[{"article_type":"original","publication_status":"published","author":[{"last_name":"Qian","full_name":"Qian, Qingyin","first_name":"Qingyin"},{"orcid":"0000-0003-1671-9434","last_name":"Nagai","full_name":"Nagai, Hiroki","id":"608df3e6-e2ab-11ed-8890-c9318cec7da4","first_name":"Hiroki"},{"first_name":"Yuya","full_name":"Sanaki, Yuya","last_name":"Sanaki"},{"first_name":"Makoto","full_name":"Hayashi, Makoto","last_name":"Hayashi"},{"last_name":"Kimura","first_name":"Kenichi","full_name":"Kimura, Kenichi"},{"last_name":"Nakajima","full_name":"Nakajima, Yu Ichiro","first_name":"Yu Ichiro"},{"last_name":"Niwa","first_name":"Ryusuke","full_name":"Niwa, Ryusuke"}],"user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","oa":1,"abstract":[{"lang":"eng","text":"Cellular plasticity, the ability of a differentiated cell to adopt another phenotypic identity, is restricted under basal conditions, but can be elicited upon damage. However, the molecular mechanism enabling such plasticity remains largely unexplored. Here, we report damage-induced cellular plasticity of secretory enteroendocrine cells (EEs) in the adult Drosophila midgut. Ionizing radiation induces EE fate conversion and activates stress-responsive programs in EE lineages, accompanied by the induction of the stress-inducible transcription factor Xrp1 and the cytokine gene upd3. Xrp1 and upd3 are both necessary for radiation-induced EE plasticity. Under basal conditions, EE-specific Xrp1 overexpression triggers ectopic expression of progenitor-specific genes, which is necessary for Xrp1 to drive EE plasticity. Our work identifies Xrp1 as a crucial regulator that coordinates damage-induced signaling and transcriptional reprogramming, enabling the reactivation of cellular plasticity in differentiated cells."}],"date_published":"2026-01-15T00:00:00Z","scopus_import":"1","status":"public","OA_type":"green","acknowledgement":"We thank Pierre Léopold, Tatsushi Igaki, Erik Storkebaum, Tobias Reiff, Masayuki Miura, Xiaohang Yang, Mikio Furuse, Bloomington Drosophila Stock Center and Developmental Studies Hybridoma Bank for providing us with fly stocks and reagents. We are also grateful to Hiromi Yanagisawa, Satoru Kobayashi, Md Al Amin Sheikh and Yaxuan Cui for allowing us to use their equipment, and to Allison Bardin, Pierre Léopold and Tadashi Uemura for helpful discussions.","article_processing_charge":"No","pmid":1,"month":"01","year":"2026","issue":"2","_id":"21039","oa_version":"Preprint","title":"Xrp1 drives damage-induced cellular plasticity of enteroendocrine cells in the adult Drosophila midgut","date_created":"2026-01-25T23:01:39Z","article_number":"dev205225","department":[{"_id":"XiFe"}],"intvolume":"       153","language":[{"iso":"eng"}],"quality_controlled":"1","publication_identifier":{"eissn":["1477-9129"],"issn":["0950-1991"]},"date_updated":"2026-02-12T12:41:18Z","OA_place":"repository","external_id":{"pmid":["41392708"]},"publication":"Development","main_file_link":[{"open_access":"1","url":"https://doi.org/10.1101/2025.07.05.662934"}],"citation":{"short":"Q. Qian, H. NAGAI, Y. Sanaki, M. Hayashi, K. Kimura, Y.I. Nakajima, R. Niwa, Development 153 (2026).","apa":"Qian, Q., NAGAI, H., Sanaki, Y., Hayashi, M., Kimura, K., Nakajima, Y. I., &#38; Niwa, R. (2026). Xrp1 drives damage-induced cellular plasticity of enteroendocrine cells in the adult Drosophila midgut. <i>Development</i>. The Company of Biologists. <a href=\"https://doi.org/10.1242/dev.205225\">https://doi.org/10.1242/dev.205225</a>","mla":"Qian, Qingyin, et al. “Xrp1 Drives Damage-Induced Cellular Plasticity of Enteroendocrine Cells in the Adult Drosophila Midgut.” <i>Development</i>, vol. 153, no. 2, dev205225, The Company of Biologists, 2026, doi:<a href=\"https://doi.org/10.1242/dev.205225\">10.1242/dev.205225</a>.","ista":"Qian Q, NAGAI H, Sanaki Y, Hayashi M, Kimura K, Nakajima YI, Niwa R. 2026. Xrp1 drives damage-induced cellular plasticity of enteroendocrine cells in the adult Drosophila midgut. Development. 153(2), dev205225.","ieee":"Q. Qian <i>et al.</i>, “Xrp1 drives damage-induced cellular plasticity of enteroendocrine cells in the adult Drosophila midgut,” <i>Development</i>, vol. 153, no. 2. The Company of Biologists, 2026.","ama":"Qian Q, NAGAI H, Sanaki Y, et al. Xrp1 drives damage-induced cellular plasticity of enteroendocrine cells in the adult Drosophila midgut. <i>Development</i>. 2026;153(2). doi:<a href=\"https://doi.org/10.1242/dev.205225\">10.1242/dev.205225</a>","chicago":"Qian, Qingyin, HIROKI NAGAI, Yuya Sanaki, Makoto Hayashi, Kenichi Kimura, Yu Ichiro Nakajima, and Ryusuke Niwa. “Xrp1 Drives Damage-Induced Cellular Plasticity of Enteroendocrine Cells in the Adult Drosophila Midgut.” <i>Development</i>. The Company of Biologists, 2026. <a href=\"https://doi.org/10.1242/dev.205225\">https://doi.org/10.1242/dev.205225</a>."},"volume":153,"doi":"10.1242/dev.205225","day":"15","publisher":"The Company of Biologists","type":"journal_article"},{"title":"Hoxb genes determine the timing of cell ingression by regulating cell surface fluctuations during zebrafish gastrulation","year":"2025","issue":"12","_id":"20048","oa_version":"Published Version","pmid":1,"month":"06","article_processing_charge":"Yes (via OA deal)","OA_type":"hybrid","acknowledgement":"We thank all the Heisenberg lab members for discussions and comments on the manuscript, and the Bioimaging and Life Science facilities of ISTA for support with microscopy and fish maintenance, respectively. This study was funded by a Japan Society for the Promotion of Science (JSPS) Overseas Research Fellowship and a Japan Science and Technology Agency PRESTO grant (JPMJPR214B) to Y.M. Open Access funding provided by the Japan Science and Technology Agency. Deposited in PMC for immediate release.","ddc":["570"],"date_published":"2025-06-27T00:00:00Z","scopus_import":"1","abstract":[{"lang":"eng","text":"During embryonic development, cell behaviors need to be tightly regulated in time and space. Yet how the temporal and spatial regulations of cell behaviors are interconnected during embryonic development remains elusive. To address this, we turned to zebrafish gastrulation, the process whereby dynamic cell behaviors generate the three principal germ layers of the early embryo. Here, we show that Hoxb cluster genes are expressed in a temporally collinear manner at the blastoderm margin, where mesodermal and endodermal (mesendoderm) progenitor cells are specified and ingress to form mesendoderm/hypoblast. Functional analysis shows that these Hoxb genes regulate the timing of cell ingression: under- or overexpression of Hoxb genes perturb the timing of mesendoderm cell ingression and, consequently, the positioning of these cells along the forming anterior-posterior body axis after gastrulation. Finally, we found that Hoxb genes control the timing of mesendoderm ingression by regulating cellular bleb formation and cell surface fluctuations in the ingressing cells. Collectively, our findings suggest that Hoxb genes interconnect the temporal and spatial pattern of cell behaviors during zebrafish gastrulation by controlling cell surface fluctuations."}],"status":"public","file":[{"date_created":"2025-07-23T08:43:01Z","creator":"dernst","access_level":"open_access","content_type":"application/pdf","file_size":25935563,"relation":"main_file","file_id":"20070","checksum":"808d8aa28df79d23fb661838d1fdc1be","success":1,"file_name":"2025_Development_Moriyama.pdf","date_updated":"2025-07-23T08:43:01Z"}],"user_id":"317138e5-6ab7-11ef-aa6d-ffef3953e345","isi":1,"oa":1,"publication_status":"published","article_type":"original","author":[{"id":"addc9b8c-67a0-11f0-b374-a2e094825470","full_name":"Moriyama, Yuuta","first_name":"Yuuta","last_name":"Moriyama","orcid":"0000-0002-2853-8051"},{"last_name":"Mitsui","first_name":"Toshiyuki","full_name":"Mitsui, Toshiyuki"},{"last_name":"Heisenberg","orcid":"0000-0002-0912-4566","first_name":"Carl-Philipp J","id":"39427864-F248-11E8-B48F-1D18A9856A87","full_name":"Heisenberg, Carl-Philipp J"}],"publisher":"The Company of Biologists","doi":"10.1242/dev.204261","day":"27","type":"journal_article","citation":{"chicago":"Moriyama, Yuuta, Toshiyuki Mitsui, and Carl-Philipp J Heisenberg. “Hoxb Genes Determine the Timing of Cell Ingression by Regulating Cell Surface Fluctuations during Zebrafish Gastrulation.” <i>Development</i>. The Company of Biologists, 2025. <a href=\"https://doi.org/10.1242/dev.204261\">https://doi.org/10.1242/dev.204261</a>.","ama":"Moriyama Y, Mitsui T, Heisenberg C-PJ. Hoxb genes determine the timing of cell ingression by regulating cell surface fluctuations during zebrafish gastrulation. <i>Development</i>. 2025;152(12). doi:<a href=\"https://doi.org/10.1242/dev.204261\">10.1242/dev.204261</a>","apa":"Moriyama, Y., Mitsui, T., &#38; Heisenberg, C.-P. J. (2025). Hoxb genes determine the timing of cell ingression by regulating cell surface fluctuations during zebrafish gastrulation. <i>Development</i>. The Company of Biologists. <a href=\"https://doi.org/10.1242/dev.204261\">https://doi.org/10.1242/dev.204261</a>","ista":"Moriyama Y, Mitsui T, Heisenberg C-PJ. 2025. Hoxb genes determine the timing of cell ingression by regulating cell surface fluctuations during zebrafish gastrulation. Development. 152(12), dev204261.","mla":"Moriyama, Yuuta, et al. “Hoxb Genes Determine the Timing of Cell Ingression by Regulating Cell Surface Fluctuations during Zebrafish Gastrulation.” <i>Development</i>, vol. 152, no. 12, dev204261, The Company of Biologists, 2025, doi:<a href=\"https://doi.org/10.1242/dev.204261\">10.1242/dev.204261</a>.","ieee":"Y. Moriyama, T. Mitsui, and C.-P. J. Heisenberg, “Hoxb genes determine the timing of cell ingression by regulating cell surface fluctuations during zebrafish gastrulation,” <i>Development</i>, vol. 152, no. 12. The Company of Biologists, 2025.","short":"Y. Moriyama, T. Mitsui, C.-P.J. Heisenberg, Development 152 (2025)."},"volume":152,"publication":"Development","date_updated":"2025-09-30T14:07:51Z","OA_place":"publisher","has_accepted_license":"1","external_id":{"pmid":["40576478"],"isi":["001525252300001"]},"corr_author":"1","intvolume":"       152","quality_controlled":"1","language":[{"iso":"eng"}],"publication_identifier":{"issn":["0950-1991"],"eissn":["1477-9129"]},"tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","image":"/images/cc_by.png","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","short":"CC BY (4.0)"},"date_created":"2025-07-21T08:10:32Z","file_date_updated":"2025-07-23T08:43:01Z","article_number":"dev204261","department":[{"_id":"CaHe"}],"PlanS_conform":"1"},{"title":"Robust axis elongation by Nodal-dependent restriction of BMP signaling","oa_version":"Published Version","issue":"4","_id":"15048","year":"2024","month":"02","pmid":1,"article_processing_charge":"Yes (via OA deal)","ddc":["570"],"acknowledgement":"We thank Patrick Müller for sharing the chordintt250 mutant zebrafish line as well as the plasmid for chrd-GFP, Katherine Rogers for sharing the bmp2b plasmid and Andrea Pauli for sharing the draculin plasmid. Diana Pinheiro generated the MZlefty1,2;Tg(sebox::EGFP) line. We are grateful to Patrick Müller, Diana Pinheiro and Katherine Rogers and members of the Heisenberg lab for discussions, technical advice and feedback on the manuscript. We also thank Anna Kicheva and Edouard Hannezo for discussions. We thank the Imaging and Optics Facility as well as the Life Science facility at IST Austria for support with microscopy and fish maintenance.\r\nThis work was supported by a European Research Council Advanced Grant\r\n(MECSPEC 742573 to C.-P.H.). A.S. is a recipient of a DOC Fellowship of the Austrian\r\nAcademy of Sciences at IST Austria. Open Access funding provided by Institute of\r\nScience and Technology Austria. ","status":"public","date_published":"2024-02-01T00:00:00Z","scopus_import":"1","abstract":[{"text":"Embryogenesis results from the coordinated activities of different signaling pathways controlling cell fate specification and morphogenesis. In vertebrate gastrulation, both Nodal and BMP signaling play key roles in germ layer specification and morphogenesis, yet their interplay to coordinate embryo patterning with morphogenesis is still insufficiently understood. Here, we took a reductionist approach using zebrafish embryonic explants to study the coordination of Nodal and BMP signaling for embryo patterning and morphogenesis. We show that Nodal signaling triggers explant elongation by inducing mesendodermal progenitors but also suppressing BMP signaling activity at the site of mesendoderm induction. Consistent with this, ectopic BMP signaling in the mesendoderm blocks cell alignment and oriented mesendoderm intercalations, key processes during explant elongation. Translating these ex vivo observations to the intact embryo showed that, similar to explants, Nodal signaling suppresses the effect of BMP signaling on cell intercalations in the dorsal domain, thus allowing robust embryonic axis elongation. These findings suggest a dual function of Nodal signaling in embryonic axis elongation by both inducing mesendoderm and suppressing BMP effects in the dorsal portion of the mesendoderm.","lang":"eng"}],"oa":1,"isi":1,"user_id":"317138e5-6ab7-11ef-aa6d-ffef3953e345","file":[{"checksum":"6961ea10012bf0d266681f9628bb8f13","success":1,"date_updated":"2024-03-04T07:24:43Z","file_name":"2024_Development_Schauer.pdf","access_level":"open_access","date_created":"2024-03-04T07:24:43Z","creator":"dernst","content_type":"application/pdf","relation":"main_file","file_size":14839986,"file_id":"15050"}],"author":[{"orcid":"0000-0001-7659-9142","last_name":"Schauer","first_name":"Alexandra","id":"30A536BA-F248-11E8-B48F-1D18A9856A87","full_name":"Schauer, Alexandra"},{"last_name":"Pranjic-Ferscha","full_name":"Pranjic-Ferscha, Kornelija","id":"4362B3C2-F248-11E8-B48F-1D18A9856A87","first_name":"Kornelija"},{"first_name":"Robert","id":"4E01D6B4-F248-11E8-B48F-1D18A9856A87","full_name":"Hauschild, Robert","orcid":"0000-0001-9843-3522","last_name":"Hauschild"},{"last_name":"Heisenberg","orcid":"0000-0002-0912-4566","first_name":"Carl-Philipp J","full_name":"Heisenberg, Carl-Philipp J","id":"39427864-F248-11E8-B48F-1D18A9856A87"}],"publication_status":"published","article_type":"original","project":[{"call_identifier":"H2020","name":"Interaction and feedback between cell mechanics and fate specification in vertebrate gastrulation","_id":"260F1432-B435-11E9-9278-68D0E5697425","grant_number":"742573"},{"name":"Mesendoderm specification in zebrafish: The role of extraembryonic tissues","grant_number":"25239","_id":"26B1E39C-B435-11E9-9278-68D0E5697425"}],"type":"journal_article","ec_funded":1,"related_material":{"record":[{"id":"14926","relation":"research_data","status":"public"}]},"doi":"10.1242/dev.202316","day":"01","publisher":"The Company of Biologists","page":"1-18","volume":151,"citation":{"short":"A. Schauer, K. Pranjic-Ferscha, R. Hauschild, C.-P.J. Heisenberg, Development 151 (2024) 1–18.","apa":"Schauer, A., Pranjic-Ferscha, K., Hauschild, R., &#38; Heisenberg, C.-P. J. (2024). Robust axis elongation by Nodal-dependent restriction of BMP signaling. <i>Development</i>. The Company of Biologists. <a href=\"https://doi.org/10.1242/dev.202316\">https://doi.org/10.1242/dev.202316</a>","mla":"Schauer, Alexandra, et al. “Robust Axis Elongation by Nodal-Dependent Restriction of BMP Signaling.” <i>Development</i>, vol. 151, no. 4, The Company of Biologists, 2024, pp. 1–18, doi:<a href=\"https://doi.org/10.1242/dev.202316\">10.1242/dev.202316</a>.","ista":"Schauer A, Pranjic-Ferscha K, Hauschild R, Heisenberg C-PJ. 2024. Robust axis elongation by Nodal-dependent restriction of BMP signaling. Development. 151(4), 1–18.","ieee":"A. Schauer, K. Pranjic-Ferscha, R. Hauschild, and C.-P. J. Heisenberg, “Robust axis elongation by Nodal-dependent restriction of BMP signaling,” <i>Development</i>, vol. 151, no. 4. The Company of Biologists, pp. 1–18, 2024.","ama":"Schauer A, Pranjic-Ferscha K, Hauschild R, Heisenberg C-PJ. Robust axis elongation by Nodal-dependent restriction of BMP signaling. <i>Development</i>. 2024;151(4):1-18. doi:<a href=\"https://doi.org/10.1242/dev.202316\">10.1242/dev.202316</a>","chicago":"Schauer, Alexandra, Kornelija Pranjic-Ferscha, Robert Hauschild, and Carl-Philipp J Heisenberg. “Robust Axis Elongation by Nodal-Dependent Restriction of BMP Signaling.” <i>Development</i>. The Company of Biologists, 2024. <a href=\"https://doi.org/10.1242/dev.202316\">https://doi.org/10.1242/dev.202316</a>."},"publication":"Development","corr_author":"1","external_id":{"isi":["001170580200001"],"pmid":["38372390"]},"has_accepted_license":"1","date_updated":"2025-09-04T12:10:40Z","publication_identifier":{"eissn":["1477-9129"],"issn":["0950-1991"]},"language":[{"iso":"eng"}],"quality_controlled":"1","intvolume":"       151","acknowledged_ssus":[{"_id":"Bio"},{"_id":"LifeSc"}],"tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","image":"/images/cc_by.png","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","short":"CC BY (4.0)"},"department":[{"_id":"CaHe"},{"_id":"Bio"}],"file_date_updated":"2024-03-04T07:24:43Z","date_created":"2024-03-03T23:00:50Z"},{"issue":"15","_id":"17458","year":"2024","oa_version":"Published Version","title":"Compensation of gene dosage on the mammalian X","article_processing_charge":"Yes (in subscription journal)","pmid":1,"month":"08","date_published":"2024-08-14T00:00:00Z","scopus_import":"1","abstract":[{"text":"Changes in gene dosage can have tremendous evolutionary potential (e.g. whole-genome duplications), but without compensatory mechanisms, they can also lead to gene dysregulation and pathologies. Sex chromosomes are a paradigmatic example of naturally occurring gene dosage differences and their compensation. In species with chromosome-based sex determination, individuals within the same population necessarily show ‘natural’ differences in gene dosage for the sex chromosomes. In this Review, we focus on the mammalian X chromosome and discuss recent new insights into the dosage-compensation mechanisms that evolved along with the emergence of sex chromosomes, namely X-inactivation and X-upregulation. We also discuss the evolution of the genetic loci and molecular players involved, as well as the regulatory diversity and potentially different requirements for dosage compensation across mammalian species.","lang":"eng"}],"status":"public","ddc":["599"],"acknowledgement":"We thank Estelle Nicolas for critical feedback on the manuscript and Ikuhiro Okamoto for critical feedback on the figures. We apologise to authors whose work we overlooked or did not discuss or cite due to limits in the number of references. We thank the anonymous reviewers for pointing us to additional literature and for their constructive feedback. Figures were prepared with BioRender.com. D.C. is supported by a fellowship from Ligue Contre le Cancer (LNCC_TAJT25850) and R.G. holds a tenured research position from the Centre National de la Recherche Scientifique (France). Research in the Galupa lab is supported by a grant from the Fondation pour la Recherche Médicale (AJE202305017142). Open Access funding provided by Fondation pour la Recherche Médicale. Deposited in PMC for immediate release.","publication_status":"published","article_type":"original","author":[{"full_name":"Cecalev, Daniela","first_name":"Daniela","last_name":"Cecalev"},{"id":"49E1C5C6-F248-11E8-B48F-1D18A9856A87","full_name":"Vicoso, Beatriz","first_name":"Beatriz","orcid":"0000-0002-4579-8306","last_name":"Vicoso"},{"first_name":"Rafael","full_name":"Galupa, Rafael","last_name":"Galupa"}],"user_id":"317138e5-6ab7-11ef-aa6d-ffef3953e345","isi":1,"file":[{"content_type":"application/pdf","access_level":"open_access","creator":"cchlebak","date_created":"2024-08-28T10:32:16Z","file_id":"17464","relation":"main_file","file_size":2085135,"success":1,"checksum":"5e428bda0440d3f957c694b315a8f2a9","date_updated":"2024-08-28T10:32:16Z","file_name":"2024_Development_Cecalev.pdf"}],"oa":1,"citation":{"ama":"Cecalev D, Vicoso B, Galupa R. Compensation of gene dosage on the mammalian X. <i>Development</i>. 2024;151(15). doi:<a href=\"https://doi.org/10.1242/dev.202891\">10.1242/dev.202891</a>","chicago":"Cecalev, Daniela, Beatriz Vicoso, and Rafael Galupa. “Compensation of Gene Dosage on the Mammalian X.” <i>Development</i>. The Company of Biologists, 2024. <a href=\"https://doi.org/10.1242/dev.202891\">https://doi.org/10.1242/dev.202891</a>.","short":"D. Cecalev, B. Vicoso, R. Galupa, Development 151 (2024).","ieee":"D. Cecalev, B. Vicoso, and R. Galupa, “Compensation of gene dosage on the mammalian X,” <i>Development</i>, vol. 151, no. 15. The Company of Biologists, 2024.","ista":"Cecalev D, Vicoso B, Galupa R. 2024. Compensation of gene dosage on the mammalian X. Development. 151(15), dev202891.","mla":"Cecalev, Daniela, et al. “Compensation of Gene Dosage on the Mammalian X.” <i>Development</i>, vol. 151, no. 15, dev202891, The Company of Biologists, 2024, doi:<a href=\"https://doi.org/10.1242/dev.202891\">10.1242/dev.202891</a>.","apa":"Cecalev, D., Vicoso, B., &#38; Galupa, R. (2024). Compensation of gene dosage on the mammalian X. <i>Development</i>. The Company of Biologists. <a href=\"https://doi.org/10.1242/dev.202891\">https://doi.org/10.1242/dev.202891</a>"},"volume":151,"day":"14","publisher":"The Company of Biologists","doi":"10.1242/dev.202891","type":"journal_article","publication":"Development","language":[{"iso":"eng"}],"quality_controlled":"1","intvolume":"       151","publication_identifier":{"eissn":["1477-9129"],"issn":["0950-1991"]},"has_accepted_license":"1","date_updated":"2025-09-08T08:58:58Z","external_id":{"isi":["001292608800003"],"pmid":["39140247"]},"file_date_updated":"2024-08-28T10:32:16Z","date_created":"2024-08-25T22:01:07Z","department":[{"_id":"BeVi"}],"article_number":"dev202891","tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","image":"/images/cc_by.png","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","short":"CC BY (4.0)"}},{"file_date_updated":"2024-12-04T22:12:04Z","date_created":"2024-12-04T22:02:52Z","tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","image":"/images/cc_by.png","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","short":"CC BY (4.0)"},"publication_identifier":{"issn":["0950-1991"],"eissn":["1477-9129"]},"language":[{"iso":"eng"}],"quality_controlled":"1","intvolume":"       150","external_id":{"pmid":["37721334"]},"has_accepted_license":"1","OA_place":"publisher","date_updated":"2024-12-09T11:43:40Z","publication":"Development","extern":"1","volume":150,"citation":{"short":"N. Ramirez, H.M. Belalcazar, M. Rahman, M. Trivedi, L.T.H. Tang, H.E. Bülow, Development 150 (2023).","ieee":"N. Ramirez, H. M. Belalcazar, M. Rahman, M. Trivedi, L. T. H. Tang, and H. E. Bülow, “Convertase-dependent regulation of membrane-tethered and secreted ligands tunes dendrite adhesion,” <i>Development</i>, vol. 150, no. 18. The Company of Biologists, 2023.","mla":"Ramirez, Nelson, et al. “Convertase-Dependent Regulation of Membrane-Tethered and Secreted Ligands Tunes Dendrite Adhesion.” <i>Development</i>, vol. 150, no. 18, The Company of Biologists, 2023, doi:<a href=\"https://doi.org/10.1242/dev.201208\">10.1242/dev.201208</a>.","apa":"Ramirez, N., Belalcazar, H. M., Rahman, M., Trivedi, M., Tang, L. T. H., &#38; Bülow, H. E. (2023). Convertase-dependent regulation of membrane-tethered and secreted ligands tunes dendrite adhesion. <i>Development</i>. The Company of Biologists. <a href=\"https://doi.org/10.1242/dev.201208\">https://doi.org/10.1242/dev.201208</a>","ista":"Ramirez N, Belalcazar HM, Rahman M, Trivedi M, Tang LTH, Bülow HE. 2023. Convertase-dependent regulation of membrane-tethered and secreted ligands tunes dendrite adhesion. Development. 150(18).","ama":"Ramirez N, Belalcazar HM, Rahman M, Trivedi M, Tang LTH, Bülow HE. Convertase-dependent regulation of membrane-tethered and secreted ligands tunes dendrite adhesion. <i>Development</i>. 2023;150(18). doi:<a href=\"https://doi.org/10.1242/dev.201208\">10.1242/dev.201208</a>","chicago":"Ramirez, Nelson, Helen M. Belalcazar, Maisha Rahman, Meera Trivedi, Leo T. H. Tang, and Hannes E. Bülow. “Convertase-Dependent Regulation of Membrane-Tethered and Secreted Ligands Tunes Dendrite Adhesion.” <i>Development</i>. The Company of Biologists, 2023. <a href=\"https://doi.org/10.1242/dev.201208\">https://doi.org/10.1242/dev.201208</a>."},"type":"journal_article","doi":"10.1242/dev.201208","day":"18","publisher":"The Company of Biologists","author":[{"id":"39831956-E4FE-11E9-85DE-0DC7E5697425","full_name":"Ramirez, Nelson","first_name":"Nelson","last_name":"Ramirez"},{"last_name":"Belalcazar","full_name":"Belalcazar, Helen M.","first_name":"Helen M."},{"full_name":"Rahman, Maisha","first_name":"Maisha","last_name":"Rahman"},{"full_name":"Trivedi, Meera","first_name":"Meera","last_name":"Trivedi"},{"last_name":"Tang","first_name":"Leo T. H.","full_name":"Tang, Leo T. H."},{"first_name":"Hannes E.","full_name":"Bülow, Hannes E.","last_name":"Bülow"}],"article_type":"original","publication_status":"published","oa":1,"user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","file":[{"relation":"main_file","file_size":9559527,"file_id":"18624","creator":"nramirez","date_created":"2024-12-04T22:12:04Z","access_level":"open_access","content_type":"application/pdf","file_name":"dev201208.pdf","date_updated":"2024-12-04T22:12:04Z","checksum":"d2158dc56db50457e6404c4afec4401c","success":1}],"status":"public","abstract":[{"lang":"eng","text":"During neural development, cellular adhesion is crucial for interactions among and between neurons and surrounding tissues. This function is mediated by conserved cell adhesion molecules, which are tightly regulated to allow for coordinated neuronal outgrowth. Here, we show that the proprotein convertase KPC-1 (homolog of mammalian furin) regulates the Menorin adhesion complex during development of PVD dendritic arbors in Caenorhabditis elegans. We found a finely regulated antagonistic balance between PVD-expressed KPC-1 and the epidermally expressed putative cell adhesion molecule MNR-1 (Menorin). Genetically, partial loss of mnr-1 suppressed partial loss of kpc-1, and both loss of kpc-1 and transgenic overexpression of mnr-1 resulted in indistinguishable phenotypes in PVD dendrites. This balance regulated cell-surface localization of the DMA-1 leucine-rich transmembrane receptor in PVD neurons. Lastly, kpc-1 mutants showed increased amounts of MNR-1 and decreased amounts of muscle-derived LECT-2 (Chondromodulin II), which is also part of the Menorin adhesion complex. These observations suggest that KPC-1 in PVD neurons directly or indirectly controls the abundance of proteins of the Menorin adhesion complex from adjacent tissues, thereby providing negative feedback from the dendrite to the instructive cues of surrounding tissues."}],"scopus_import":"1","date_published":"2023-09-18T00:00:00Z","ddc":["570"],"acknowledgement":"We thank members of the Bülow laboratory for comments on the manuscript and discussions throughout the course of this work; and Ryan Peer and William Corman for their initial help with the modifier genetic screen. We acknowledge the Genomics Core facility and the Advanced Imaging Facility at Albert Einstein College of Medicine for help during these studies. We are grateful to Kang Shen, David Miller and the Caenorhabditis Genetics Center (which is funded by National Institutes of Health Office of Research Infrastructure Programs P40OD0104400) for some of the strains used in this study, and Lhisia Chen for the anti-SAX-7 antibody.\r\nThis work was supported by grants from the National Institutes of Health (F31NS100370 to M.R.; T32GM007288 and F31NS111939 to M.T.; R01NS096672, R21NS081505 and R01NS129992 to H.E.B.; and P30HD071593 to Albert Einstein College of Medicine). N.J.R.-S. was the recipient of a Colciencias-Fulbright Fellowship [funded by Departamento Administrativo de Ciencia, Tecnología e Innovación (COLCIENCIAS) and Fulbright Colombia], L.T.H.T. of a Croucher Foundation Fellowship, and H.E.B. of an Irma T. Hirschl Trust/Monique Weill-Caulier Trust research fellowship. Open Access funding provided by Albert Einstein College of Medicine, Yeshiva University. Deposited in PMC for immediate release.","OA_type":"hybrid","article_processing_charge":"No","month":"09","pmid":1,"oa_version":"Published Version","_id":"18621","issue":"18","year":"2023","title":"Convertase-dependent regulation of membrane-tethered and secreted ligands tunes dendrite adhesion"},{"author":[{"full_name":"Harish, Rohit K","id":"1bae78aa-ee0e-11ec-9b76-bc42990f409d","first_name":"Rohit K","last_name":"Harish"},{"first_name":"Mansi","full_name":"Gupta, Mansi","last_name":"Gupta"},{"full_name":"Zöller, Daniela","first_name":"Daniela","last_name":"Zöller"},{"full_name":"Hartmann, Hella","first_name":"Hella","last_name":"Hartmann"},{"last_name":"Gheisari","first_name":"Ali","full_name":"Gheisari, Ali"},{"first_name":"Anja","full_name":"Machate, Anja","last_name":"Machate"},{"full_name":"Hans, Stefan","first_name":"Stefan","last_name":"Hans"},{"full_name":"Brand, Michael","first_name":"Michael","last_name":"Brand"}],"publication_status":"published","article_type":"original","oa":1,"file":[{"creator":"dernst","date_created":"2024-01-10T12:41:13Z","access_level":"open_access","content_type":"application/pdf","relation":"main_file","file_size":12836306,"file_id":"14790","checksum":"2d6f52dc33260a9b2352b8f28374ba5f","success":1,"file_name":"2023_Development_Harish.pdf","date_updated":"2024-01-10T12:41:13Z"}],"isi":1,"user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","status":"public","date_published":"2023-10-01T00:00:00Z","abstract":[{"lang":"eng","text":"Morphogen gradients impart positional information to cells in a homogenous tissue field. Fgf8a, a highly conserved growth factor, has been proposed to act as a morphogen during zebrafish gastrulation. However, technical limitations have so far prevented direct visualization of the endogenous Fgf8a gradient and confirmation of its morphogenic activity. Here, we monitor Fgf8a propagation in the developing neural plate using a CRISPR/Cas9-mediated EGFP knock-in at the endogenous fgf8a locus. By combining sensitive imaging with single-molecule fluorescence correlation spectroscopy, we demonstrate that Fgf8a, which is produced at the embryonic margin, propagates by diffusion through the extracellular space and forms a graded distribution towards the animal pole. Overlaying the Fgf8a gradient curve with expression profiles of its downstream targets determines the precise input-output relationship of Fgf8a-mediated patterning. Manipulation of the extracellular Fgf8a levels alters the signaling outcome, thus establishing Fgf8a as a bona fide morphogen during zebrafish gastrulation. Furthermore, by hindering Fgf8a diffusion, we demonstrate that extracellular diffusion of the protein from the source is crucial for it to achieve its morphogenic potential."}],"acknowledgement":"We thank members of the Brand lab, as well as Justina Stark (Ivo Sbalzarini group, Max Planck Institute of Molecular Cell Biology and Genetics, Dresden, Germany) for project-related discussions; Darren Gilmour (University of Zurich), Karuna Sampath (University of Warwick) and Gokul Kesavan (Vowels Lifesciences Private Limited, Bangalore) for comments on the manuscript; personnel of the CMCB technology platform, TU Dresden for imaging and image analysis-related support; and Maurizio Abbate (Technical support, Arivis) for help with image analysis. We are also grateful to Stapornwongkul and Briscoe for commenting on a preprint version of our work (Stapornwongkul and Briscoe, 2022).\r\nThis work was supported by the Deutsche Forschungsgemeinschaft (BR 1746/6-2, BR 1746/11-1 and BR 1746/3 to M.B.), by a Cluster of Excellence ‘Physics of Life’ seed grant and by institutional funds from Technische Universitat Dresden (to M.B.). Open Access funding provided by Technische Universitat Dresden. Deposited in PMC for immediate release.","ddc":["570"],"article_processing_charge":"Yes (via OA deal)","month":"10","pmid":1,"oa_version":"Published Version","year":"2023","_id":"14774","issue":"19","title":"Real-time monitoring of an endogenous Fgf8a gradient attests to its role as a morphogen during zebrafish gastrulation","keyword":["Developmental Biology","Molecular Biology"],"article_number":"dev201559","department":[{"_id":"AnKi"}],"date_created":"2024-01-10T09:18:54Z","file_date_updated":"2024-01-10T12:41:13Z","tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","image":"/images/cc_by.png","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","short":"CC BY (4.0)"},"publication_identifier":{"issn":["0950-1991"],"eissn":["1477-9129"]},"intvolume":"       150","language":[{"iso":"eng"}],"quality_controlled":"1","external_id":{"isi":["001097449100002"],"pmid":["37665167"]},"date_updated":"2024-01-10T12:45:25Z","has_accepted_license":"1","publication":"Development","volume":150,"citation":{"ista":"Harish RK, Gupta M, Zöller D, Hartmann H, Gheisari A, Machate A, Hans S, Brand M. 2023. Real-time monitoring of an endogenous Fgf8a gradient attests to its role as a morphogen during zebrafish gastrulation. Development. 150(19), dev201559.","apa":"Harish, R. K., Gupta, M., Zöller, D., Hartmann, H., Gheisari, A., Machate, A., … Brand, M. (2023). Real-time monitoring of an endogenous Fgf8a gradient attests to its role as a morphogen during zebrafish gastrulation. <i>Development</i>. The Company of Biologists. <a href=\"https://doi.org/10.1242/dev.201559\">https://doi.org/10.1242/dev.201559</a>","mla":"Harish, Rohit K., et al. “Real-Time Monitoring of an Endogenous Fgf8a Gradient Attests to Its Role as a Morphogen during Zebrafish Gastrulation.” <i>Development</i>, vol. 150, no. 19, dev201559, The Company of Biologists, 2023, doi:<a href=\"https://doi.org/10.1242/dev.201559\">10.1242/dev.201559</a>.","ieee":"R. K. Harish <i>et al.</i>, “Real-time monitoring of an endogenous Fgf8a gradient attests to its role as a morphogen during zebrafish gastrulation,” <i>Development</i>, vol. 150, no. 19. The Company of Biologists, 2023.","short":"R.K. Harish, M. Gupta, D. Zöller, H. Hartmann, A. Gheisari, A. Machate, S. Hans, M. Brand, Development 150 (2023).","chicago":"Harish, Rohit K, Mansi Gupta, Daniela Zöller, Hella Hartmann, Ali Gheisari, Anja Machate, Stefan Hans, and Michael Brand. “Real-Time Monitoring of an Endogenous Fgf8a Gradient Attests to Its Role as a Morphogen during Zebrafish Gastrulation.” <i>Development</i>. The Company of Biologists, 2023. <a href=\"https://doi.org/10.1242/dev.201559\">https://doi.org/10.1242/dev.201559</a>.","ama":"Harish RK, Gupta M, Zöller D, et al. Real-time monitoring of an endogenous Fgf8a gradient attests to its role as a morphogen during zebrafish gastrulation. <i>Development</i>. 2023;150(19). doi:<a href=\"https://doi.org/10.1242/dev.201559\">10.1242/dev.201559</a>"},"type":"journal_article","publisher":"The Company of Biologists","day":"01","doi":"10.1242/dev.201559"},{"publication_status":"published","article_type":"original","author":[{"last_name":"Kogure","full_name":"Kogure, Yuki S.","first_name":"Yuki S."},{"last_name":"Muraoka","full_name":"Muraoka, Hiromochi","first_name":"Hiromochi"},{"first_name":"Wataru C.","full_name":"Koizumi, Wataru C.","last_name":"Koizumi"},{"full_name":"Gelin-alessi, Raphaël","first_name":"Raphaël","last_name":"Gelin-alessi"},{"id":"33280250-F248-11E8-B48F-1D18A9856A87","full_name":"Godard, Benoit G","first_name":"Benoit G","last_name":"Godard"},{"last_name":"Oka","full_name":"Oka, Kotaro","first_name":"Kotaro"},{"orcid":"0000-0002-0912-4566","last_name":"Heisenberg","first_name":"Carl-Philipp J","id":"39427864-F248-11E8-B48F-1D18A9856A87","full_name":"Heisenberg, Carl-Philipp J"},{"last_name":"Hotta","full_name":"Hotta, Kohji","first_name":"Kohji"}],"file":[{"relation":"main_file","file_size":9160451,"file_id":"12423","creator":"dernst","date_created":"2023-01-27T10:36:50Z","access_level":"open_access","content_type":"application/pdf","file_name":"2022_Development_Kogure.pdf","date_updated":"2023-01-27T10:36:50Z","checksum":"871b9c58eb79b9e60752de25a46938d6","success":1}],"user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","isi":1,"oa":1,"scopus_import":"1","date_published":"2022-11-01T00:00:00Z","abstract":[{"lang":"eng","text":"Ventral tail bending, which is transient but pronounced, is found in many chordate embryos and constitutes an interesting model of how tissue interactions control embryo shape. Here, we identify one key upstream regulator of ventral tail bending in embryos of the ascidian Ciona. We show that during the early tailbud stages, ventral epidermal cells exhibit a boat-shaped morphology (boat cell) with a narrow apical surface where phosphorylated myosin light chain (pMLC) accumulates. We further show that interfering with the function of the BMP ligand Admp led to pMLC localizing to the basal instead of the apical side of ventral epidermal cells and a reduced number of boat cells. Finally, we show that cutting ventral epidermal midline cells at their apex using an ultraviolet laser relaxed ventral tail bending. Based on these results, we propose a previously unreported function for Admp in localizing pMLC to the apical side of ventral epidermal cells, which causes the tail to bend ventrally by resisting antero-posterior notochord extension at the ventral side of the tail."}],"status":"public","acknowledgement":"iona intestinalis adults were provided by Dr Yutaka Satou (Kyoto University) and Dr Manabu Yoshida (the University of Tokyo) with support from the National Bio-Resource Project of AMED, Japan. We thank Dr Hidehiko Hashimoto and Dr Yuji Mizotani for technical information about 1P-myosin antibody staining. We thank Dr Kaoru Imai and Dr Yutaka Satou for valuable discussion about Admp and for the DNA construct of Bmp2/4 under the Dlx.b upstream sequence. We thank Ms Maki Kogure for constructing the FUSION360 of the intercalating epidermal cell.\r\nThis work was supported by funding from the Japan Society for the Promotion of Science (JP16H01451, JP21H00440). Open Access funding provided by Keio University: Keio Gijuku Daigaku.","ddc":["570"],"article_processing_charge":"No","pmid":1,"month":"11","year":"2022","issue":"21","_id":"12231","oa_version":"Published Version","title":"Admp regulates tail bending by controlling ventral epidermal cell polarity via phosphorylated myosin localization in Ciona","keyword":["Developmental Biology","Molecular Biology"],"date_created":"2023-01-16T09:50:12Z","file_date_updated":"2023-01-27T10:36:50Z","article_number":"dev200215","department":[{"_id":"CaHe"}],"tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","image":"/images/cc_by.png","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","short":"CC BY (4.0)"},"intvolume":"       149","language":[{"iso":"eng"}],"quality_controlled":"1","publication_identifier":{"eissn":["1477-9129"],"issn":["0950-1991"]},"date_updated":"2024-10-09T21:03:48Z","has_accepted_license":"1","external_id":{"isi":["000903991700002"],"pmid":["36227591"]},"corr_author":"1","publication":"Development","citation":{"chicago":"Kogure, Yuki S., Hiromochi Muraoka, Wataru C. Koizumi, Raphaël Gelin-alessi, Benoit G Godard, Kotaro Oka, Carl-Philipp J Heisenberg, and Kohji Hotta. “Admp Regulates Tail Bending by Controlling Ventral Epidermal Cell Polarity via Phosphorylated Myosin Localization in Ciona.” <i>Development</i>. The Company of Biologists, 2022. <a href=\"https://doi.org/10.1242/dev.200215\">https://doi.org/10.1242/dev.200215</a>.","ama":"Kogure YS, Muraoka H, Koizumi WC, et al. Admp regulates tail bending by controlling ventral epidermal cell polarity via phosphorylated myosin localization in Ciona. <i>Development</i>. 2022;149(21). doi:<a href=\"https://doi.org/10.1242/dev.200215\">10.1242/dev.200215</a>","ieee":"Y. S. Kogure <i>et al.</i>, “Admp regulates tail bending by controlling ventral epidermal cell polarity via phosphorylated myosin localization in Ciona,” <i>Development</i>, vol. 149, no. 21. The Company of Biologists, 2022.","mla":"Kogure, Yuki S., et al. “Admp Regulates Tail Bending by Controlling Ventral Epidermal Cell Polarity via Phosphorylated Myosin Localization in Ciona.” <i>Development</i>, vol. 149, no. 21, dev200215, The Company of Biologists, 2022, doi:<a href=\"https://doi.org/10.1242/dev.200215\">10.1242/dev.200215</a>.","apa":"Kogure, Y. S., Muraoka, H., Koizumi, W. C., Gelin-alessi, R., Godard, B. G., Oka, K., … Hotta, K. (2022). Admp regulates tail bending by controlling ventral epidermal cell polarity via phosphorylated myosin localization in Ciona. <i>Development</i>. The Company of Biologists. <a href=\"https://doi.org/10.1242/dev.200215\">https://doi.org/10.1242/dev.200215</a>","ista":"Kogure YS, Muraoka H, Koizumi WC, Gelin-alessi R, Godard BG, Oka K, Heisenberg C-PJ, Hotta K. 2022. Admp regulates tail bending by controlling ventral epidermal cell polarity via phosphorylated myosin localization in Ciona. Development. 149(21), dev200215.","short":"Y.S. Kogure, H. Muraoka, W.C. Koizumi, R. Gelin-alessi, B.G. Godard, K. Oka, C.-P.J. Heisenberg, K. Hotta, Development 149 (2022)."},"volume":149,"publisher":"The Company of Biologists","day":"01","doi":"10.1242/dev.200215","type":"journal_article"},{"publication":"Development","publisher":"The Company of Biologists","day":"01","doi":"10.1242/dev.200474","type":"journal_article","related_material":{"link":[{"relation":"software","url":" https://github.com/burtonjosh/StepwiseMir9"}]},"citation":{"ama":"Soto X, Burton J, Manning CS, et al. Sequential and additive expression of miR-9 precursors control timing of neurogenesis. <i>Development</i>. 2022;149(19). doi:<a href=\"https://doi.org/10.1242/dev.200474\">10.1242/dev.200474</a>","chicago":"Soto, Ximena, Joshua Burton, Cerys S. Manning, Thomas Minchington, Robert Lea, Jessica Lee, Jochen Kursawe, Magnus Rattray, and Nancy Papalopulu. “Sequential and Additive Expression of MiR-9 Precursors Control Timing of Neurogenesis.” <i>Development</i>. The Company of Biologists, 2022. <a href=\"https://doi.org/10.1242/dev.200474\">https://doi.org/10.1242/dev.200474</a>.","short":"X. Soto, J. Burton, C.S. Manning, T. Minchington, R. Lea, J. Lee, J. Kursawe, M. Rattray, N. Papalopulu, Development 149 (2022).","ieee":"X. Soto <i>et al.</i>, “Sequential and additive expression of miR-9 precursors control timing of neurogenesis,” <i>Development</i>, vol. 149, no. 19. The Company of Biologists, 2022.","apa":"Soto, X., Burton, J., Manning, C. S., Minchington, T., Lea, R., Lee, J., … Papalopulu, N. (2022). Sequential and additive expression of miR-9 precursors control timing of neurogenesis. <i>Development</i>. The Company of Biologists. <a href=\"https://doi.org/10.1242/dev.200474\">https://doi.org/10.1242/dev.200474</a>","mla":"Soto, Ximena, et al. “Sequential and Additive Expression of MiR-9 Precursors Control Timing of Neurogenesis.” <i>Development</i>, vol. 149, no. 19, dev200474, The Company of Biologists, 2022, doi:<a href=\"https://doi.org/10.1242/dev.200474\">10.1242/dev.200474</a>.","ista":"Soto X, Burton J, Manning CS, Minchington T, Lea R, Lee J, Kursawe J, Rattray M, Papalopulu N. 2022. Sequential and additive expression of miR-9 precursors control timing of neurogenesis. Development. 149(19), dev200474."},"volume":149,"tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","image":"/images/cc_by.png","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","short":"CC BY (4.0)"},"file_date_updated":"2023-01-30T08:35:44Z","date_created":"2023-01-16T09:53:17Z","department":[{"_id":"AnKi"}],"article_number":"dev200474","has_accepted_license":"1","date_updated":"2023-08-04T09:41:08Z","external_id":{"pmid":["36189829"],"isi":["000918161000003"]},"quality_controlled":"1","language":[{"iso":"eng"}],"intvolume":"       149","publication_identifier":{"eissn":["1477-9129"],"issn":["0950-1991"]},"pmid":1,"month":"10","article_processing_charge":"No","keyword":["Developmental Biology","Molecular Biology"],"title":"Sequential and additive expression of miR-9 precursors control timing of neurogenesis","issue":"19","_id":"12245","year":"2022","oa_version":"Published Version","user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","isi":1,"file":[{"relation":"main_file","file_size":9348839,"file_id":"12438","creator":"dernst","date_created":"2023-01-30T08:35:44Z","access_level":"open_access","content_type":"application/pdf","file_name":"2022_Development_Soto.pdf","date_updated":"2023-01-30T08:35:44Z","checksum":"d7c29b74e9e4032308228cc704a30e88","success":1}],"oa":1,"publication_status":"published","article_type":"original","author":[{"full_name":"Soto, Ximena","first_name":"Ximena","last_name":"Soto"},{"full_name":"Burton, Joshua","first_name":"Joshua","last_name":"Burton"},{"full_name":"Manning, Cerys S.","first_name":"Cerys S.","last_name":"Manning"},{"first_name":"Thomas","full_name":"Minchington, Thomas","id":"7d1648cb-19e9-11eb-8e7a-f8c037fb3e3f","last_name":"Minchington"},{"first_name":"Robert","full_name":"Lea, Robert","last_name":"Lea"},{"last_name":"Lee","full_name":"Lee, Jessica","first_name":"Jessica"},{"last_name":"Kursawe","first_name":"Jochen","full_name":"Kursawe, Jochen"},{"last_name":"Rattray","full_name":"Rattray, Magnus","first_name":"Magnus"},{"last_name":"Papalopulu","first_name":"Nancy","full_name":"Papalopulu, Nancy"}],"ddc":["570"],"acknowledgement":"We are grateful to Dr Tom Pettini for the advice on smiFISH technique and Dr Laure Bally-Cuif for sharing plasmids. The authors also thank the Biological Services Facility, Bioimaging and Systems Microscopy Facilities of the University of Manchester for technical support.\r\nThis work was supported by a Wellcome Trust Senior Research Fellowship (090868/Z/09/Z) and a Wellcome Trust Investigator Award (224394/Z/21/Z) to N.P. and a Medical Research Council Career Development Award to C.S.M. (MR/V032534/1). J.B. was supported by a Wellcome Trust Four-Year PhD Studentship in Basic Science (219992/Z/19/Z). Open Access funding provided by The University of Manchester. Deposited in PMC for immediate release.","scopus_import":"1","abstract":[{"text":"MicroRNAs (miRs) have an important role in tuning dynamic gene expression. However, the mechanism by which they are quantitatively controlled is unknown. We show that the amount of mature miR-9, a key regulator of neuronal development, increases during zebrafish neurogenesis in a sharp stepwise manner. We characterize the spatiotemporal profile of seven distinct microRNA primary transcripts (pri-mir)-9s that produce the same mature miR-9 and show that they are sequentially expressed during hindbrain neurogenesis. Expression of late-onset pri-mir-9-1 is added on to, rather than replacing, the expression of early onset pri-mir-9-4 and -9-5 in single cells. CRISPR/Cas9 mutation of the late-onset pri-mir-9-1 prevents the developmental increase of mature miR-9, reduces late neuronal differentiation and fails to downregulate Her6 at late stages. Mathematical modelling shows that an adaptive network containing Her6 is insensitive to linear increases in miR-9 but responds to stepwise increases of miR-9. We suggest that a sharp stepwise increase of mature miR-9 is created by sequential and additive temporal activation of distinct loci. This may be a strategy to overcome adaptation and facilitate a transition of Her6 to a new dynamic regime or steady state.","lang":"eng"}],"date_published":"2022-10-01T00:00:00Z","status":"public"},{"tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","image":"/images/cc_by.png","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","short":"CC BY (4.0)"},"article_number":"dev196121.","department":[{"_id":"AnKi"}],"file_date_updated":"2024-04-03T13:58:51Z","date_created":"2024-04-03T07:26:41Z","external_id":{"pmid":["33722899 "]},"date_updated":"2024-04-03T14:00:33Z","has_accepted_license":"1","publication_identifier":{"eissn":["1477-9129"],"issn":["0950-1991"]},"intvolume":"       148","quality_controlled":"1","language":[{"iso":"eng"}],"publication":"Development","type":"journal_article","publisher":"The Company of Biologists","day":"01","doi":"10.1242/dev.196121","volume":148,"citation":{"ama":"Vinter DJ, Hoppe C, Minchington T, Sutcliffe C, Ashe HL. Dynamics of hunchback translation in real-time and at single-mRNA resolution in the Drosophila embryo. <i>Development</i>. 2021;148(18). doi:<a href=\"https://doi.org/10.1242/dev.196121\">10.1242/dev.196121</a>","chicago":"Vinter, Daisy J., Caroline Hoppe, Thomas Minchington, Catherine Sutcliffe, and Hilary L. Ashe. “Dynamics of Hunchback Translation in Real-Time and at Single-MRNA Resolution in the Drosophila Embryo.” <i>Development</i>. The Company of Biologists, 2021. <a href=\"https://doi.org/10.1242/dev.196121\">https://doi.org/10.1242/dev.196121</a>.","short":"D.J. Vinter, C. Hoppe, T. Minchington, C. Sutcliffe, H.L. Ashe, Development 148 (2021).","ista":"Vinter DJ, Hoppe C, Minchington T, Sutcliffe C, Ashe HL. 2021. Dynamics of hunchback translation in real-time and at single-mRNA resolution in the Drosophila embryo. Development. 148(18), dev196121.","mla":"Vinter, Daisy J., et al. “Dynamics of Hunchback Translation in Real-Time and at Single-MRNA Resolution in the Drosophila Embryo.” <i>Development</i>, vol. 148, no. 18, dev196121., The Company of Biologists, 2021, doi:<a href=\"https://doi.org/10.1242/dev.196121\">10.1242/dev.196121</a>.","apa":"Vinter, D. J., Hoppe, C., Minchington, T., Sutcliffe, C., &#38; Ashe, H. L. (2021). Dynamics of hunchback translation in real-time and at single-mRNA resolution in the Drosophila embryo. <i>Development</i>. The Company of Biologists. <a href=\"https://doi.org/10.1242/dev.196121\">https://doi.org/10.1242/dev.196121</a>","ieee":"D. J. Vinter, C. Hoppe, T. Minchington, C. Sutcliffe, and H. L. Ashe, “Dynamics of hunchback translation in real-time and at single-mRNA resolution in the Drosophila embryo,” <i>Development</i>, vol. 148, no. 18. The Company of Biologists, 2021."},"oa":1,"file":[{"success":1,"checksum":"6d0533fe9c712448b3f9feb15e05ec4b","file_name":"2021_CompanyBiologists_Vinter.pdf","date_updated":"2024-04-03T13:58:51Z","content_type":"application/pdf","creator":"dernst","date_created":"2024-04-03T13:58:51Z","access_level":"open_access","file_id":"15290","relation":"main_file","file_size":16258500}],"user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","author":[{"last_name":"Vinter","first_name":"Daisy J.","full_name":"Vinter, Daisy J."},{"last_name":"Hoppe","first_name":"Caroline","full_name":"Hoppe, Caroline"},{"last_name":"Minchington","first_name":"Thomas","full_name":"Minchington, Thomas","id":"7d1648cb-19e9-11eb-8e7a-f8c037fb3e3f"},{"last_name":"Sutcliffe","first_name":"Catherine","full_name":"Sutcliffe, Catherine"},{"first_name":"Hilary L.","full_name":"Ashe, Hilary L.","last_name":"Ashe"}],"publication_status":"published","article_type":"original","ddc":["570"],"status":"public","scopus_import":"1","abstract":[{"text":"The Hunchback (Hb) transcription factor is crucial for anterior-posterior patterning of the Drosophila embryo. The maternal hb mRNA acts as a paradigm for translational regulation due to its repression in the posterior of the embryo. However, little is known about the translatability of zygotically transcribed hb mRNAs. Here, we adapt the SunTag system, developed for imaging translation at single-mRNA resolution in tissue culture cells, to the Drosophila embryo to study the translation dynamics of zygotic hb mRNAs. Using single-molecule imaging in fixed and live embryos, we provide evidence for translational repression of zygotic SunTag-hb mRNAs. Whereas the proportion of SunTag-hb mRNAs translated is initially uniform, translation declines from the anterior over time until it becomes restricted to a posterior band in the expression domain. We discuss how regulated hb mRNA translation may help establish the sharp Hb expression boundary, which is a model for precision and noise during developmental patterning. Overall, our data show how use of the SunTag method on fixed and live embryos is a powerful combination for elucidating spatiotemporal regulation of mRNA translation in Drosophila.","lang":"eng"}],"date_published":"2021-09-01T00:00:00Z","month":"09","pmid":1,"article_processing_charge":"No","title":"Dynamics of hunchback translation in real-time and at single-mRNA resolution in the Drosophila embryo","keyword":["Developmental Biology","Molecular Biology"],"oa_version":"Published Version","year":"2021","issue":"18","_id":"15262"},{"abstract":[{"lang":"eng","text":"Cell division, movement and differentiation contribute to pattern formation in developing tissues. This is the case in the vertebrate neural tube, in which neurons differentiate in a characteristic pattern from a highly dynamic proliferating pseudostratified epithelium. To investigate how progenitor proliferation and differentiation affect cell arrangement and growth of the neural tube, we used experimental measurements to develop a mechanical model of the apical surface of the neuroepithelium that incorporates the effect of interkinetic nuclear movement and spatially varying rates of neuronal differentiation. Simulations predict that tissue growth and the shape of lineage-related clones of cells differ with the rate of differentiation. Growth is isotropic in regions of high differentiation, but dorsoventrally biased in regions of low differentiation. This is consistent with experimental observations. The absence of directional signalling in the simulations indicates that global mechanical constraints are sufficient to explain the observed differences in anisotropy. This provides insight into how the tissue growth rate affects cell dynamics and growth anisotropy and opens up possibilities to study the coupling between mechanics, pattern formation and growth in the neural tube."}],"scopus_import":"1","date_published":"2019-12-04T00:00:00Z","status":"public","ddc":["570"],"publication_status":"published","article_type":"original","project":[{"grant_number":"680037","_id":"B6FC0238-B512-11E9-945C-1524E6697425","call_identifier":"H2020","name":"Coordination of Patterning And Growth In the Spinal Cord"}],"author":[{"last_name":"Guerrero","first_name":"Pilar","full_name":"Guerrero, Pilar"},{"first_name":"Ruben","full_name":"Perez-Carrasco, Ruben","last_name":"Perez-Carrasco"},{"id":"343DA0DC-F248-11E8-B48F-1D18A9856A87","full_name":"Zagórski, Marcin P","first_name":"Marcin P","orcid":"0000-0001-7896-7762","last_name":"Zagórski"},{"last_name":"Page","full_name":"Page, David","first_name":"David"},{"orcid":"0000-0003-4509-4998","last_name":"Kicheva","id":"3959A2A0-F248-11E8-B48F-1D18A9856A87","full_name":"Kicheva, Anna","first_name":"Anna"},{"full_name":"Briscoe, James","first_name":"James","last_name":"Briscoe"},{"first_name":"Karen M.","full_name":"Page, Karen M.","last_name":"Page"}],"isi":1,"user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","file":[{"date_created":"2019-12-13T07:34:06Z","creator":"dernst","access_level":"open_access","content_type":"application/pdf","relation":"main_file","file_size":7797881,"file_id":"7177","checksum":"b6533c37dc8fbd803ffeca216e0a8b8a","file_name":"2019_Development_Guerrero.pdf","date_updated":"2020-07-14T12:47:50Z"}],"oa":1,"issue":"23","_id":"7165","year":"2019","oa_version":"Published Version","title":"Neuronal differentiation influences progenitor arrangement in the vertebrate neuroepithelium","article_processing_charge":"No","pmid":1,"month":"12","quality_controlled":"1","language":[{"iso":"eng"}],"intvolume":"       146","publication_identifier":{"eissn":["1477-9129"],"issn":["0950-1991"]},"has_accepted_license":"1","date_updated":"2025-04-14T07:27:30Z","corr_author":"1","external_id":{"pmid":["31784457"],"isi":["000507575700004"]},"date_created":"2019-12-10T14:39:50Z","file_date_updated":"2020-07-14T12:47:50Z","department":[{"_id":"AnKi"}],"article_number":"dev176297","tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","image":"/images/cc_by.png","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","short":"CC BY (4.0)"},"citation":{"mla":"Guerrero, Pilar, et al. “Neuronal Differentiation Influences Progenitor Arrangement in the Vertebrate Neuroepithelium.” <i>Development</i>, vol. 146, no. 23, dev176297, The Company of Biologists, 2019, doi:<a href=\"https://doi.org/10.1242/dev.176297\">10.1242/dev.176297</a>.","ista":"Guerrero P, Perez-Carrasco R, Zagórski MP, Page D, Kicheva A, Briscoe J, Page KM. 2019. Neuronal differentiation influences progenitor arrangement in the vertebrate neuroepithelium. Development. 146(23), dev176297.","apa":"Guerrero, P., Perez-Carrasco, R., Zagórski, M. P., Page, D., Kicheva, A., Briscoe, J., &#38; Page, K. M. (2019). Neuronal differentiation influences progenitor arrangement in the vertebrate neuroepithelium. <i>Development</i>. The Company of Biologists. <a href=\"https://doi.org/10.1242/dev.176297\">https://doi.org/10.1242/dev.176297</a>","ieee":"P. Guerrero <i>et al.</i>, “Neuronal differentiation influences progenitor arrangement in the vertebrate neuroepithelium,” <i>Development</i>, vol. 146, no. 23. The Company of Biologists, 2019.","short":"P. Guerrero, R. Perez-Carrasco, M.P. Zagórski, D. Page, A. Kicheva, J. Briscoe, K.M. Page, Development 146 (2019).","chicago":"Guerrero, Pilar, Ruben Perez-Carrasco, Marcin P Zagórski, David Page, Anna Kicheva, James Briscoe, and Karen M. Page. “Neuronal Differentiation Influences Progenitor Arrangement in the Vertebrate Neuroepithelium.” <i>Development</i>. The Company of Biologists, 2019. <a href=\"https://doi.org/10.1242/dev.176297\">https://doi.org/10.1242/dev.176297</a>.","ama":"Guerrero P, Perez-Carrasco R, Zagórski MP, et al. Neuronal differentiation influences progenitor arrangement in the vertebrate neuroepithelium. <i>Development</i>. 2019;146(23). doi:<a href=\"https://doi.org/10.1242/dev.176297\">10.1242/dev.176297</a>"},"volume":146,"day":"04","publisher":"The Company of Biologists","doi":"10.1242/dev.176297","ec_funded":1,"type":"journal_article","publication":"Development"},{"author":[{"last_name":"Stürner","full_name":"Stürner, Tomke","first_name":"Tomke"},{"first_name":"Anastasia","full_name":"Tatarnikova, Anastasia","last_name":"Tatarnikova"},{"first_name":"Jan","id":"AD07FDB4-0F61-11EA-8158-C4CC64CEAA8D","full_name":"Müller, Jan","last_name":"Müller"},{"last_name":"Schaffran","full_name":"Schaffran, Barbara","first_name":"Barbara"},{"last_name":"Cuntz","first_name":"Hermann","full_name":"Cuntz, Hermann"},{"first_name":"Yun","full_name":"Zhang, Yun","last_name":"Zhang"},{"full_name":"Nemethova, Maria","id":"34E27F1C-F248-11E8-B48F-1D18A9856A87","first_name":"Maria","last_name":"Nemethova"},{"last_name":"Bogdan","first_name":"Sven","full_name":"Bogdan, Sven"},{"last_name":"Small","first_name":"Vic","full_name":"Small, Vic"},{"first_name":"Gaia","full_name":"Tavosanis, Gaia","last_name":"Tavosanis"}],"article_type":"original","publication_status":"published","oa":1,"user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","isi":1,"status":"public","scopus_import":"1","date_published":"2019-04-04T00:00:00Z","abstract":[{"lang":"eng","text":"The formation of neuronal dendrite branches is fundamental for the wiring and function of the nervous system. Indeed, dendrite branching enhances the coverage of the neuron's receptive field and modulates the initial processing of incoming stimuli. Complex dendrite patterns are achieved in vivo through a dynamic process of de novo branch formation, branch extension and retraction. The first step towards branch formation is the generation of a dynamic filopodium-like branchlet. The mechanisms underlying the initiation of dendrite branchlets are therefore crucial to the shaping of dendrites. Through in vivo time-lapse imaging of the subcellular localization of actin during the process of branching of Drosophila larva sensory neurons, combined with genetic analysis and electron tomography, we have identified the Actin-related protein (Arp) 2/3 complex as the major actin nucleator involved in the initiation of dendrite branchlet formation, under the control of the activator WAVE and of the small GTPase Rac1. Transient recruitment of an Arp2/3 component marks the site of branchlet initiation in vivo. These data position the activation of Arp2/3 as an early hub for the initiation of branchlet formation."}],"article_processing_charge":"No","month":"04","pmid":1,"oa_version":"Published Version","year":"2019","issue":"7","_id":"7404","title":"Transient localization of the Arp2/3 complex initiates neuronal dendrite branching in vivo","article_number":"dev171397","department":[{"_id":"MiSi"}],"date_created":"2020-01-29T16:27:10Z","publication_identifier":{"eissn":["1477-9129"],"issn":["0950-1991"]},"intvolume":"       146","quality_controlled":"1","language":[{"iso":"eng"}],"external_id":{"isi":["000464583200006"],"pmid":["30910826"]},"date_updated":"2023-09-07T14:47:00Z","publication":"Development","main_file_link":[{"url":"https://doi.org/10.1242/dev.171397","open_access":"1"}],"volume":146,"citation":{"short":"T. Stürner, A. Tatarnikova, J. Müller, B. Schaffran, H. Cuntz, Y. Zhang, M. Nemethova, S. Bogdan, V. Small, G. Tavosanis, Development 146 (2019).","ieee":"T. Stürner <i>et al.</i>, “Transient localization of the Arp2/3 complex initiates neuronal dendrite branching in vivo,” <i>Development</i>, vol. 146, no. 7. The Company of Biologists, 2019.","apa":"Stürner, T., Tatarnikova, A., Müller, J., Schaffran, B., Cuntz, H., Zhang, Y., … Tavosanis, G. (2019). Transient localization of the Arp2/3 complex initiates neuronal dendrite branching in vivo. <i>Development</i>. The Company of Biologists. <a href=\"https://doi.org/10.1242/dev.171397\">https://doi.org/10.1242/dev.171397</a>","ista":"Stürner T, Tatarnikova A, Müller J, Schaffran B, Cuntz H, Zhang Y, Nemethova M, Bogdan S, Small V, Tavosanis G. 2019. Transient localization of the Arp2/3 complex initiates neuronal dendrite branching in vivo. Development. 146(7), dev171397.","mla":"Stürner, Tomke, et al. “Transient Localization of the Arp2/3 Complex Initiates Neuronal Dendrite Branching in Vivo.” <i>Development</i>, vol. 146, no. 7, dev171397, The Company of Biologists, 2019, doi:<a href=\"https://doi.org/10.1242/dev.171397\">10.1242/dev.171397</a>.","ama":"Stürner T, Tatarnikova A, Müller J, et al. Transient localization of the Arp2/3 complex initiates neuronal dendrite branching in vivo. <i>Development</i>. 2019;146(7). doi:<a href=\"https://doi.org/10.1242/dev.171397\">10.1242/dev.171397</a>","chicago":"Stürner, Tomke, Anastasia Tatarnikova, Jan Müller, Barbara Schaffran, Hermann Cuntz, Yun Zhang, Maria Nemethova, Sven Bogdan, Vic Small, and Gaia Tavosanis. “Transient Localization of the Arp2/3 Complex Initiates Neuronal Dendrite Branching in Vivo.” <i>Development</i>. The Company of Biologists, 2019. <a href=\"https://doi.org/10.1242/dev.171397\">https://doi.org/10.1242/dev.171397</a>."},"type":"journal_article","day":"04","publisher":"The Company of Biologists","doi":"10.1242/dev.171397"},{"has_accepted_license":"1","date_updated":"2026-04-16T09:59:52Z","corr_author":"1","external_id":{"isi":["000395650100001"]},"quality_controlled":"1","language":[{"iso":"eng"}],"intvolume":"       144","publication_identifier":{"issn":["0950-1991"]},"file_date_updated":"2020-07-14T12:47:33Z","date_created":"2018-12-11T11:47:44Z","department":[{"_id":"AnKi"}],"doi":"10.1242/dev.144915","publisher":"Company of Biologists","day":"01","page":"733 - 736","pubrep_id":"987","type":"journal_article","ec_funded":1,"citation":{"short":"A. Kicheva, N. Rivron, Development 144 (2017) 733–736.","mla":"Kicheva, Anna, and Nicolas Rivron. “Creating to Understand – Developmental Biology Meets Engineering in Paris.” <i>Development</i>, vol. 144, no. 5, Company of Biologists, 2017, pp. 733–36, doi:<a href=\"https://doi.org/10.1242/dev.144915\">10.1242/dev.144915</a>.","ista":"Kicheva A, Rivron N. 2017. Creating to understand – developmental biology meets engineering in Paris. Development. 144(5), 733–736.","apa":"Kicheva, A., &#38; Rivron, N. (2017). Creating to understand – developmental biology meets engineering in Paris. <i>Development</i>. Company of Biologists. <a href=\"https://doi.org/10.1242/dev.144915\">https://doi.org/10.1242/dev.144915</a>","ieee":"A. Kicheva and N. Rivron, “Creating to understand – developmental biology meets engineering in Paris,” <i>Development</i>, vol. 144, no. 5. Company of Biologists, pp. 733–736, 2017.","ama":"Kicheva A, Rivron N. Creating to understand – developmental biology meets engineering in Paris. <i>Development</i>. 2017;144(5):733-736. doi:<a href=\"https://doi.org/10.1242/dev.144915\">10.1242/dev.144915</a>","chicago":"Kicheva, Anna, and Nicolas Rivron. “Creating to Understand – Developmental Biology Meets Engineering in Paris.” <i>Development</i>. Company of Biologists, 2017. <a href=\"https://doi.org/10.1242/dev.144915\">https://doi.org/10.1242/dev.144915</a>."},"volume":144,"publist_id":"7089","publication":"Development","ddc":["571"],"abstract":[{"lang":"eng","text":"In November 2016, developmental biologists, synthetic biologists and engineers gathered in Paris for a meeting called ‘Engineering the embryo’. The participants shared an interest in exploring how synthetic systems can reveal new principles of embryonic development, and how the in vitro manipulation and modeling of development using stem cells can be used to integrate ideas and expertise from physics, developmental biology and tissue engineering. As we review here, the conference pinpointed some of the challenges arising at the intersection of these fields, along with great enthusiasm for finding new approaches and collaborations."}],"date_published":"2017-03-01T00:00:00Z","scopus_import":"1","status":"public","isi":1,"user_id":"ba8df636-2132-11f1-aed0-ed93e2281fdd","file":[{"file_name":"IST-2018-987-v1+1_2017_KichevaRivron__Creating_to.pdf","date_updated":"2020-07-14T12:47:33Z","checksum":"eef22a0f42a55b232cb2d1188a2322cb","file_size":228206,"relation":"main_file","file_id":"5139","date_created":"2018-12-12T10:15:20Z","creator":"system","access_level":"open_access","content_type":"application/pdf"}],"oa":1,"publication_status":"published","project":[{"call_identifier":"H2020","name":"Coordination of Patterning And Growth In the Spinal Cord","_id":"B6FC0238-B512-11E9-945C-1524E6697425","grant_number":"680037"}],"author":[{"first_name":"Anna","full_name":"Kicheva, Anna","id":"3959A2A0-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0003-4509-4998","last_name":"Kicheva"},{"last_name":"Rivron","full_name":"Rivron, Nicolas","first_name":"Nicolas"}],"title":"Creating to understand – developmental biology meets engineering in Paris","_id":"654","issue":"5","year":"2017","oa_version":"Submitted Version","month":"03","article_processing_charge":"No"},{"publication_status":"published","article_type":"original","author":[{"orcid":"0000-0003-4761-5996","last_name":"Krens","first_name":"Gabriel","full_name":"Krens, Gabriel","id":"2B819732-F248-11E8-B48F-1D18A9856A87"},{"last_name":"Veldhuis","full_name":"Veldhuis, Jim","first_name":"Jim"},{"id":"419EECCC-F248-11E8-B48F-1D18A9856A87","full_name":"Barone, Vanessa","first_name":"Vanessa","last_name":"Barone","orcid":"0000-0003-2676-3367"},{"orcid":"0000-0001-5199-9940","last_name":"Capek","id":"31C42484-F248-11E8-B48F-1D18A9856A87","full_name":"Capek, Daniel","first_name":"Daniel"},{"full_name":"Maître, Jean-Léon","id":"48F1E0D8-F248-11E8-B48F-1D18A9856A87","first_name":"Jean-Léon","orcid":"0000-0002-3688-1474","last_name":"Maître"},{"last_name":"Brodland","full_name":"Brodland, Wayne","first_name":"Wayne"},{"last_name":"Heisenberg","orcid":"0000-0002-0912-4566","first_name":"Carl-Philipp J","full_name":"Heisenberg, Carl-Philipp J","id":"39427864-F248-11E8-B48F-1D18A9856A87"}],"user_id":"ba8df636-2132-11f1-aed0-ed93e2281fdd","isi":1,"file":[{"checksum":"bc25125fb664706cdf180e061429f91d","file_name":"2017_Development_Krens.pdf","date_updated":"2020-07-14T12:47:39Z","creator":"dernst","date_created":"2019-09-24T06:56:22Z","access_level":"open_access","content_type":"application/pdf","relation":"main_file","file_size":8194516,"file_id":"6905"}],"oa":1,"date_published":"2017-05-15T00:00:00Z","scopus_import":"1","abstract":[{"lang":"eng","text":"The segregation of different cell types into distinct tissues is a fundamental process in metazoan development. Differences in cell adhesion and cortex tension are commonly thought to drive cell sorting by regulating tissue surface tension (TST). However, the role that differential TST plays in cell segregation within the developing embryo is as yet unclear. Here, we have analyzed the role of differential TST for germ layer progenitor cell segregation during zebrafish gastrulation. Contrary to previous observations that differential TST drives germ layer progenitor cell segregation in vitro, we show that germ layers display indistinguishable TST within the gastrulating embryo, arguing against differential TST driving germ layer progenitor cell segregation in vivo. We further show that the osmolarity of the interstitial fluid (IF) is an important factor that influences germ layer TST in vivo, and that lower osmolarity of the IF compared with standard cell culture medium can explain why germ layers display differential TST in culture but not in vivo. Finally, we show that directed migration of mesendoderm progenitors is required for germ layer progenitor cell segregation and germ layer formation."}],"status":"public","ddc":["570"],"article_processing_charge":"No","pmid":1,"month":"05","_id":"676","issue":"10","year":"2017","oa_version":"Published Version","title":"Interstitial fluid osmolarity modulates the action of differential tissue surface tension in progenitor cell segregation during gastrulation","file_date_updated":"2020-07-14T12:47:39Z","date_created":"2018-12-11T11:47:52Z","department":[{"_id":"Bio"},{"_id":"CaHe"}],"tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","image":"/images/cc_by.png","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","short":"CC BY (4.0)"},"language":[{"iso":"eng"}],"quality_controlled":"1","intvolume":"       144","publication_identifier":{"issn":["0950-1991"]},"has_accepted_license":"1","date_updated":"2026-05-04T22:31:03Z","corr_author":"1","external_id":{"pmid":["28512197"],"isi":["000402275900007"]},"publication":"Development","publist_id":"7047","citation":{"chicago":"Krens, Gabriel, Jim Veldhuis, Vanessa Barone, Daniel Capek, Jean-Léon Maître, Wayne Brodland, and Carl-Philipp J Heisenberg. “Interstitial Fluid Osmolarity Modulates the Action of Differential Tissue Surface Tension in Progenitor Cell Segregation during Gastrulation.” <i>Development</i>. Company of Biologists, 2017. <a href=\"https://doi.org/10.1242/dev.144964\">https://doi.org/10.1242/dev.144964</a>.","ama":"Krens G, Veldhuis J, Barone V, et al. Interstitial fluid osmolarity modulates the action of differential tissue surface tension in progenitor cell segregation during gastrulation. <i>Development</i>. 2017;144(10):1798-1806. doi:<a href=\"https://doi.org/10.1242/dev.144964\">10.1242/dev.144964</a>","ieee":"G. Krens <i>et al.</i>, “Interstitial fluid osmolarity modulates the action of differential tissue surface tension in progenitor cell segregation during gastrulation,” <i>Development</i>, vol. 144, no. 10. Company of Biologists, pp. 1798–1806, 2017.","ista":"Krens G, Veldhuis J, Barone V, Capek D, Maître J-L, Brodland W, Heisenberg C-PJ. 2017. Interstitial fluid osmolarity modulates the action of differential tissue surface tension in progenitor cell segregation during gastrulation. Development. 144(10), 1798–1806.","mla":"Krens, Gabriel, et al. “Interstitial Fluid Osmolarity Modulates the Action of Differential Tissue Surface Tension in Progenitor Cell Segregation during Gastrulation.” <i>Development</i>, vol. 144, no. 10, Company of Biologists, 2017, pp. 1798–806, doi:<a href=\"https://doi.org/10.1242/dev.144964\">10.1242/dev.144964</a>.","apa":"Krens, G., Veldhuis, J., Barone, V., Capek, D., Maître, J.-L., Brodland, W., &#38; Heisenberg, C.-P. J. (2017). Interstitial fluid osmolarity modulates the action of differential tissue surface tension in progenitor cell segregation during gastrulation. <i>Development</i>. Company of Biologists. <a href=\"https://doi.org/10.1242/dev.144964\">https://doi.org/10.1242/dev.144964</a>","short":"G. Krens, J. Veldhuis, V. Barone, D. Capek, J.-L. Maître, W. Brodland, C.-P.J. Heisenberg, Development 144 (2017) 1798–1806."},"volume":144,"publisher":"Company of Biologists","doi":"10.1242/dev.144964","day":"15","page":"1798 - 1806","type":"journal_article","related_material":{"record":[{"status":"public","relation":"dissertation_contains","id":"961"},{"status":"public","relation":"dissertation_contains","id":"50"}]}},{"month":"07","pmid":1,"article_processing_charge":"No","title":"Tapetal cell fate, lineage and proliferation in the Arabidopsis anther","keyword":["Developmental Biology","Molecular Biology","Anther Tapetum","Arabidopsis","Cell Fate Establishment","EMS1","Reproductive Cell Lineage"],"oa_version":"None","year":"2010","_id":"12199","issue":"14","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","author":[{"first_name":"Xiaoqi","full_name":"Feng, Xiaoqi","id":"e0164712-22ee-11ed-b12a-d80fcdf35958","orcid":"0000-0002-4008-1234","last_name":"Feng"},{"first_name":"Hugh G.","full_name":"Dickinson, Hugh G.","last_name":"Dickinson"}],"publication_status":"published","article_type":"original","acknowledgement":"We thank the following for providing mutant lines and reagents: Hong Ma, De Ye, Sacco De Vries, and Rod Scott for providing the pA9::Barnase lines and information on A9 expression patterns. Carla Galinha and Paolo Piazza gave valuable help with in situ hybridisation and qRT-PCR, respectively, and we acknowledge Qing Zhang, Helen Prescott and Matthew Dicks for providing excellent technical assistance. We are indebted to Miltos Tsiantis and Angela Hay for helpful discussion, and the research was funded by Oxford University through a Clarendon Scholarship to X.F., with additional financial support from Magdalen College (Oxford).","status":"public","abstract":[{"text":"The four microsporangia of the flowering plant anther develop from archesporial cells in the L2 of the primordium. Within each microsporangium, developing microsporocytes are surrounded by concentric monolayers of tapetal, middle layer and endothecial cells. How this intricate array of tissues, each containing relatively few cells, is established in an organ possessing no formal meristems is poorly understood. We describe here the pivotal role of the LRR receptor kinase EXCESS MICROSPOROCYTES 1 (EMS1) in forming the monolayer of tapetal nurse cells in Arabidopsis. Unusually for plants, tapetal cells are specified very early in development, and are subsequently stimulated to proliferate by a receptor-like kinase (RLK) complex that includes EMS1. Mutations in members of this EMS1 signalling complex and its putative ligand result in male-sterile plants in which tapetal initials fail to proliferate. Surprisingly, these cells continue to develop, isolated at the locular periphery. Mutant and wild-type microsporangia expand at similar rates and the ‘tapetal’ space at the periphery of mutant locules becomes occupied by microsporocytes. However, induction of late expression of EMS1 in the few tapetal initials in ems1 plants results in their proliferation to generate a functional tapetum, and this proliferation suppresses microsporocyte number. Our experiments also show that integrity of the tapetal monolayer is crucial for the maintenance of the polarity of divisions within it. This unexpected autonomy of the tapetal ‘lineage’ is discussed in the context of tissue development in complex plant organs, where constancy in size, shape and cell number is crucial.","lang":"eng"}],"date_published":"2010-07-15T00:00:00Z","scopus_import":"1","extern":"1","publication":"Development","type":"journal_article","page":"2409-2416","doi":"10.1242/dev.049320","publisher":"The Company of Biologists","day":"15","volume":137,"citation":{"chicago":"Feng, Xiaoqi, and Hugh G. Dickinson. “Tapetal Cell Fate, Lineage and Proliferation in the Arabidopsis Anther.” <i>Development</i>. The Company of Biologists, 2010. <a href=\"https://doi.org/10.1242/dev.049320\">https://doi.org/10.1242/dev.049320</a>.","ama":"Feng X, Dickinson HG. Tapetal cell fate, lineage and proliferation in the Arabidopsis anther. <i>Development</i>. 2010;137(14):2409-2416. doi:<a href=\"https://doi.org/10.1242/dev.049320\">10.1242/dev.049320</a>","ieee":"X. Feng and H. G. Dickinson, “Tapetal cell fate, lineage and proliferation in the Arabidopsis anther,” <i>Development</i>, vol. 137, no. 14. The Company of Biologists, pp. 2409–2416, 2010.","ista":"Feng X, Dickinson HG. 2010. Tapetal cell fate, lineage and proliferation in the Arabidopsis anther. Development. 137(14), 2409–2416.","mla":"Feng, Xiaoqi, and Hugh G. Dickinson. “Tapetal Cell Fate, Lineage and Proliferation in the Arabidopsis Anther.” <i>Development</i>, vol. 137, no. 14, The Company of Biologists, 2010, pp. 2409–16, doi:<a href=\"https://doi.org/10.1242/dev.049320\">10.1242/dev.049320</a>.","apa":"Feng, X., &#38; Dickinson, H. G. (2010). Tapetal cell fate, lineage and proliferation in the Arabidopsis anther. <i>Development</i>. The Company of Biologists. <a href=\"https://doi.org/10.1242/dev.049320\">https://doi.org/10.1242/dev.049320</a>","short":"X. Feng, H.G. Dickinson, Development 137 (2010) 2409–2416."},"department":[{"_id":"XiFe"}],"date_created":"2023-01-16T09:21:54Z","external_id":{"pmid":["20570940"]},"date_updated":"2023-05-08T10:57:11Z","publication_identifier":{"issn":["1477-9129","0950-1991"]},"intvolume":"       137","quality_controlled":"1","language":[{"iso":"eng"}]},{"oa_version":"Published Version","year":"2007","_id":"9524","issue":"22","title":"Genome-wide analysis of DNA methylation patterns","article_processing_charge":"No","month":"11","pmid":1,"status":"public","abstract":[{"lang":"eng","text":"Cytosine methylation is the most common covalent modification of DNA in eukaryotes. DNA methylation has an important role in many aspects of biology, including development and disease. Methylation can be detected using bisulfite conversion, methylation-sensitive restriction enzymes, methyl-binding proteins and anti-methylcytosine antibodies. Combining these techniques with DNA microarrays and high-throughput sequencing has made the mapping of DNA methylation feasible on a genome-wide scale. Here we discuss recent developments and future directions for identifying and mapping methylation, in an effort to help colleagues to identify the approaches that best serve their research interests."}],"date_published":"2007-11-15T00:00:00Z","scopus_import":"1","author":[{"last_name":"Zilberman","orcid":"0000-0002-0123-8649","first_name":"Daniel","full_name":"Zilberman, Daniel","id":"6973db13-dd5f-11ea-814e-b3e5455e9ed1"},{"first_name":"Steven","full_name":"Henikoff, Steven","last_name":"Henikoff"}],"publication_status":"published","article_type":"review","oa":1,"user_id":"8b945eb4-e2f2-11eb-945a-df72226e66a9","volume":134,"citation":{"chicago":"Zilberman, Daniel, and Steven Henikoff. “Genome-Wide Analysis of DNA Methylation Patterns.” <i>Development</i>. The Company of Biologists, 2007. <a href=\"https://doi.org/10.1242/dev.001131\">https://doi.org/10.1242/dev.001131</a>.","ama":"Zilberman D, Henikoff S. Genome-wide analysis of DNA methylation patterns. <i>Development</i>. 2007;134(22):3959-3965. doi:<a href=\"https://doi.org/10.1242/dev.001131\">10.1242/dev.001131</a>","apa":"Zilberman, D., &#38; Henikoff, S. (2007). Genome-wide analysis of DNA methylation patterns. <i>Development</i>. The Company of Biologists. <a href=\"https://doi.org/10.1242/dev.001131\">https://doi.org/10.1242/dev.001131</a>","ista":"Zilberman D, Henikoff S. 2007. Genome-wide analysis of DNA methylation patterns. Development. 134(22), 3959–3965.","mla":"Zilberman, Daniel, and Steven Henikoff. “Genome-Wide Analysis of DNA Methylation Patterns.” <i>Development</i>, vol. 134, no. 22, The Company of Biologists, 2007, pp. 3959–65, doi:<a href=\"https://doi.org/10.1242/dev.001131\">10.1242/dev.001131</a>.","ieee":"D. Zilberman and S. Henikoff, “Genome-wide analysis of DNA methylation patterns,” <i>Development</i>, vol. 134, no. 22. The Company of Biologists, pp. 3959–3965, 2007.","short":"D. Zilberman, S. Henikoff, Development 134 (2007) 3959–3965."},"type":"journal_article","page":"3959-3965","day":"15","publisher":"The Company of Biologists","doi":"10.1242/dev.001131","publication":"Development","extern":"1","main_file_link":[{"open_access":"1","url":"https://doi.org/10.1242/dev.001131"}],"publication_identifier":{"issn":["0950-1991"],"eissn":["1477-9129"]},"intvolume":"       134","language":[{"iso":"eng"}],"quality_controlled":"1","external_id":{"pmid":["17928417"]},"date_updated":"2021-12-14T08:57:58Z","department":[{"_id":"DaZi"}],"date_created":"2021-06-08T06:29:50Z"},{"year":"2002","_id":"4209","issue":"14","oa_version":"None","title":"Planar cell polarization requires Widerborst, a B′ regulatory subunit of protein phosphatase 2A","article_processing_charge":"No","pmid":1,"month":"07","date_published":"2002-07-15T00:00:00Z","scopus_import":"1","abstract":[{"lang":"eng","text":"We have identified widerborst (wdb), a B' regulatory subunit of PP2A, as a conserved component of planar cell polarization mechanisms in both Drosophila and in zebrafish. In Drosophila, wdb acts at two steps during planar polarization of wing epithelial cells. It is required to organize tissue polarity proteins into proximal and distal cortical domains, thus determining wing hair orientation. It is also needed to generate the polarized membrane outgrowth that becomes the wing hair. Widerborst activates the catalytic subunit of PP2A and localizes to the distal side of a planar microtubule web that lies at the level of apical cell junctions. This suggests that polarized PP2A activation along the planar microtubule web is important for planar polarization. In zebrafish, two wdb homologs are required for convergent extension during gastrulation, supporting the conjecture that Drosophila planar cell polarization and vertebrate gastrulation movements are regulated by similar mechanisms."}],"status":"public","acknowledgement":"We gratefully acknowledge Bianca Habermann for assistance with bioinformatics, Jens Rietdorf and Arshad Desai for help with deconvolution, and Tadashi Uemura and Rick Fehon for providing antibodies. Arshad Desai, Christian Dahmann, Tony Hyman and Elly Tanaka provided helpful comments on the manuscript. Part of this work was performed at the EMBL in Heidelberg.","article_type":"original","publication_status":"published","author":[{"first_name":"Michael","full_name":"Hannus, Michael","last_name":"Hannus"},{"last_name":"Feiguin","full_name":"Feiguin, Fabian","first_name":"Fabian"},{"orcid":"0000-0002-0912-4566","last_name":"Heisenberg","full_name":"Heisenberg, Carl-Philipp J","id":"39427864-F248-11E8-B48F-1D18A9856A87","first_name":"Carl-Philipp J"},{"full_name":"Eaton, Suzanne","first_name":"Suzanne","last_name":"Eaton"}],"user_id":"ea97e931-d5af-11eb-85d4-e6957dddbf17","citation":{"short":"M. Hannus, F. Feiguin, C.-P.J. Heisenberg, S. Eaton, Development 129 (2002) 3493–3503.","ieee":"M. Hannus, F. Feiguin, C.-P. J. Heisenberg, and S. Eaton, “Planar cell polarization requires Widerborst, a B′ regulatory subunit of protein phosphatase 2A,” <i>Development</i>, vol. 129, no. 14. Company of Biologists, pp. 3493–3503, 2002.","ista":"Hannus M, Feiguin F, Heisenberg C-PJ, Eaton S. 2002. Planar cell polarization requires Widerborst, a B′ regulatory subunit of protein phosphatase 2A. Development. 129(14), 3493–3503.","mla":"Hannus, Michael, et al. “Planar Cell Polarization Requires Widerborst, a B′ Regulatory Subunit of Protein Phosphatase 2A.” <i>Development</i>, vol. 129, no. 14, Company of Biologists, 2002, pp. 3493–503, doi:<a href=\"https://doi.org/10.1242/dev.129.14.3493\">10.1242/dev.129.14.3493</a>.","apa":"Hannus, M., Feiguin, F., Heisenberg, C.-P. J., &#38; Eaton, S. (2002). Planar cell polarization requires Widerborst, a B′ regulatory subunit of protein phosphatase 2A. <i>Development</i>. Company of Biologists. <a href=\"https://doi.org/10.1242/dev.129.14.3493\">https://doi.org/10.1242/dev.129.14.3493</a>","ama":"Hannus M, Feiguin F, Heisenberg C-PJ, Eaton S. Planar cell polarization requires Widerborst, a B′ regulatory subunit of protein phosphatase 2A. <i>Development</i>. 2002;129(14):3493-3503. doi:<a href=\"https://doi.org/10.1242/dev.129.14.3493\">10.1242/dev.129.14.3493</a>","chicago":"Hannus, Michael, Fabian Feiguin, Carl-Philipp J Heisenberg, and Suzanne Eaton. “Planar Cell Polarization Requires Widerborst, a B′ Regulatory Subunit of Protein Phosphatase 2A.” <i>Development</i>. Company of Biologists, 2002. <a href=\"https://doi.org/10.1242/dev.129.14.3493\">https://doi.org/10.1242/dev.129.14.3493</a>."},"volume":129,"page":"3493 - 3503","doi":"10.1242/dev.129.14.3493","day":"15","publisher":"Company of Biologists","type":"journal_article","publication":"Development","extern":"1","publist_id":"1909","intvolume":"       129","language":[{"iso":"eng"}],"quality_controlled":"1","publication_identifier":{"issn":["0950-1991"]},"date_updated":"2023-06-06T14:07:49Z","external_id":{"pmid":["12091318"]},"date_created":"2018-12-11T12:07:36Z"},{"page":"2129 - 2140","day":"15","doi":"10.1242/dev.126.10.2129","publisher":"Company of Biologists","type":"journal_article","citation":{"chicago":"Heisenberg, Carl-Philipp J, Caroline Brennan, and Stephen Wilson. “Zebrafish Aussicht Mutant Embryos Exhibit Widespread Overexpression of Ace (Fgf8) and Coincident Defects in CNS Development.” <i>Development</i>. Company of Biologists, 1999. <a href=\"https://doi.org/10.1242/dev.126.10.2129\">https://doi.org/10.1242/dev.126.10.2129</a>.","ama":"Heisenberg C-PJ, Brennan C, Wilson S. Zebrafish aussicht mutant embryos exhibit widespread overexpression of ace (fgf8) and coincident defects in CNS development. <i>Development</i>. 1999;126(10):2129-2140. doi:<a href=\"https://doi.org/10.1242/dev.126.10.2129\">10.1242/dev.126.10.2129</a>","ieee":"C.-P. J. Heisenberg, C. Brennan, and S. Wilson, “Zebrafish aussicht mutant embryos exhibit widespread overexpression of ace (fgf8) and coincident defects in CNS development,” <i>Development</i>, vol. 126, no. 10. Company of Biologists, pp. 2129–2140, 1999.","mla":"Heisenberg, Carl-Philipp J., et al. “Zebrafish Aussicht Mutant Embryos Exhibit Widespread Overexpression of Ace (Fgf8) and Coincident Defects in CNS Development.” <i>Development</i>, vol. 126, no. 10, Company of Biologists, 1999, pp. 2129–40, doi:<a href=\"https://doi.org/10.1242/dev.126.10.2129\">10.1242/dev.126.10.2129</a>.","ista":"Heisenberg C-PJ, Brennan C, Wilson S. 1999. Zebrafish aussicht mutant embryos exhibit widespread overexpression of ace (fgf8) and coincident defects in CNS development. Development. 126(10), 2129–2140.","apa":"Heisenberg, C.-P. J., Brennan, C., &#38; Wilson, S. (1999). Zebrafish aussicht mutant embryos exhibit widespread overexpression of ace (fgf8) and coincident defects in CNS development. <i>Development</i>. Company of Biologists. <a href=\"https://doi.org/10.1242/dev.126.10.2129\">https://doi.org/10.1242/dev.126.10.2129</a>","short":"C.-P.J. Heisenberg, C. Brennan, S. Wilson, Development 126 (1999) 2129–2140."},"volume":126,"extern":"1","publist_id":"1914","publication":"Development","date_updated":"2022-09-06T08:38:01Z","external_id":{"pmid":["10207138"]},"intvolume":"       126","quality_controlled":"1","language":[{"iso":"eng"}],"publication_identifier":{"issn":["0950-1991"]},"date_created":"2018-12-11T12:07:34Z","title":"Zebrafish aussicht mutant embryos exhibit widespread overexpression of ace (fgf8) and coincident defects in CNS development","year":"1999","_id":"4204","issue":"10","oa_version":"None","pmid":1,"month":"05","article_processing_charge":"No","acknowledgement":"We thank Corinne Houart, Michael Brand and the late Nigel Holder for comments and advice on this study, many colleagues for providing probes used in this analysis, other members of our laboratories for suggestions throughout the course of the work and Michael Brand, Jörg Rauch and Pascal Haffter for providing data prior to publication. We also would like to thank Christiane Nüsslein-Volhard in whose laboratory the mutant described in this study was initially isolated.\r\nThis study was supported by grants from The Wellcome Trust and\r\nBBSRC. C. P. H. was supported by Fellowships from EMBO and the\r\nEC, and S. W. W. is a Wellcome Trust Senior Research Fellow.\r\n","scopus_import":"1","date_published":"1999-05-15T00:00:00Z","abstract":[{"lang":"eng","text":"During the development of the zebrafish nervous system both noi, a zebrafish pax2 homolog, and ace, a zebrafish fgf8 homolog, are required for development of the midbrain and cerebellum. Here we describe a dominant mutation, aussicht (aus), in which the expression of noi and ace is upregulated, In aus mutant embryos, ace is upregulated at many sites in the embryo, while Itoi expression is only upregulated in regions of the forebrain and midbrain which also express ace. Subsequent to the alterations in noi and ace expression, aus mutants exhibit defects in the differentiation of the forebrain, midbrain and eyes. Within the forebrain, the formation of the anterior and postoptic commissures is delayed and the expression of markers within the pretectal area is reduced. Within the midbrain, En and wnt1 expression is expanded. In heterozygous aus embryos, there is ectopic outgrowth of neural retina in the temporal half of the eyes, whereas in putative homozygous aus embryos, the ventral retina is reduced and the pigmented retinal epithelium is expanded towards the midline, The observation that ans mutant embryos exhibit widespread upregulation of ace raised the possibility that aus might represent an allele of the ace gene itself. However, by crossing carriers for both aus and ace, we were able to generate homozygous ace mutant embryos that also exhibited the aus phenotype, This indicated that aus is not tightly linked to ace and is unlikely to be a mutation directly affecting the ace locus. However, increased Ace activity may underly many aspects of the aus phenotype and we show that the upregulation of noi in the forebrain of aus mutants is partially dependent upon functional Ace activity. Conversely, increased ace expression in the forebrain of arcs mutants is not dependent upon functional Noi activity. We conclude that aus represents a mutation involving a locus normally required for the regulation of ace expression during embryogenesis."}],"status":"public","user_id":"ea97e931-d5af-11eb-85d4-e6957dddbf17","article_type":"original","publication_status":"published","author":[{"first_name":"Carl-Philipp J","id":"39427864-F248-11E8-B48F-1D18A9856A87","full_name":"Heisenberg, Carl-Philipp J","orcid":"0000-0002-0912-4566","last_name":"Heisenberg"},{"last_name":"Brennan","first_name":"Caroline","full_name":"Brennan, Caroline"},{"first_name":"Stephen","full_name":"Wilson, Stephen","last_name":"Wilson"}]},{"publication_status":"published","article_type":"original","author":[{"last_name":"Whitfield","first_name":"Tanya","full_name":"Whitfield, Tanya"},{"last_name":"Granato","full_name":"Granato, Michael","first_name":"Michael"},{"first_name":"Fredericus","full_name":"Van Eeden, Fredericus","last_name":"Van Eeden"},{"first_name":"Ursula","full_name":"Schach, Ursula","last_name":"Schach"},{"full_name":"Brand, Michael","first_name":"Michael","last_name":"Brand"},{"first_name":"Makoto","full_name":"Furutani Seiki, Makoto","last_name":"Furutani Seiki"},{"first_name":"Pascal","full_name":"Haffter, Pascal","last_name":"Haffter"},{"full_name":"Hammerschmidt, Matthias","first_name":"Matthias","last_name":"Hammerschmidt"},{"first_name":"Carl-Philipp J","full_name":"Heisenberg, Carl-Philipp J","id":"39427864-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-0912-4566","last_name":"Heisenberg"},{"last_name":"Jiang","full_name":"Jiang, Yunjin","first_name":"Yunjin"},{"last_name":"Kane","first_name":"Donald","full_name":"Kane, Donald"},{"last_name":"Kelsh","first_name":"Robert","full_name":"Kelsh, Robert"},{"full_name":"Mullins, Mary","first_name":"Mary","last_name":"Mullins"},{"full_name":"Odenthal, Jörg","first_name":"Jörg","last_name":"Odenthal"},{"last_name":"Nüsslein Volhard","first_name":"Christiane","full_name":"Nüsslein Volhard, Christiane"}],"user_id":"ea97e931-d5af-11eb-85d4-e6957dddbf17","date_published":"1996-12-01T00:00:00Z","abstract":[{"text":"Mutations giving rise to anatomical defects in the inner ear have been isolated in a large scale screen for mutations causing visible abnormalities in the zebrafish embryo (Haffter, P., Granato, M., Brand, M. et al. (1996) Development 123, 1-36). 58 mutants have been classified as having a primary ear phenotype; these fall into several phenotypic classes, affecting presence or size of the otoliths, size and shape of the otic vesicle and formation of the semicircular canals, and define at least 20 complementation groups. Mutations in seven genes cause loss of one or both otoliths, but do not appear to affect development of other structures within the ear. Mutations in seven genes affect morphology and patterning of the inner ear epithelium, including formation of the semicircular canals and, in some, development of sensory patches (maculae and cristae). Within this class, dog-eared mutants show abnormal development of semicircular canals and lack cristae within the ear, while in van gogh, semicircular canals fail to form altogether, resulting in a tiny otic vesicle containing a single sensory patch. Both these mutants show defects in the expression of homeobox genes within the otic vesicle. In a further class of mutants, ear size is affected while patterning appears to be relatively normal; mutations in three genes cause expansion of the otic vesicle, while in little ears and microtic, the ear is abnormally small, but still contains all five sensory patches, as in the wild type. Many of the ear and otolith mutants show an expected behavioural phenotype: embryos fail to balance correctly, and may swim on their sides, upside down, or in circles. Several mutants with similar balance defects have also been isolated that have no obvious structural ear defect, but that may include mutants with vestibular dysfunction of the inner ear (Granato, M., van Eeden, F. J. M., Schach, U. et al. (1996) Development, 123, 399-413,). Mutations in 19 genes causing primary defects in other structures also show an ear defect. In particular, ear phenotypes are often found in conjunction with defects of neural crest derivatives (pigment cells and/or cartilaginous elements of the jaw). At least one mutant, dog-eared, shows defects in both the ear and another placodally derived sensory system, the lateral line, while hypersensitive mutants have additional trunk lateral line organs.","lang":"eng"}],"scopus_import":"1","status":"public","acknowledgement":"T. T. W. thanks all members of the Tübingen fish and fly groups for their hospitality and generosity during her visits to the laboratory. We thank Julian Lewis, in whose laboratory much of this work was carried out, for many helpful discussions and suggestions, Catherine Haddon for advice on wild-type ear development and techniques, and Stephen Massey for fish husbandry in Oxford. We are grateful to Julian Lewis, Catherine Haddon, Nick Monk and Patrick Blader for comments on the manuscript, and to Trevor Jowett, Tom Schilling,Eric Weinberg and Monte Westerfield for providing cDNAs. We also thank Jarema Malicki and Wolfgang Driever for making some of the Boston otolith mutants available before publication. T. T. W. thanks the EMBO (ASTF 7668; ASTF 7918), the Imperial Cancer Research Fund and the Wellcome Trust (03643/Z/92) for support.","article_processing_charge":"No","pmid":1,"month":"12","_id":"4142","year":"1996","oa_version":"None","title":"Mutations affecting development of the zebrafish inner ear and lateral line","date_created":"2018-12-11T12:07:11Z","language":[{"iso":"eng"}],"quality_controlled":"1","intvolume":"       123","publication_identifier":{"issn":["0950-1991"]},"date_updated":"2022-08-08T08:45:59Z","external_id":{"pmid":["9007244"]},"publication":"Development","extern":"1","publist_id":"1979","citation":{"ama":"Whitfield T, Granato M, Van Eeden F, et al. Mutations affecting development of the zebrafish inner ear and lateral line. <i>Development</i>. 1996;123:241-254. doi:<a href=\"https://doi.org/10.1242/dev.123.1.241\">10.1242/dev.123.1.241</a>","chicago":"Whitfield, Tanya, Michael Granato, Fredericus Van Eeden, Ursula Schach, Michael Brand, Makoto Furutani Seiki, Pascal Haffter, et al. “Mutations Affecting Development of the Zebrafish Inner Ear and Lateral Line.” <i>Development</i>. Company of Biologists, 1996. <a href=\"https://doi.org/10.1242/dev.123.1.241\">https://doi.org/10.1242/dev.123.1.241</a>.","short":"T. Whitfield, M. Granato, F. Van Eeden, U. Schach, M. Brand, M. Furutani Seiki, P. Haffter, M. Hammerschmidt, C.-P.J. Heisenberg, Y. Jiang, D. Kane, R. Kelsh, M. Mullins, J. Odenthal, C. Nüsslein Volhard, Development 123 (1996) 241–254.","mla":"Whitfield, Tanya, et al. “Mutations Affecting Development of the Zebrafish Inner Ear and Lateral Line.” <i>Development</i>, vol. 123, Company of Biologists, 1996, pp. 241–54, doi:<a href=\"https://doi.org/10.1242/dev.123.1.241\">10.1242/dev.123.1.241</a>.","apa":"Whitfield, T., Granato, M., Van Eeden, F., Schach, U., Brand, M., Furutani Seiki, M., … Nüsslein Volhard, C. (1996). Mutations affecting development of the zebrafish inner ear and lateral line. <i>Development</i>. Company of Biologists. <a href=\"https://doi.org/10.1242/dev.123.1.241\">https://doi.org/10.1242/dev.123.1.241</a>","ista":"Whitfield T, Granato M, Van Eeden F, Schach U, Brand M, Furutani Seiki M, Haffter P, Hammerschmidt M, Heisenberg C-PJ, Jiang Y, Kane D, Kelsh R, Mullins M, Odenthal J, Nüsslein Volhard C. 1996. Mutations affecting development of the zebrafish inner ear and lateral line. Development. 123, 241–254.","ieee":"T. Whitfield <i>et al.</i>, “Mutations affecting development of the zebrafish inner ear and lateral line,” <i>Development</i>, vol. 123. Company of Biologists, pp. 241–254, 1996."},"volume":123,"day":"01","doi":"10.1242/dev.123.1.241","publisher":"Company of Biologists","page":"241 - 254","type":"journal_article"},{"citation":{"short":"T. Schilling, T. Piotrowski, H. Grandel, M. Brand, C.-P.J. Heisenberg, Y. Jiang, D. Beuchle, M. Hammerschmidt, D. Kane, M. Mullins, F. Van Eeden, R. Kelsh, M. Furutani Seiki, M. Granato, P. Haffter, J. Odenthal, R. Warga, T. Trowe, C. Nüsslein Volhard, Development 123 (1996) 329–344.","mla":"Schilling, Thomas, et al. “Jaw and Branchial Arch Mutants in Zebrafish I: Branchial Arches.” <i>Development</i>, vol. 123, no. 1, Company of Biologists, 1996, pp. 329–44, doi:<a href=\"https://doi.org/10.1242/dev.123.1.329\">10.1242/dev.123.1.329</a>.","apa":"Schilling, T., Piotrowski, T., Grandel, H., Brand, M., Heisenberg, C.-P. J., Jiang, Y., … Nüsslein Volhard, C. (1996). Jaw and branchial arch mutants in zebrafish I: Branchial arches. <i>Development</i>. Company of Biologists. <a href=\"https://doi.org/10.1242/dev.123.1.329\">https://doi.org/10.1242/dev.123.1.329</a>","ista":"Schilling T, Piotrowski T, Grandel H, Brand M, Heisenberg C-PJ, Jiang Y, Beuchle D, Hammerschmidt M, Kane D, Mullins M, Van Eeden F, Kelsh R, Furutani Seiki M, Granato M, Haffter P, Odenthal J, Warga R, Trowe T, Nüsslein Volhard C. 1996. Jaw and branchial arch mutants in zebrafish I: Branchial arches. Development. 123(1), 329–344.","ieee":"T. Schilling <i>et al.</i>, “Jaw and branchial arch mutants in zebrafish I: Branchial arches,” <i>Development</i>, vol. 123, no. 1. Company of Biologists, pp. 329–344, 1996.","ama":"Schilling T, Piotrowski T, Grandel H, et al. Jaw and branchial arch mutants in zebrafish I: Branchial arches. <i>Development</i>. 1996;123(1):329-344. doi:<a href=\"https://doi.org/10.1242/dev.123.1.329\">10.1242/dev.123.1.329</a>","chicago":"Schilling, Thomas, Tatjana Piotrowski, Heiner Grandel, Michael Brand, Carl-Philipp J Heisenberg, Yunjin Jiang, Dirk Beuchle, et al. “Jaw and Branchial Arch Mutants in Zebrafish I: Branchial Arches.” <i>Development</i>. Company of Biologists, 1996. <a href=\"https://doi.org/10.1242/dev.123.1.329\">https://doi.org/10.1242/dev.123.1.329</a>."},"volume":123,"publisher":"Company of Biologists","doi":"10.1242/dev.123.1.329","day":"01","page":"329 - 344","type":"journal_article","publication":"Development","extern":"1","publist_id":"1968","language":[{"iso":"eng"}],"quality_controlled":"1","intvolume":"       123","publication_identifier":{"issn":["0950-1991"]},"date_updated":"2022-08-08T08:41:00Z","external_id":{"pmid":["9007253"]},"date_created":"2018-12-11T12:07:15Z","_id":"4151","issue":"1","year":"1996","oa_version":"None","title":"Jaw and branchial arch mutants in zebrafish I: Branchial arches","article_processing_charge":"No","pmid":1,"month":"12","scopus_import":"1","date_published":"1996-12-01T00:00:00Z","abstract":[{"lang":"eng","text":"Jaws and branchial arches together are a basic, segmented feature of the vertebrate head, Seven arches develop in the zebrafish embryo (Danio rerio), derived largely from neural crest cells that form the cartilaginous skeleton, In this and the following paper we describe the phenotypes of 109 arch mutants, focusing here on three classes that affect the posterior pharyngeal arches, including the hyoid and five gill-bearing arches, In lockjaw, the hyoid arch is strongly reduced and subsets of branchial arches do not develop, Mutants of a large second class, designated the flathead group, lack several adjacent branchial arches and their associated cartilages. Five alleles at the flathead locus all lead to larvae that lack arches 4-6, Among 34 other flathead group members complementation tests are incomplete, but at least six unique phenotypes can be distinguished, These all delete continuous stretches of adjacent branchial arches and unpaired cartilages in the ventral midline, Many show cell death in the midbrain, from which some neural crest precursors of the arches originate, lockjaw and a few mutants in the flathead group, including pistachio, affect both jaw cartilage and pigmentation, reflecting essential functions of these genes in at least two neural crest lineages, Mutants of a third class, including boxer, dackel and pincher, affect pectoral fins and axonal trajectories in the brain, as well as the arches. Their skeletal phenotypes suggest that they disrupt cartilage morphogenesis in all arches, Our results suggest that there are sets of genes that: (1) specify neural crest cells in groups of adjacent head segments, and (2) function in common genetic pathways in a variety of tissues including the brain, pectoral fins and pigment cells as well as pharyngeal arches."}],"status":"public","acknowledgement":"We thank Drs Charles Kimmel, Philip Ingham, Paula Mabee and members of the Ingham lab for critical comments on the manuscript.","publication_status":"published","article_type":"original","author":[{"first_name":"Thomas","full_name":"Schilling, Thomas","last_name":"Schilling"},{"last_name":"Piotrowski","first_name":"Tatjana","full_name":"Piotrowski, Tatjana"},{"last_name":"Grandel","first_name":"Heiner","full_name":"Grandel, Heiner"},{"first_name":"Michael","full_name":"Brand, Michael","last_name":"Brand"},{"first_name":"Carl-Philipp J","id":"39427864-F248-11E8-B48F-1D18A9856A87","full_name":"Heisenberg, Carl-Philipp J","orcid":"0000-0002-0912-4566","last_name":"Heisenberg"},{"last_name":"Jiang","full_name":"Jiang, Yunjin","first_name":"Yunjin"},{"full_name":"Beuchle, Dirk","first_name":"Dirk","last_name":"Beuchle"},{"last_name":"Hammerschmidt","first_name":"Matthias","full_name":"Hammerschmidt, Matthias"},{"first_name":"Donald","full_name":"Kane, Donald","last_name":"Kane"},{"last_name":"Mullins","first_name":"Mary","full_name":"Mullins, Mary"},{"last_name":"Van Eeden","full_name":"Van Eeden, Fredericus","first_name":"Fredericus"},{"first_name":"Robert","full_name":"Kelsh, Robert","last_name":"Kelsh"},{"last_name":"Furutani Seiki","full_name":"Furutani Seiki, Makoto","first_name":"Makoto"},{"last_name":"Granato","first_name":"Michael","full_name":"Granato, Michael"},{"last_name":"Haffter","full_name":"Haffter, Pascal","first_name":"Pascal"},{"full_name":"Odenthal, Jörg","first_name":"Jörg","last_name":"Odenthal"},{"last_name":"Warga","full_name":"Warga, Rachel","first_name":"Rachel"},{"first_name":"Torsten","full_name":"Trowe, Torsten","last_name":"Trowe"},{"last_name":"Nüsslein Volhard","first_name":"Christiane","full_name":"Nüsslein Volhard, Christiane"}],"user_id":"ea97e931-d5af-11eb-85d4-e6957dddbf17"},{"article_processing_charge":"No","month":"12","pmid":1,"oa_version":"None","_id":"4154","issue":"1","year":"1996","title":"Characterization of zebrafish mutants with defects in embryonic hematopoiesis","author":[{"last_name":"Ransom","first_name":"David","full_name":"Ransom, David"},{"first_name":"Pascal","full_name":"Haffter, Pascal","last_name":"Haffter"},{"last_name":"Odenthal","full_name":"Odenthal, Jörg","first_name":"Jörg"},{"last_name":"Brownlie","full_name":"Brownlie, Alison","first_name":"Alison"},{"last_name":"Vogelsang","full_name":"Vogelsang, Elisabeth","first_name":"Elisabeth"},{"full_name":"Kelsh, Robert","first_name":"Robert","last_name":"Kelsh"},{"last_name":"Brand","full_name":"Brand, Michael","first_name":"Michael"},{"last_name":"Van Eeden","first_name":"Fredericus","full_name":"Van Eeden, Fredericus"},{"full_name":"Furutani Seiki, Makoto","first_name":"Makoto","last_name":"Furutani Seiki"},{"full_name":"Granato, Michael","first_name":"Michael","last_name":"Granato"},{"first_name":"Matthias","full_name":"Hammerschmidt, Matthias","last_name":"Hammerschmidt"},{"first_name":"Carl-Philipp J","id":"39427864-F248-11E8-B48F-1D18A9856A87","full_name":"Heisenberg, Carl-Philipp J","orcid":"0000-0002-0912-4566","last_name":"Heisenberg"},{"full_name":"Jiang, Yunjin","first_name":"Yunjin","last_name":"Jiang"},{"last_name":"Kane","first_name":"Donald","full_name":"Kane, Donald"},{"full_name":"Mullins, Mary","first_name":"Mary","last_name":"Mullins"},{"last_name":"Nüsslein Volhard","first_name":"Christiane","full_name":"Nüsslein Volhard, Christiane"}],"publication_status":"published","article_type":"original","user_id":"ea97e931-d5af-11eb-85d4-e6957dddbf17","status":"public","date_published":"1996-12-01T00:00:00Z","scopus_import":"1","abstract":[{"text":"As part of a large scale chemical mutagenesis screen of the zebrafish (Danio rerio) genome, we have identified 33 mutants with defects in hematopoiesis, Complementation analysis placed 32 of these mutants into 17 complementation groups, The allelism of the remaining 1 blood mutant is currently unresolved, We have categorized these blood mutants into four phenotypic classes based on analyses of whole embryos and isolated blood cells, as well as by in situ hybridization using the hematopoietic transcription factors GATA-1 and GATA-2, Embryos mutant for the gene moonshine have few if any proerythroblasts visible on the day circulation begins and normal erythroid cell differentiation is blocked as determined by staining for hemoglobin and GATA-1 expression, Mutations in five genes, chablis, frascati, merlot, retsina, thunderbird and two possibly unique mutations cause a progressive decrease in the number of blood cells during the first 5 days of development, Mutations in another seven genes, chardonnay, chianti, grenache, sauternes, weibherbst and zinfandel, and two additional mutations result in hypochromic blood cells which also decrease in number as development proceeds, Several of these mutants have immature cells in the circulation, indicating a block in normal erythroid development. The mutation in zinfandel is dominant, and 2-day old heterozygous carriers fail to express detectable levels of hemoglobin and have decreasing numbers of circulating cells during the first 5 days of development, Mutations in two genes, freixenet and yquem, result in the animals that are photosensitive with autofluorescent blood, similar to that found in the human congenital porphyrias, The collection of mutants presented here represent several steps required for normal erythropoiesis, The analysis of these mutants provides a powerful approach towards defining the molecular mechanisms involved in vertebrate hematopoietic development.","lang":"eng"}],"acknowledgement":"We thank Leonard Zon for his generous support of D. G. R. and A. B., for critical review of this manuscript and for many helpful discussions. We also thank Lauren Barone and Stephen Pratt for technical assistance. D. G. R. is a postdoctoral fellow of the Howard Hughes Medical Institute. ","publication":"Development","publist_id":"1966","extern":"1","volume":123,"citation":{"chicago":"Ransom, David, Pascal Haffter, Jörg Odenthal, Alison Brownlie, Elisabeth Vogelsang, Robert Kelsh, Michael Brand, et al. “Characterization of Zebrafish Mutants with Defects in Embryonic Hematopoiesis.” <i>Development</i>. Company of Biologists, 1996. <a href=\"https://doi.org/10.1242/dev.123.1.311\">https://doi.org/10.1242/dev.123.1.311</a>.","ama":"Ransom D, Haffter P, Odenthal J, et al. Characterization of zebrafish mutants with defects in embryonic hematopoiesis. <i>Development</i>. 1996;123(1):311-319. doi:<a href=\"https://doi.org/10.1242/dev.123.1.311\">10.1242/dev.123.1.311</a>","ieee":"D. Ransom <i>et al.</i>, “Characterization of zebrafish mutants with defects in embryonic hematopoiesis,” <i>Development</i>, vol. 123, no. 1. Company of Biologists, pp. 311–319, 1996.","apa":"Ransom, D., Haffter, P., Odenthal, J., Brownlie, A., Vogelsang, E., Kelsh, R., … Nüsslein Volhard, C. (1996). Characterization of zebrafish mutants with defects in embryonic hematopoiesis. <i>Development</i>. Company of Biologists. <a href=\"https://doi.org/10.1242/dev.123.1.311\">https://doi.org/10.1242/dev.123.1.311</a>","ista":"Ransom D, Haffter P, Odenthal J, Brownlie A, Vogelsang E, Kelsh R, Brand M, Van Eeden F, Furutani Seiki M, Granato M, Hammerschmidt M, Heisenberg C-PJ, Jiang Y, Kane D, Mullins M, Nüsslein Volhard C. 1996. Characterization of zebrafish mutants with defects in embryonic hematopoiesis. Development. 123(1), 311–319.","mla":"Ransom, David, et al. “Characterization of Zebrafish Mutants with Defects in Embryonic Hematopoiesis.” <i>Development</i>, vol. 123, no. 1, Company of Biologists, 1996, pp. 311–19, doi:<a href=\"https://doi.org/10.1242/dev.123.1.311\">10.1242/dev.123.1.311</a>.","short":"D. Ransom, P. Haffter, J. Odenthal, A. Brownlie, E. Vogelsang, R. Kelsh, M. Brand, F. Van Eeden, M. Furutani Seiki, M. Granato, M. Hammerschmidt, C.-P.J. Heisenberg, Y. Jiang, D. Kane, M. Mullins, C. Nüsslein Volhard, Development 123 (1996) 311–319."},"type":"journal_article","doi":"10.1242/dev.123.1.311","day":"01","publisher":"Company of Biologists","page":"311 - 319","date_created":"2018-12-11T12:07:16Z","publication_identifier":{"issn":["0950-1991"]},"quality_controlled":"1","language":[{"iso":"eng"}],"intvolume":"       123","external_id":{"pmid":["9007251"]},"date_updated":"2022-08-08T08:23:35Z"}]