main_file","content_type":"application/pdf","success":1,"date_created":"2022-05-13T08:03:37Z","file_size":9010446,"creator":"dernst","file_name":"2021_eLife_Pulgar.pdf","access_level":"open_access","date_updated":"2022-05-13T08:03:37Z","checksum":"a3f82b0499cc822ac1eab48a01f3f57e"}],"article_number":"e66483","date_published":"2021-08-27T00:00:00Z","_id":"9999","abstract":[{"text":"The developmental strategies used by progenitor cells to endure a safe journey from their induction place towards the site of terminal differentiation are still poorly understood. Here we uncovered a progenitor cell allocation mechanism that stems from an incomplete process of epithelial delamination that allows progenitors to coordinate their movement with adjacent extra-embryonic tissues. Progenitors of the zebrafish laterality organ originate from the surface epithelial enveloping layer by an apical constriction process of cell delamination. During this process, progenitors retain long-term apical contacts that enable the epithelial layer to pull a subset of progenitors along their way towards the vegetal pole. The remaining delaminated progenitors follow apically-attached progenitors’ movement by a co-attraction mechanism, avoiding sequestration by the adjacent endoderm, ensuring their fate and collective allocation at the differentiation site. Thus, we reveal that incomplete delamination serves as a cellular platform for coordinated tissue movements during development. Impact Statement: Incomplete delamination serves as a cellular platform for coordinated tissue movements during development, guiding newly formed progenitor cell groups to the differentiation site.","lang":"eng"}],"article_processing_charge":"Yes","external_id":{"isi":["000700428500001"],"pmid":["34448451"]},"scopus_import":"1","date_updated":"2023-08-14T06:53:33Z","user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","publication_identifier":{"eissn":["2050-084X"]},"article_type":"original","year":"2021","has_accepted_license":"1","oa_version":"Published Version"},{"external_id":{"pmid":["31907035"]},"date_updated":"2021-01-12T08:19:02Z","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","publication_identifier":{"issn":["1741-7007"]},"article_type":"original","year":"2020","oa_version":"Published Version","publication_status":"published","oa":1,"main_file_link":[{"url":"https://doi.org/10.1186/s12915-019-0733-6","open_access":"1"}],"volume":18,"article_processing_charge":"No","article_number":"2","_id":"8402","abstract":[{"lang":"eng","text":"Background: The mitochondrial pyruvate carrier (MPC) plays a central role in energy metabolism by transporting pyruvate across the inner mitochondrial membrane. Its heterodimeric composition and homology to SWEET and semiSWEET transporters set the MPC apart from the canonical mitochondrial carrier family (named MCF or SLC25). The import of the canonical carriers is mediated by the carrier translocase of the inner membrane (TIM22) pathway and is dependent on their structure, which features an even number of transmembrane segments and both termini in the intermembrane space. The import pathway of MPC proteins has not been elucidated. The odd number of transmembrane segments and positioning of the N-terminus in the matrix argues against an import via the TIM22 carrier pathway but favors an import via the flexible presequence pathway.\r\nResults: Here, we systematically analyzed the import pathways of Mpc2 and Mpc3 and report that, contrary to an expected import via the flexible presequence pathway, yeast MPC proteins with an odd number of transmembrane segments and matrix-exposed N-terminus are imported by the carrier pathway, using the receptor Tom70, small TIM chaperones, and the TIM22 complex. The TIM9·10 complex chaperones MPC proteins through the mitochondrial intermembrane space using conserved hydrophobic motifs that are also required for the interaction with canonical carrier proteins.\r\nConclusions: The carrier pathway can import paired and non-paired transmembrane helices and translocate N-termini to either side of the mitochondrial inner membrane, revealing an unexpected versatility of the mitochondrial import pathway for non-cleavable inner membrane proteins."}],"date_published":"2020-01-06T00:00:00Z","pmid":1,"keyword":["Biotechnology","Plant Science","General Biochemistry","Genetics and Molecular Biology","Developmental Biology","Cell Biology","Physiology","Ecology","Evolution","Behavior and Systematics","Structural Biology","General Agricultural and Biological Sciences"],"language":[{"iso":"eng"}],"doi":"10.1186/s12915-019-0733-6","citation":{"mla":"Rampelt, Heike, et al. “The Mitochondrial Carrier Pathway Transports Non-Canonical Substrates with an Odd Number of Transmembrane Segments.” <i>BMC Biology</i>, vol. 18, 2, Springer Nature, 2020, doi:<a href=\"https://doi.org/10.1186/s12915-019-0733-6\">10.1186/s12915-019-0733-6</a>.","ieee":"H. Rampelt <i>et al.</i>, “The mitochondrial carrier pathway transports non-canonical substrates with an odd number of transmembrane segments,” <i>BMC Biology</i>, vol. 18. Springer Nature, 2020.","ista":"Rampelt H, Sucec I, Bersch B, Horten P, Perschil I, Martinou J-C, van der Laan M, Wiedemann N, Schanda P, Pfanner N. 2020. The mitochondrial carrier pathway transports non-canonical substrates with an odd number of transmembrane segments. BMC Biology. 18, 2.","chicago":"Rampelt, Heike, Iva Sucec, Beate Bersch, Patrick Horten, Inge Perschil, Jean-Claude Martinou, Martin van der Laan, Nils Wiedemann, Paul Schanda, and Nikolaus Pfanner. “The Mitochondrial Carrier Pathway Transports Non-Canonical Substrates with an Odd Number of Transmembrane Segments.” <i>BMC Biology</i>. Springer Nature, 2020. <a href=\"https://doi.org/10.1186/s12915-019-0733-6\">https://doi.org/10.1186/s12915-019-0733-6</a>.","apa":"Rampelt, H., Sucec, I., Bersch, B., Horten, P., Perschil, I., Martinou, J.-C., … Pfanner, N. (2020). The mitochondrial carrier pathway transports non-canonical substrates with an odd number of transmembrane segments. <i>BMC Biology</i>. Springer Nature. <a href=\"https://doi.org/10.1186/s12915-019-0733-6\">https://doi.org/10.1186/s12915-019-0733-6</a>","ama":"Rampelt H, Sucec I, Bersch B, et al. The mitochondrial carrier pathway transports non-canonical substrates with an odd number of transmembrane segments. <i>BMC Biology</i>. 2020;18. doi:<a href=\"https://doi.org/10.1186/s12915-019-0733-6\">10.1186/s12915-019-0733-6</a>","short":"H. Rampelt, I. Sucec, B. Bersch, P. Horten, I. Perschil, J.-C. Martinou, M. van der Laan, N. Wiedemann, P. Schanda, N. Pfanner, BMC Biology 18 (2020)."},"title":"The mitochondrial carrier pathway transports non-canonical substrates with an odd number of transmembrane segments","day":"06","author":[{"full_name":"Rampelt, Heike","first_name":"Heike","last_name":"Rampelt"},{"last_name":"Sucec","first_name":"Iva","full_name":"Sucec, Iva"},{"full_name":"Bersch, Beate","first_name":"Beate","last_name":"Bersch"},{"last_name":"Horten","first_name":"Patrick","full_name":"Horten, Patrick"},{"full_name":"Perschil, Inge","first_name":"Inge","last_name":"Perschil"},{"full_name":"Martinou, Jean-Claude","first_name":"Jean-Claude","last_name":"Martinou"},{"last_name":"van der Laan","full_name":"van der Laan, Martin","first_name":"Martin"},{"last_name":"Wiedemann","first_name":"Nils","full_name":"Wiedemann, Nils"},{"id":"7B541462-FAF6-11E9-A490-E8DFE5697425","orcid":"0000-0002-9350-7606","first_name":"Paul","full_name":"Schanda, Paul","last_name":"Schanda"},{"full_name":"Pfanner, Nikolaus","first_name":"Nikolaus","last_name":"Pfanner"}],"type":"journal_article","publisher":"Springer Nature","publication":"BMC Biology","quality_controlled":"1","status":"public","intvolume":"        18","month":"01","extern":"1","date_created":"2020-09-17T10:26:53Z"},{"date_created":"2020-09-17T14:00:33Z","month":"04","intvolume":"       133","status":"public","department":[{"_id":"FlSc"}],"quality_controlled":"1","publication":"Journal of Cell Science","isi":1,"publisher":"The Company of Biologists","type":"journal_article","author":[{"full_name":"Dimchev, Georgi A","first_name":"Georgi A","last_name":"Dimchev","orcid":"0000-0001-8370-6161","id":"38C393BE-F248-11E8-B48F-1D18A9856A87"},{"full_name":"Amiri, Behnam","first_name":"Behnam","last_name":"Amiri"},{"full_name":"Humphries, Ashley C.","first_name":"Ashley C.","last_name":"Humphries"},{"last_name":"Schaks","full_name":"Schaks, Matthias","first_name":"Matthias"},{"full_name":"Dimchev, Vanessa","first_name":"Vanessa","last_name":"Dimchev"},{"last_name":"Stradal","full_name":"Stradal, Theresia E. B.","first_name":"Theresia E. B."},{"last_name":"Faix","first_name":"Jan","full_name":"Faix, Jan"},{"first_name":"Matthias","full_name":"Krause, Matthias","last_name":"Krause"},{"last_name":"Way","first_name":"Michael","full_name":"Way, Michael"},{"first_name":"Martin","full_name":"Falcke, Martin","last_name":"Falcke"},{"first_name":"Klemens","full_name":"Rottner, Klemens","last_name":"Rottner"}],"day":"09","title":"Lamellipodin tunes cell migration by stabilizing protrusions and promoting adhesion formation","citation":{"mla":"Dimchev, Georgi A., et al. “Lamellipodin Tunes Cell Migration by Stabilizing Protrusions and Promoting Adhesion Formation.” <i>Journal of Cell Science</i>, vol. 133, no. 7, jcs239020, The Company of Biologists, 2020, doi:<a href=\"https://doi.org/10.1242/jcs.239020\">10.1242/jcs.239020</a>.","chicago":"Dimchev, Georgi A, Behnam Amiri, Ashley C. Humphries, Matthias Schaks, Vanessa Dimchev, Theresia E. B. Stradal, Jan Faix, et al. “Lamellipodin Tunes Cell Migration by Stabilizing Protrusions and Promoting Adhesion Formation.” <i>Journal of Cell Science</i>. The Company of Biologists, 2020. <a href=\"https://doi.org/10.1242/jcs.239020\">https://doi.org/10.1242/jcs.239020</a>.","ieee":"G. A. Dimchev <i>et al.</i>, “Lamellipodin tunes cell migration by stabilizing protrusions and promoting adhesion formation,” <i>Journal of Cell Science</i>, vol. 133, no. 7. The Company of Biologists, 2020.","ista":"Dimchev GA, Amiri B, Humphries AC, Schaks M, Dimchev V, Stradal TEB, Faix J, Krause M, Way M, Falcke M, Rottner K. 2020. Lamellipodin tunes cell migration by stabilizing protrusions and promoting adhesion formation. Journal of Cell Science. 133(7), jcs239020.","ama":"Dimchev GA, Amiri B, Humphries AC, et al. Lamellipodin tunes cell migration by stabilizing protrusions and promoting adhesion formation. <i>Journal of Cell Science</i>. 2020;133(7). doi:<a href=\"https://doi.org/10.1242/jcs.239020\">10.1242/jcs.239020</a>","apa":"Dimchev, G. A., Amiri, B., Humphries, A. C., Schaks, M., Dimchev, V., Stradal, T. E. B., … Rottner, K. (2020). Lamellipodin tunes cell migration by stabilizing protrusions and promoting adhesion formation. <i>Journal of Cell Science</i>. The Company of Biologists. <a href=\"https://doi.org/10.1242/jcs.239020\">https://doi.org/10.1242/jcs.239020</a>","short":"G.A. Dimchev, B. Amiri, A.C. Humphries, M. Schaks, V. Dimchev, T.E.B. Stradal, J. Faix, M. Krause, M. Way, M. Falcke, K. Rottner, Journal of Cell Science 133 (2020)."},"ddc":["570"],"doi":"10.1242/jcs.239020","language":[{"iso":"eng"}],"keyword":["Cell Biology"],"acknowledgement":"This work was supported in part by Deutsche Forschungsgemeinschaft (DFG)[GRK2223/1, RO2414/5-1 (to K.R.), FA350/11-1 (to M.F.) and FA330/11-1 (to J.F.)],as well as by intramural funding from the Helmholtz Association (to T.E.B.S. andK.R.). G.D. was additionally funded by the Austrian Science Fund (FWF) LiseMeitner Program [M-2495]. A.C.H. and M.W. are supported by the Francis CrickInstitute, which receives its core funding from Cancer Research UK [FC001209], theMedical Research Council [FC001209] and the Wellcome Trust [FC001209]. M.K. issupported by the Biotechnology and Biological Sciences Research Council [BB/F011431/1, BB/J000590/1, BB/N000226/1]. Deposited in PMC for release after 6months.","pmid":1,"project":[{"grant_number":"M02495","name":"Protein structure and function in filopodia across scales","_id":"2674F658-B435-11E9-9278-68D0E5697425","call_identifier":"FWF"}],"_id":"8434","date_published":"2020-04-09T00:00:00Z","abstract":[{"lang":"eng","text":"Efficient migration on adhesive surfaces involves the protrusion of lamellipodial actin networks and their subsequent stabilization by nascent adhesions. The actin-binding protein lamellipodin (Lpd) is thought to play a critical role in lamellipodium protrusion, by delivering Ena/VASP proteins onto the growing plus ends of actin filaments and by interacting with the WAVE regulatory complex, an activator of the Arp2/3 complex, at the leading edge. Using B16-F1 melanoma cell lines, we demonstrate that genetic ablation of Lpd compromises protrusion efficiency and coincident cell migration without altering essential parameters of lamellipodia, including their maximal rate of forward advancement and actin polymerization. We also confirmed lamellipodia and migration phenotypes with CRISPR/Cas9-mediated Lpd knockout Rat2 fibroblasts, excluding cell type-specific effects. Moreover, computer-aided analysis of cell-edge morphodynamics on B16-F1 cell lamellipodia revealed that loss of Lpd correlates with reduced temporal protrusion maintenance as a prerequisite of nascent adhesion formation. We conclude that Lpd optimizes protrusion and nascent adhesion formation by counteracting frequent, chaotic retraction and membrane ruffling.This article has an associated First Person interview with the first author of the paper. "}],"article_number":"jcs239020","file":[{"date_created":"2020-09-17T14:07:51Z","relation":"main_file","file_id":"8435","content_type":"application/pdf","access_level":"open_access","date_updated":"2020-10-11T22:30:02Z","checksum":"ba917e551acc4ece2884b751434df9ae","embargo":"2020-10-10","creator":"dernst","file_size":13493302,"file_name":"2020_JournalCellScience_Dimchev.pdf"}],"issue":"7","article_processing_charge":"No","volume":133,"file_date_updated":"2020-10-11T22:30:02Z","oa":1,"publication_status":"published","oa_version":"Published Version","year":"2020","has_accepted_license":"1","article_type":"original","publication_identifier":{"issn":["0021-9533"],"eissn":["1477-9137"]},"date_updated":"2023-09-05T15:41:48Z","user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","external_id":{"pmid":[" 32094266"],"isi":["000534387800005"]}},{"publication":"Journal of Structural Biology","quality_controlled":"1","department":[{"_id":"FlSc"}],"intvolume":"       212","status":"public","publisher":"Elsevier","isi":1,"month":"12","date_created":"2020-09-29T13:24:06Z","keyword":["electron microscopy","cryo-EM","EM sample preparation","3D printing","cell culture"],"language":[{"iso":"eng"}],"ddc":["570"],"doi":"10.1016/j.jsb.2020.107633","related_material":{"record":[{"status":"public","id":"14592","relation":"used_in_publication"},{"status":"public","id":"12491","relation":"dissertation_contains"}]},"project":[{"_id":"9B954C5C-BA93-11EA-9121-9846C619BF3A","name":"Structure and isoform diversity of the Arp2/3 complex","grant_number":"P33367"},{"name":"NÖ-Fonds Preis für die Jungforscherin des Jahres am IST Austria","_id":"059B463C-7A3F-11EA-A408-12923DDC885E"}],"acknowledgement":"This work was supported by the Austrian Science Fund (FWF, P33367) to FKMS. BZ acknowledges support by the Niederösterreich Fond. This research was also supported by the Scientific Service Units (SSU) of IST Austria through resources provided by Scientific Computing (SciComp), the Life Science Facility (LSF), the BioImaging Facility (BIF) and the Electron Microscopy Facility (EMF). We thank Georgi Dimchev (IST Austria) and Sonja Jacob (Vienna Biocenter Core Facilities) for testing our grid holders in different experimental setups and Daniel Gütl and the Kondrashov group (IST Austria) for granting us repeated access to their 3D printers. We also thank Jonna Alanko and the Sixt lab (IST Austria) for providing us HeLa cells, primary BL6 mouse tail fibroblasts, NIH 3T3 fibroblasts and human telomerase immortalised foreskin fibroblasts for our experiments. We are thankful to Ori Avinoam and William Wan for helpful comments on the manuscript and also thank Dorotea Fracchiolla (Art&Science) for illustrating the graphical abstract.","day":"01","author":[{"first_name":"Florian","full_name":"Fäßler, Florian","last_name":"Fäßler","id":"404F5528-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0001-7149-769X"},{"id":"45FD126C-F248-11E8-B48F-1D18A9856A87","full_name":"Zens, Bettina","first_name":"Bettina","last_name":"Zens"},{"first_name":"Robert","full_name":"Hauschild, Robert","last_name":"Hauschild","id":"4E01D6B4-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0001-9843-3522"},{"orcid":"0000-0003-4790-8078","id":"48AD8942-F248-11E8-B48F-1D18A9856A87","last_name":"Schur","full_name":"Schur, Florian KM","first_name":"Florian KM"}],"type":"journal_article","citation":{"short":"F. Fäßler, B. Zens, R. Hauschild, F.K. Schur, Journal of Structural Biology 212 (2020).","ama":"Fäßler F, Zens B, Hauschild R, Schur FK. 3D printed cell culture grid holders for improved cellular specimen preparation in cryo-electron microscopy. <i>Journal of Structural Biology</i>. 2020;212(3). doi:<a href=\"https://doi.org/10.1016/j.jsb.2020.107633\">10.1016/j.jsb.2020.107633</a>","apa":"Fäßler, F., Zens, B., Hauschild, R., &#38; Schur, F. K. (2020). 3D printed cell culture grid holders for improved cellular specimen preparation in cryo-electron microscopy. <i>Journal of Structural Biology</i>. Elsevier. <a href=\"https://doi.org/10.1016/j.jsb.2020.107633\">https://doi.org/10.1016/j.jsb.2020.107633</a>","chicago":"Fäßler, Florian, Bettina Zens, Robert Hauschild, and Florian KM Schur. “3D Printed Cell Culture Grid Holders for Improved Cellular Specimen Preparation in Cryo-Electron Microscopy.” <i>Journal of Structural Biology</i>. Elsevier, 2020. <a href=\"https://doi.org/10.1016/j.jsb.2020.107633\">https://doi.org/10.1016/j.jsb.2020.107633</a>.","ista":"Fäßler F, Zens B, Hauschild R, Schur FK. 2020. 3D printed cell culture grid holders for improved cellular specimen preparation in cryo-electron microscopy. Journal of Structural Biology. 212(3), 107633.","ieee":"F. Fäßler, B. Zens, R. Hauschild, and F. K. Schur, “3D printed cell culture grid holders for improved cellular specimen preparation in cryo-electron microscopy,” <i>Journal of Structural Biology</i>, vol. 212, no. 3. Elsevier, 2020.","mla":"Fäßler, Florian, et al. “3D Printed Cell Culture Grid Holders for Improved Cellular Specimen Preparation in Cryo-Electron Microscopy.” <i>Journal of Structural Biology</i>, vol. 212, no. 3, 107633, Elsevier, 2020, doi:<a href=\"https://doi.org/10.1016/j.jsb.2020.107633\">10.1016/j.jsb.2020.107633</a>."},"title":"3D printed cell culture grid holders for improved cellular specimen preparation in cryo-electron microscopy","file_date_updated":"2020-12-10T14:01:10Z","tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","image":"/images/cc_by.png","short":"CC BY (4.0)"},"volume":212,"publication_status":"published","oa":1,"article_number":"107633","file":[{"success":1,"date_created":"2020-12-10T14:01:10Z","content_type":"application/pdf","file_id":"8937","relation":"main_file","date_updated":"2020-12-10T14:01:10Z","access_level":"open_access","checksum":"c48cbf594e84fc2f91966ffaafc0918c","file_name":"2020_JourStrucBiology_Faessler.pdf","file_size":7076870,"creator":"dernst"}],"_id":"8586","date_published":"2020-12-01T00:00:00Z","abstract":[{"lang":"eng","text":"Cryo-electron microscopy (cryo-EM) of cellular specimens provides insights into biological processes and structures within a native context. However, a major challenge still lies in the efficient and reproducible preparation of adherent cells for subsequent cryo-EM analysis. This is due to the sensitivity of many cellular specimens to the varying seeding and culturing conditions required for EM experiments, the often limited amount of cellular material and also the fragility of EM grids and their substrate. Here, we present low-cost and reusable 3D printed grid holders, designed to improve specimen preparation when culturing challenging cellular samples directly on grids. The described grid holders increase cell culture reproducibility and throughput, and reduce the resources required for cell culturing. We show that grid holders can be integrated into various cryo-EM workflows, including micro-patterning approaches to control cell seeding on grids, and for generating samples for cryo-focused ion beam milling and cryo-electron tomography experiments. Their adaptable design allows for the generation of specialized grid holders customized to a large variety of applications."}],"article_processing_charge":"Yes (via OA deal)","issue":"3","external_id":{"isi":["000600997800008"]},"scopus_import":"1","user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","date_updated":"2024-03-25T23:30:04Z","publication_identifier":{"issn":["1047-8477"]},"acknowledged_ssus":[{"_id":"ScienComp"},{"_id":"LifeSc"},{"_id":"Bio"},{"_id":"EM-Fac"}],"article_type":"original","oa_version":"Published Version","has_accepted_license":"1","year":"2020"},{"citation":{"ista":"Toyama BH, Arrojo e Drigo R, Lev-Ram V, Ramachandra R, Deerinck TJ, Lechene C, Ellisman MH, Hetzer M. 2019. Visualization of long-lived proteins reveals age mosaicism within nuclei of postmitotic cells. Journal of Cell Biology. 218(2), 433–444.","ieee":"B. H. Toyama <i>et al.</i>, “Visualization of long-lived proteins reveals age mosaicism within nuclei of postmitotic cells,” <i>Journal of Cell Biology</i>, vol. 218, no. 2. Rockefeller University Press, pp. 433–444, 2019.","chicago":"Toyama, Brandon H., Rafael Arrojo e Drigo, Varda Lev-Ram, Ranjan Ramachandra, Thomas J. Deerinck, Claude Lechene, Mark H. Ellisman, and Martin Hetzer. “Visualization of Long-Lived Proteins Reveals Age Mosaicism within Nuclei of Postmitotic Cells.” <i>Journal of Cell Biology</i>. Rockefeller University Press, 2019. <a href=\"https://doi.org/10.1083/jcb.201809123\">https://doi.org/10.1083/jcb.201809123</a>.","mla":"Toyama, Brandon H., et al. “Visualization of Long-Lived Proteins Reveals Age Mosaicism within Nuclei of Postmitotic Cells.” <i>Journal of Cell Biology</i>, vol. 218, no. 2, Rockefeller University Press, 2019, pp. 433–44, doi:<a href=\"https://doi.org/10.1083/jcb.201809123\">10.1083/jcb.201809123</a>.","short":"B.H. Toyama, R. Arrojo e Drigo, V. Lev-Ram, R. Ramachandra, T.J. Deerinck, C. Lechene, M.H. Ellisman, M. Hetzer, Journal of Cell Biology 218 (2019) 433–444.","apa":"Toyama, B. H., Arrojo e Drigo, R., Lev-Ram, V., Ramachandra, R., Deerinck, T. J., Lechene, C., … Hetzer, M. (2019). Visualization of long-lived proteins reveals age mosaicism within nuclei of postmitotic cells. <i>Journal of Cell Biology</i>. Rockefeller University Press. <a href=\"https://doi.org/10.1083/jcb.201809123\">https://doi.org/10.1083/jcb.201809123</a>","ama":"Toyama BH, Arrojo e Drigo R, Lev-Ram V, et al. Visualization of long-lived proteins reveals age mosaicism within nuclei of postmitotic cells. <i>Journal of Cell Biology</i>. 2019;218(2):433-444. doi:<a href=\"https://doi.org/10.1083/jcb.201809123\">10.1083/jcb.201809123</a>"},"title":"Visualization of long-lived proteins reveals age mosaicism within nuclei of postmitotic cells","day":"04","type":"journal_article","author":[{"last_name":"Toyama","full_name":"Toyama, Brandon H.","first_name":"Brandon H."},{"first_name":"Rafael","full_name":"Arrojo e Drigo, Rafael","last_name":"Arrojo e Drigo"},{"last_name":"Lev-Ram","full_name":"Lev-Ram, Varda","first_name":"Varda"},{"last_name":"Ramachandra","full_name":"Ramachandra, Ranjan","first_name":"Ranjan"},{"first_name":"Thomas J.","full_name":"Deerinck, Thomas J.","last_name":"Deerinck"},{"last_name":"Lechene","first_name":"Claude","full_name":"Lechene, Claude"},{"last_name":"Ellisman","first_name":"Mark H.","full_name":"Ellisman, Mark H."},{"id":"86c0d31b-b4eb-11ec-ac5a-eae7b2e135ed","orcid":"0000-0002-2111-992X","full_name":"HETZER, Martin W","first_name":"Martin W","last_name":"HETZER"}],"pmid":1,"language":[{"iso":"eng"}],"keyword":["Cell Biology"],"ddc":["570"],"doi":"10.1083/jcb.201809123","page":"433-444","extern":"1","month":"02","date_created":"2022-04-07T07:45:11Z","publisher":"Rockefeller University Press","quality_controlled":"1","publication":"Journal of Cell Biology","intvolume":"       218","status":"public","article_type":"original","year":"2019","has_accepted_license":"1","oa_version":"Published Version","date_updated":"2022-07-18T08:31:52Z","user_id":"72615eeb-f1f3-11ec-aa25-d4573ddc34fd","external_id":{"pmid":["30552100"]},"scopus_import":"1","publication_identifier":{"eissn":["1540-8140"],"issn":["0021-9525"]},"issue":"2","article_processing_charge":"No","file":[{"date_updated":"2022-04-08T08:26:32Z","access_level":"open_access","checksum":"7964ebbf833b0b35f9fba840eea9531d","file_name":"2019_JCB_Toyama.pdf","creator":"dernst","file_size":2503838,"success":1,"date_created":"2022-04-08T08:26:32Z","content_type":"application/pdf","file_id":"11139","relation":"main_file"}],"_id":"11061","date_published":"2019-02-04T00:00:00Z","abstract":[{"lang":"eng","text":"Many adult tissues contain postmitotic cells as old as the host organism. The only organelle that does not turn over in these cells is the nucleus, and its maintenance represents a formidable challenge, as it harbors regulatory proteins that persist throughout adulthood. Here we developed strategies to visualize two classes of such long-lived proteins, histones and nucleoporins, to understand the function of protein longevity in nuclear maintenance. Genome-wide mapping of histones revealed specific enrichment of long-lived variants at silent gene loci. Interestingly, nuclear pores are maintained by piecemeal replacement of subunits, resulting in mosaic complexes composed of polypeptides with vastly different ages. In contrast, nondividing quiescent cells remove old nuclear pores in an ESCRT-dependent manner. Our findings reveal distinct molecular strategies of nuclear maintenance, linking lifelong protein persistence to gene regulation and nuclear integrity."}],"publication_status":"published","oa":1,"file_date_updated":"2022-04-08T08:26:32Z","volume":218,"tmp":{"legal_code_url":"https://creativecommons.org/licenses/by-nc-sa/4.0/legalcode","image":"/images/cc_by_nc_sa.png","name":"Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC BY-NC-SA 4.0)","short":"CC BY-NC-SA (4.0)"}},{"extern":"1","month":"08","date_created":"2022-04-07T07:45:21Z","page":"343-351.e3","quality_controlled":"1","publication":"Cell Metabolism","status":"public","intvolume":"        30","publisher":"Elsevier","day":"06","type":"journal_article","author":[{"last_name":"Arrojo e Drigo","full_name":"Arrojo e Drigo, Rafael","first_name":"Rafael"},{"last_name":"Lev-Ram","full_name":"Lev-Ram, Varda","first_name":"Varda"},{"first_name":"Swati","full_name":"Tyagi, Swati","last_name":"Tyagi"},{"last_name":"Ramachandra","first_name":"Ranjan","full_name":"Ramachandra, Ranjan"},{"full_name":"Deerinck, Thomas","first_name":"Thomas","last_name":"Deerinck"},{"first_name":"Eric","full_name":"Bushong, Eric","last_name":"Bushong"},{"last_name":"Phan","full_name":"Phan, Sebastien","first_name":"Sebastien"},{"last_name":"Orphan","first_name":"Victoria","full_name":"Orphan, Victoria"},{"last_name":"Lechene","first_name":"Claude","full_name":"Lechene, Claude"},{"full_name":"Ellisman, Mark H.","first_name":"Mark H.","last_name":"Ellisman"},{"id":"86c0d31b-b4eb-11ec-ac5a-eae7b2e135ed","orcid":"0000-0002-2111-992X","full_name":"HETZER, Martin W","first_name":"Martin W","last_name":"HETZER"}],"citation":{"short":"R. Arrojo e Drigo, V. Lev-Ram, S. Tyagi, R. Ramachandra, T. Deerinck, E. Bushong, S. Phan, V. Orphan, C. Lechene, M.H. Ellisman, M. Hetzer, Cell Metabolism 30 (2019) 343–351.e3.","ama":"Arrojo e Drigo R, Lev-Ram V, Tyagi S, et al. Age mosaicism across multiple scales in adult tissues. <i>Cell Metabolism</i>. 2019;30(2):343-351.e3. doi:<a href=\"https://doi.org/10.1016/j.cmet.2019.05.010\">10.1016/j.cmet.2019.05.010</a>","apa":"Arrojo e Drigo, R., Lev-Ram, V., Tyagi, S., Ramachandra, R., Deerinck, T., Bushong, E., … Hetzer, M. (2019). Age mosaicism across multiple scales in adult tissues. <i>Cell Metabolism</i>. Elsevier. <a href=\"https://doi.org/10.1016/j.cmet.2019.05.010\">https://doi.org/10.1016/j.cmet.2019.05.010</a>","chicago":"Arrojo e Drigo, Rafael, Varda Lev-Ram, Swati Tyagi, Ranjan Ramachandra, Thomas Deerinck, Eric Bushong, Sebastien Phan, et al. “Age Mosaicism across Multiple Scales in Adult Tissues.” <i>Cell Metabolism</i>. Elsevier, 2019. <a href=\"https://doi.org/10.1016/j.cmet.2019.05.010\">https://doi.org/10.1016/j.cmet.2019.05.010</a>.","ista":"Arrojo e Drigo R, Lev-Ram V, Tyagi S, Ramachandra R, Deerinck T, Bushong E, Phan S, Orphan V, Lechene C, Ellisman MH, Hetzer M. 2019. Age mosaicism across multiple scales in adult tissues. Cell Metabolism. 30(2), 343–351.e3.","ieee":"R. Arrojo e Drigo <i>et al.</i>, “Age mosaicism across multiple scales in adult tissues,” <i>Cell Metabolism</i>, vol. 30, no. 2. Elsevier, p. 343–351.e3, 2019.","mla":"Arrojo e Drigo, Rafael, et al. “Age Mosaicism across Multiple Scales in Adult Tissues.” <i>Cell Metabolism</i>, vol. 30, no. 2, Elsevier, 2019, p. 343–351.e3, doi:<a href=\"https://doi.org/10.1016/j.cmet.2019.05.010\">10.1016/j.cmet.2019.05.010</a>."},"title":"Age mosaicism across multiple scales in adult tissues","language":[{"iso":"eng"}],"keyword":["Cell Biology","Molecular Biology","Physiology"],"doi":"10.1016/j.cmet.2019.05.010","pmid":1,"_id":"11062","abstract":[{"lang":"eng","text":"Most neurons are not replaced during an animal’s lifetime. This nondividing state is characterized by extreme longevity and age-dependent decline of key regulatory proteins. To study the lifespans of cells and proteins in adult tissues, we combined isotope labeling of mice with a hybrid imaging method (MIMS-EM). Using 15N mapping, we show that liver and pancreas are composed of cells with vastly different ages, many as old as the animal. Strikingly, we also found that a subset of fibroblasts and endothelial cells, both known for their replicative potential, are characterized by the absence of cell division during adulthood. In addition, we show that the primary cilia of beta cells and neurons contains different structural regions with vastly different lifespans. Based on these results, we propose that age mosaicism across multiple scales is a fundamental principle of adult tissue, cell, and protein complex organization."}],"date_published":"2019-08-06T00:00:00Z","issue":"2","article_processing_charge":"No","volume":30,"publication_status":"published","oa":1,"main_file_link":[{"url":"https://doi.org/10.1016/j.cmet.2019.05.010","open_access":"1"}],"article_type":"original","year":"2019","oa_version":"Published Version","user_id":"72615eeb-f1f3-11ec-aa25-d4573ddc34fd","date_updated":"2022-07-18T08:32:30Z","external_id":{"pmid":["31178361"]},"scopus_import":"1","publication_identifier":{"issn":["1550-4131"]}},{"date_updated":"2023-10-18T08:49:17Z","user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","publication_identifier":{"eissn":["2663-337X"],"isbn":["978-3-99078-002-2"]},"oa_version":"Published Version","year":"2019","has_accepted_license":"1","publication_status":"published","oa":1,"file_date_updated":"2020-10-17T22:30:03Z","article_processing_charge":"No","file":[{"embargo_to":"open_access","date_created":"2019-10-15T05:28:42Z","relation":"source_file","file_id":"6950","content_type":"application/vnd.openxmlformats-officedocument.wordprocessingml.document","checksum":"00d100d6468e31e583051e0a006b640c","access_level":"closed","date_updated":"2020-10-17T22:30:03Z","creator":"akopf","file_size":74735267,"file_name":"Kopf_PhD_Thesis.docx"},{"file_size":52787224,"creator":"akopf","file_name":"Kopf_PhD_Thesis1.pdf","embargo":"2020-10-16","checksum":"5d1baa899993ae6ca81aebebe1797000","access_level":"open_access","date_updated":"2020-10-17T22:30:03Z","file_id":"6951","relation":"main_file","content_type":"application/pdf","date_created":"2019-10-15T05:28:47Z"}],"_id":"6891","date_published":"2019-07-24T00:00:00Z","abstract":[{"lang":"eng","text":"While cells of mesenchymal or epithelial origin perform their effector functions in a purely anchorage dependent manner, cells derived from the hematopoietic lineage are not committed to operate only within a specific niche. Instead, these cells are able to function autonomously of the molecular composition in a broad range of tissue compartments. By this means, cells of the hematopoietic lineage retain the capacity to disseminate into connective tissue and recirculate between organs, building the foundation for essential processes such as tissue regeneration or immune surveillance. \r\nCells of the immune system, specifically leukocytes, are extraordinarily good at performing this task. These cells are able to flexibly shift their mode of migration between an adhesion-mediated and an adhesion-independent manner, instantaneously accommodating for any changes in molecular composition of the external scaffold. The key component driving directed leukocyte migration is the chemokine receptor 7, which guides the cell along gradients of chemokine ligand. Therefore, the physical destination of migrating leukocytes is purely deterministic, i.e. given by global directional cues such as chemokine gradients. \r\nNevertheless, these cells typically reside in three-dimensional scaffolds of inhomogeneous complexity, raising the question whether cells are able to locally discriminate between multiple optional migration routes. Current literature provides evidence that leukocytes, specifically dendritic cells, do indeed probe their surrounding by virtue of multiple explorative protrusions. However, it remains enigmatic how these cells decide which one is the more favorable route to follow and what are the key players involved in performing this task. Due to the heterogeneous environment of most tissues, and the vast adaptability of migrating leukocytes, at this time it is not clear to what extent leukocytes are able to optimize their migratory strategy by adapting their level of adhesiveness. And, given the fact that leukocyte migration is characterized by branched cell shapes in combination with high migration velocities, it is reasonable to assume that these cells require fine tuned shape maintenance mechanisms that tightly coordinate protrusion and adhesion dynamics in a spatiotemporal manner. \r\nTherefore, this study aimed to elucidate how rapidly migrating leukocytes opt for an ideal migratory path while maintaining a continuous cell shape and balancing adhesive forces to efficiently navigate through complex microenvironments. \r\nThe results of this study unraveled a role for the microtubule cytoskeleton in promoting the decision making process during path finding and for the first time point towards a microtubule-mediated function in cell shape maintenance of highly ramified cells such as dendritic cells. Furthermore, we found that migrating low-adhesive leukocytes are able to instantaneously adapt to increased tensile load by engaging adhesion receptors. This response was only occurring tangential to the substrate while adhesive properties in the vertical direction were not increased. As leukocytes are primed for rapid migration velocities, these results demonstrate that leukocyte integrins are able to confer a high level of traction forces parallel to the cell membrane along the direction of migration without wasting energy in gluing the cell to the substrate. \r\nThus, the data in the here presented thesis provide new insights into the pivotal role of cytoskeletal dynamics and the mechanisms of force transduction during leukocyte migration. \r\nThereby the here presented results help to further define fundamental principles underlying leukocyte migration and open up potential therapeutic avenues of clinical relevance.\r\n"}],"project":[{"_id":"265E2996-B435-11E9-9278-68D0E5697425","call_identifier":"FWF","name":"Nano-Analytics of Cellular Systems","grant_number":"W01250-B20"}],"related_material":{"record":[{"status":"public","id":"6328","relation":"part_of_dissertation"},{"status":"public","id":"15","relation":"part_of_dissertation"},{"id":"6877","relation":"part_of_dissertation","status":"public"}],"link":[{"relation":"press_release","url":"https://ist.ac.at/en/news/feeling-like-a-cell/"}]},"language":[{"iso":"eng"}],"keyword":["cell biology","immunology","leukocyte","migration","microfluidics"],"ddc":["570"],"doi":"10.15479/AT:ISTA:6891","citation":{"mla":"Kopf, Aglaja. <i>The Implication of Cytoskeletal Dynamics on Leukocyte Migration</i>. Institute of Science and Technology Austria, 2019, doi:<a href=\"https://doi.org/10.15479/AT:ISTA:6891\">10.15479/AT:ISTA:6891</a>.","ista":"Kopf A. 2019. The implication of cytoskeletal dynamics on leukocyte migration. Institute of Science and Technology Austria.","ieee":"A. Kopf, “The implication of cytoskeletal dynamics on leukocyte migration,” Institute of Science and Technology Austria, 2019.","chicago":"Kopf, Aglaja. “The Implication of Cytoskeletal Dynamics on Leukocyte Migration.” Institute of Science and Technology Austria, 2019. <a href=\"https://doi.org/10.15479/AT:ISTA:6891\">https://doi.org/10.15479/AT:ISTA:6891</a>.","apa":"Kopf, A. (2019). <i>The implication of cytoskeletal dynamics on leukocyte migration</i>. Institute of Science and Technology Austria. <a href=\"https://doi.org/10.15479/AT:ISTA:6891\">https://doi.org/10.15479/AT:ISTA:6891</a>","ama":"Kopf A. The implication of cytoskeletal dynamics on leukocyte migration. 2019. doi:<a href=\"https://doi.org/10.15479/AT:ISTA:6891\">10.15479/AT:ISTA:6891</a>","short":"A. Kopf, The Implication of Cytoskeletal Dynamics on Leukocyte Migration, Institute of Science and Technology Austria, 2019."},"title":"The implication of cytoskeletal dynamics on leukocyte migration","day":"24","alternative_title":["ISTA Thesis"],"type":"dissertation","author":[{"orcid":"0000-0002-2187-6656","id":"31DAC7B6-F248-11E8-B48F-1D18A9856A87","first_name":"Aglaja","full_name":"Kopf, Aglaja","last_name":"Kopf"}],"publisher":"Institute of Science and Technology Austria","degree_awarded":"PhD","department":[{"_id":"MiSi"}],"status":"public","page":"171","month":"07","date_created":"2019-09-19T08:19:44Z","supervisor":[{"orcid":"0000-0002-6620-9179","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","last_name":"Sixt","first_name":"Michael K","full_name":"Sixt, Michael K"}]},{"doi":"10.1016/j.celrep.2019.05.005","ddc":["576"],"keyword":["cardiomyocyte","cell cycle","Cofilin2","cytoskeleton","Hippo","microRNA","regeneration","YAP"],"language":[{"iso":"eng"}],"pmid":1,"type":"journal_article","author":[{"first_name":"Consuelo","full_name":"Torrini, Consuelo","last_name":"Torrini"},{"last_name":"Cubero","first_name":"Ryan J","full_name":"Cubero, Ryan J","orcid":"0000-0003-0002-1867","id":"850B2E12-9CD4-11E9-837F-E719E6697425"},{"first_name":"Ellen","full_name":"Dirkx, Ellen","last_name":"Dirkx"},{"first_name":"Luca","full_name":"Braga, Luca","last_name":"Braga"},{"first_name":"Hashim","full_name":"Ali, Hashim","last_name":"Ali"},{"last_name":"Prosdocimo","first_name":"Giulia","full_name":"Prosdocimo, Giulia"},{"full_name":"Gutierrez, Maria Ines","first_name":"Maria Ines","last_name":"Gutierrez"},{"last_name":"Collesi","full_name":"Collesi, Chiara","first_name":"Chiara"},{"full_name":"Licastro, Danilo","first_name":"Danilo","last_name":"Licastro"},{"full_name":"Zentilin, Lorena","first_name":"Lorena","last_name":"Zentilin"},{"first_name":"Miguel","full_name":"Mano, Miguel","last_name":"Mano"},{"full_name":"Zacchigna, Serena","first_name":"Serena","last_name":"Zacchigna"},{"last_name":"Vendruscolo","full_name":"Vendruscolo, Michele","first_name":"Michele"},{"full_name":"Marsili, Matteo","first_name":"Matteo","last_name":"Marsili"},{"last_name":"Samal","full_name":"Samal, Areejit","first_name":"Areejit"},{"last_name":"Giacca","first_name":"Mauro","full_name":"Giacca, Mauro"}],"day":"28","title":"Common regulatory pathways mediate activity of microRNAs inducing cardiomyocyte proliferation","citation":{"apa":"Torrini, C., Cubero, R. J., Dirkx, E., Braga, L., Ali, H., Prosdocimo, G., … Giacca, M. (2019). Common regulatory pathways mediate activity of microRNAs inducing cardiomyocyte proliferation. <i>Cell Reports</i>. Elsevier. <a href=\"https://doi.org/10.1016/j.celrep.2019.05.005\">https://doi.org/10.1016/j.celrep.2019.05.005</a>","ama":"Torrini C, Cubero RJ, Dirkx E, et al. Common regulatory pathways mediate activity of microRNAs inducing cardiomyocyte proliferation. <i>Cell Reports</i>. 2019;27(9):2759-2771.e5. doi:<a href=\"https://doi.org/10.1016/j.celrep.2019.05.005\">10.1016/j.celrep.2019.05.005</a>","short":"C. Torrini, R.J. Cubero, E. Dirkx, L. Braga, H. Ali, G. Prosdocimo, M.I. Gutierrez, C. Collesi, D. Licastro, L. Zentilin, M. Mano, S. Zacchigna, M. Vendruscolo, M. Marsili, A. Samal, M. Giacca, Cell Reports 27 (2019) 2759–2771.e5.","mla":"Torrini, Consuelo, et al. “Common Regulatory Pathways Mediate Activity of MicroRNAs Inducing Cardiomyocyte Proliferation.” <i>Cell Reports</i>, vol. 27, no. 9, Elsevier, 2019, p. 2759–2771.e5, doi:<a href=\"https://doi.org/10.1016/j.celrep.2019.05.005\">10.1016/j.celrep.2019.05.005</a>.","ista":"Torrini C, Cubero RJ, Dirkx E, Braga L, Ali H, Prosdocimo G, Gutierrez MI, Collesi C, Licastro D, Zentilin L, Mano M, Zacchigna S, Vendruscolo M, Marsili M, Samal A, Giacca M. 2019. Common regulatory pathways mediate activity of microRNAs inducing cardiomyocyte proliferation. Cell Reports. 27(9), 2759–2771.e5.","ieee":"C. Torrini <i>et al.</i>, “Common regulatory pathways mediate activity of microRNAs inducing cardiomyocyte proliferation,” <i>Cell Reports</i>, vol. 27, no. 9. Elsevier, p. 2759–2771.e5, 2019.","chicago":"Torrini, Consuelo, Ryan J Cubero, Ellen Dirkx, Luca Braga, Hashim Ali, Giulia Prosdocimo, Maria Ines Gutierrez, et al. “Common Regulatory Pathways Mediate Activity of MicroRNAs Inducing Cardiomyocyte Proliferation.” <i>Cell Reports</i>. Elsevier, 2019. <a href=\"https://doi.org/10.1016/j.celrep.2019.05.005\">https://doi.org/10.1016/j.celrep.2019.05.005</a>."},"intvolume":"        27","status":"public","publication":"Cell Reports","quality_controlled":"1","publisher":"Elsevier","date_created":"2019-11-26T22:30:07Z","month":"05","extern":"1","page":"2759-2771.e5","publication_identifier":{"issn":["2211-1247"]},"external_id":{"pmid":["31141697"]},"user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","date_updated":"2021-01-12T08:11:56Z","has_accepted_license":"1","year":"2019","oa_version":"Published Version","article_type":"original","tmp":{"name":"Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0)","image":"/images/cc_by_nc_nd.png","legal_code_url":"https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode","short":"CC BY-NC-ND (4.0)"},"volume":27,"file_date_updated":"2020-07-14T12:47:50Z","oa":1,"publication_status":"published","date_published":"2019-05-28T00:00:00Z","_id":"7128","abstract":[{"text":"Loss of functional cardiomyocytes is a major determinant of heart failure after myocardial infarction. Previous high throughput screening studies have identified a few microRNAs (miRNAs) that can induce cardiomyocyte proliferation and stimulate cardiac regeneration in mice. Here, we show that all of the most effective of these miRNAs activate nuclear localization of the master transcriptional cofactor Yes-associated protein (YAP) and induce expression of YAP-responsive genes. In particular, miR-199a-3p directly targets two mRNAs coding for proteins impinging on the Hippo pathway, the upstream YAP inhibitory kinase TAOK1, and the E3 ubiquitin ligase β-TrCP, which leads to YAP degradation. Several of the pro-proliferative miRNAs (including miR-199a-3p) also inhibit filamentous actin depolymerization by targeting Cofilin2, a process that by itself activates YAP nuclear translocation. Thus, activation of YAP and modulation of the actin cytoskeleton are major components of the pro-proliferative action of miR-199a-3p and other miRNAs that induce cardiomyocyte proliferation.","lang":"eng"}],"file":[{"file_id":"7129","relation":"main_file","content_type":"application/pdf","date_created":"2019-11-26T22:30:43Z","creator":"rcubero","file_size":4650750,"file_name":"torrini_cellreports_2019.pdf","checksum":"c5d855d07263bfec718673385d0ea2d7","access_level":"open_access","date_updated":"2020-07-14T12:47:50Z"}],"article_processing_charge":"Yes","issue":"9"},{"quality_controlled":"1","publication":"BMC Biology","status":"public","intvolume":"        17","publisher":"Springer Nature","extern":"1","month":"10","date_created":"2021-11-26T11:25:03Z","language":[{"iso":"eng"}],"keyword":["cell biology"],"doi":"10.1186/s12915-019-0700-2","ddc":["570"],"acknowledgement":"We thank Jeremy Carlton, Mike Staddon, Geraint Harker, and the Wellcome Trust Consortium “Archaeal Origins of Eukaryotic Cell Organisation” for fruitful conversations. We thank Peter Wirnsberger and Tine Curk for discussions about the membrane model implementation.","pmid":1,"day":"22","author":[{"last_name":"Harker-Kirschneck","first_name":"Lena","full_name":"Harker-Kirschneck, Lena"},{"last_name":"Baum","full_name":"Baum, Buzz","first_name":"Buzz"},{"last_name":"Šarić","first_name":"Anđela","full_name":"Šarić, Anđela","id":"bf63d406-f056-11eb-b41d-f263a6566d8b","orcid":"0000-0002-7854-2139"}],"type":"journal_article","citation":{"apa":"Harker-Kirschneck, L., Baum, B., &#38; Šarić, A. (2019). Changes in ESCRT-III filament geometry drive membrane remodelling and fission in silico. <i>BMC Biology</i>. Springer Nature. <a href=\"https://doi.org/10.1186/s12915-019-0700-2\">https://doi.org/10.1186/s12915-019-0700-2</a>","ama":"Harker-Kirschneck L, Baum B, Šarić A. Changes in ESCRT-III filament geometry drive membrane remodelling and fission in silico. <i>BMC Biology</i>. 2019;17(1). doi:<a href=\"https://doi.org/10.1186/s12915-019-0700-2\">10.1186/s12915-019-0700-2</a>","short":"L. Harker-Kirschneck, B. Baum, A. Šarić, BMC Biology 17 (2019).","mla":"Harker-Kirschneck, Lena, et al. “Changes in ESCRT-III Filament Geometry Drive Membrane Remodelling and Fission in Silico.” <i>BMC Biology</i>, vol. 17, no. 1, 82, Springer Nature, 2019, doi:<a href=\"https://doi.org/10.1186/s12915-019-0700-2\">10.1186/s12915-019-0700-2</a>.","ista":"Harker-Kirschneck L, Baum B, Šarić A. 2019. Changes in ESCRT-III filament geometry drive membrane remodelling and fission in silico. BMC Biology. 17(1), 82.","ieee":"L. Harker-Kirschneck, B. Baum, and A. Šarić, “Changes in ESCRT-III filament geometry drive membrane remodelling and fission in silico,” <i>BMC Biology</i>, vol. 17, no. 1. Springer Nature, 2019.","chicago":"Harker-Kirschneck, Lena, Buzz Baum, and Anđela Šarić. “Changes in ESCRT-III Filament Geometry Drive Membrane Remodelling and Fission in Silico.” <i>BMC Biology</i>. Springer Nature, 2019. <a href=\"https://doi.org/10.1186/s12915-019-0700-2\">https://doi.org/10.1186/s12915-019-0700-2</a>."},"title":"Changes in ESCRT-III filament geometry drive membrane remodelling and fission in silico","file_date_updated":"2021-11-26T11:37:54Z","volume":17,"tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","image":"/images/cc_by.png","short":"CC BY (4.0)"},"publication_status":"published","oa":1,"main_file_link":[{"open_access":"1","url":"https://www.biorxiv.org/content/10.1101/559898"}],"file":[{"content_type":"application/pdf","file_id":"10356","relation":"main_file","date_created":"2021-11-26T11:37:54Z","success":1,"file_name":"2019_BMCBio_Harker_Kirschneck.pdf","creator":"cchlebak","file_size":1648926,"checksum":"31d8bae55a376d30925f53f7e1a02396","date_updated":"2021-11-26T11:37:54Z","access_level":"open_access"}],"article_number":"82","_id":"10354","date_published":"2019-10-22T00:00:00Z","abstract":[{"text":"Background\r\nESCRT-III is a membrane remodelling filament with the unique ability to cut membranes from the inside of the membrane neck. It is essential for the final stage of cell division, the formation of vesicles, the release of viruses, and membrane repair. Distinct from other cytoskeletal filaments, ESCRT-III filaments do not consume energy themselves, but work in conjunction with another ATP-consuming complex. Despite rapid progress in describing the cell biology of ESCRT-III, we lack an understanding of the physical mechanisms behind its force production and membrane remodelling.\r\nResults\r\nHere we present a minimal coarse-grained model that captures all the experimentally reported cases of ESCRT-III driven membrane sculpting, including the formation of downward and upward cones and tubules. This model suggests that a change in the geometry of membrane bound ESCRT-III filaments—from a flat spiral to a 3D helix—drives membrane deformation. We then show that such repetitive filament geometry transitions can induce the fission of cargo-containing vesicles.\r\nConclusions\r\nOur model provides a general physical mechanism that explains the full range of ESCRT-III-dependent membrane remodelling and scission events observed in cells. This mechanism for filament force production is distinct from the mechanisms described for other cytoskeletal elements discovered so far. The mechanistic principles revealed here suggest new ways of manipulating ESCRT-III-driven processes in cells and could be used to guide the engineering of synthetic membrane-sculpting systems.","lang":"eng"}],"issue":"1","article_processing_charge":"No","user_id":"8b945eb4-e2f2-11eb-945a-df72226e66a9","date_updated":"2021-11-26T11:54:29Z","scopus_import":"1","external_id":{"pmid":["31640700"]},"publication_identifier":{"issn":["1741-7007"]},"article_type":"original","year":"2019","oa_version":"Published Version","has_accepted_license":"1"},{"page":"8379-8393","article_processing_charge":"No","issue":"22","month":"06","extern":"1","_id":"8440","date_created":"2020-09-18T10:05:18Z","abstract":[{"lang":"eng","text":"Mycobacterium tuberculosis can remain dormant in the host, an ability that explains the failure of many current tuberculosis treatments. Recently, the natural products cyclomarin, ecumicin, and lassomycin have been shown to efficiently kill Mycobacterium tuberculosis persisters. Their target is the N-terminal domain of the hexameric AAA+ ATPase ClpC1, which recognizes, unfolds, and translocates protein substrates, such as proteins containing phosphorylated arginine residues, to the ClpP1P2 protease for degradation. Surprisingly, these antibiotics do not inhibit ClpC1 ATPase activity, and how they cause cell death is still unclear. Here, using NMR and small-angle X-ray scattering, we demonstrate that arginine-phosphate binding to the ClpC1 N-terminal domain induces millisecond dynamics. We show that these dynamics are caused by conformational changes and do not result from unfolding or oligomerization of this domain. Cyclomarin binding to this domain specifically blocked these N-terminal dynamics. On the basis of these results, we propose a mechanism of action involving cyclomarin-induced restriction of ClpC1 dynamics, which modulates the chaperone enzymatic activity leading eventually to cell death."}],"date_published":"2018-06-01T00:00:00Z","publisher":"American Society for Biochemistry & Molecular Biology","publication_status":"published","publication":"Journal of Biological Chemistry","quality_controlled":"1","status":"public","intvolume":"       293","volume":293,"citation":{"apa":"Weinhäupl, K., Brennich, M., Kazmaier, U., Lelievre, J., Ballell, L., Goldberg, A., … Fraga, H. (2018). The antibiotic cyclomarin blocks arginine-phosphate–induced millisecond dynamics in the N-terminal domain of ClpC1 from Mycobacterium tuberculosis. <i>Journal of Biological Chemistry</i>. American Society for Biochemistry &#38; Molecular Biology. <a href=\"https://doi.org/10.1074/jbc.ra118.002251\">https://doi.org/10.1074/jbc.ra118.002251</a>","ama":"Weinhäupl K, Brennich M, Kazmaier U, et al. The antibiotic cyclomarin blocks arginine-phosphate–induced millisecond dynamics in the N-terminal domain of ClpC1 from Mycobacterium tuberculosis. <i>Journal of Biological Chemistry</i>. 2018;293(22):8379-8393. doi:<a href=\"https://doi.org/10.1074/jbc.ra118.002251\">10.1074/jbc.ra118.002251</a>","short":"K. Weinhäupl, M. Brennich, U. Kazmaier, J. Lelievre, L. Ballell, A. Goldberg, P. Schanda, H. Fraga, Journal of Biological Chemistry 293 (2018) 8379–8393.","mla":"Weinhäupl, Katharina, et al. “The Antibiotic Cyclomarin Blocks Arginine-Phosphate–Induced Millisecond Dynamics in the N-Terminal Domain of ClpC1 from Mycobacterium Tuberculosis.” <i>Journal of Biological Chemistry</i>, vol. 293, no. 22, American Society for Biochemistry &#38; Molecular Biology, 2018, pp. 8379–93, doi:<a href=\"https://doi.org/10.1074/jbc.ra118.002251\">10.1074/jbc.ra118.002251</a>.","ista":"Weinhäupl K, Brennich M, Kazmaier U, Lelievre J, Ballell L, Goldberg A, Schanda P, Fraga H. 2018. The antibiotic cyclomarin blocks arginine-phosphate–induced millisecond dynamics in the N-terminal domain of ClpC1 from Mycobacterium tuberculosis. Journal of Biological Chemistry. 293(22), 8379–8393.","ieee":"K. Weinhäupl <i>et al.</i>, “The antibiotic cyclomarin blocks arginine-phosphate–induced millisecond dynamics in the N-terminal domain of ClpC1 from Mycobacterium tuberculosis,” <i>Journal of Biological Chemistry</i>, vol. 293, no. 22. American Society for Biochemistry &#38; Molecular Biology, pp. 8379–8393, 2018.","chicago":"Weinhäupl, Katharina, Martha Brennich, Uli Kazmaier, Joel Lelievre, Lluis Ballell, Alfred Goldberg, Paul Schanda, and Hugo Fraga. “The Antibiotic Cyclomarin Blocks Arginine-Phosphate–Induced Millisecond Dynamics in the N-Terminal Domain of ClpC1 from Mycobacterium Tuberculosis.” <i>Journal of Biological Chemistry</i>. American Society for Biochemistry &#38; Molecular Biology, 2018. <a href=\"https://doi.org/10.1074/jbc.ra118.002251\">https://doi.org/10.1074/jbc.ra118.002251</a>."},"title":"The antibiotic cyclomarin blocks arginine-phosphate–induced millisecond dynamics in the N-terminal domain of ClpC1 from Mycobacterium tuberculosis","article_type":"original","day":"01","author":[{"last_name":"Weinhäupl","full_name":"Weinhäupl, Katharina","first_name":"Katharina"},{"last_name":"Brennich","full_name":"Brennich, Martha","first_name":"Martha"},{"full_name":"Kazmaier, Uli","first_name":"Uli","last_name":"Kazmaier"},{"last_name":"Lelievre","first_name":"Joel","full_name":"Lelievre, Joel"},{"first_name":"Lluis","full_name":"Ballell, Lluis","last_name":"Ballell"},{"full_name":"Goldberg, Alfred","first_name":"Alfred","last_name":"Goldberg"},{"id":"7B541462-FAF6-11E9-A490-E8DFE5697425","orcid":"0000-0002-9350-7606","full_name":"Schanda, Paul","first_name":"Paul","last_name":"Schanda"},{"last_name":"Fraga","first_name":"Hugo","full_name":"Fraga, Hugo"}],"type":"journal_article","year":"2018","oa_version":"None","keyword":["Cell Biology","Biochemistry","Molecular Biology"],"language":[{"iso":"eng"}],"date_updated":"2021-01-12T08:19:17Z","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","publication_identifier":{"issn":["0021-9258","1083-351X"]},"doi":"10.1074/jbc.ra118.002251"}]