[{"publication_status":"published","intvolume":"        22","language":[{"iso":"eng"}],"date_published":"2026-01-05T00:00:00Z","oaworkid":1,"_id":"21015","related_material":{"link":[{"description":"News on ISTA website","relation":"research_data","url":"https://ista.ac.at/en/news/geometry-shapes-life/"}]},"corr_author":"1","acknowledgement":"We thank N. Petridou (EMBL) for sharing results before publication. N.M. was supported by funding from the European Union’s Horizon 2020 programme under the Marie Skłodowska-Curie COFUND Actions ISTplus grant agreement number 754411. Y.I.L. acknowledges funding from the European Union’s Horizon 2020 research and innovation programme under the Marie Skłodowska-Curie grant agreement number 101034413. The research was supported by funding to C.-P.H. from the NOMIS Foundation, Project ID 1.844. We would like to thank past and present members of the Heisenberg and Hannezo groups for discussions, particularly S. Shamipour, V. Doddihal, M. Jovic, N. Hino, F. N. Arslan, R. Kobylinska and C. Camelo for feedback on the draft manuscript. This research was supported by the Scientific Service Units (SSU) of Institute of Science and Technology Austria through resources provided by the Aquatics Facility, Imaging & Optics Facility (IOF), Scientific Computing (SciComp) facility and Lab Support Facility (LSF). Open access funding provided by Institute of Science and Technology (IST Austria).","publication_identifier":{"eissn":["1745-2481"],"issn":["1745-2473"],"issnl":[" 1745-2473"]},"project":[{"name":"ISTplus - Postdoctoral Fellowships","grant_number":"754411","_id":"260C2330-B435-11E9-9278-68D0E5697425","call_identifier":"H2020"},{"call_identifier":"H2020","_id":"fc2ed2f7-9c52-11eb-aca3-c01059dda49c","grant_number":"101034413","name":"IST-BRIDGE: International postdoctoral program"},{"name":"Cytoplasmic self-organization into cell-like compartments as a common guiding principle in early animal development","_id":"917c023a-16d5-11f0-9cad-eb5cafc52090"}],"external_id":{"oaworkid":["W7118187193"]},"abstract":[{"text":"Early embryo geometry is one of the most invariant species-specific traits, yet its role in ensuring developmental reproducibility and robustness remains underexplored. Here we show that in zebrafish, the geometry of the fertilized egg—specifically its curvature and volume—serves as a critical initial condition triggering a cascade of events that influence development. The embryo geometry guides patterned asymmetric cell divisions in the blastoderm, generating radial gradients of cell volume and nucleocytoplasmic ratio. These gradients generate mitotic phase waves, with the nucleocytoplasmic ratio determining individual cell cycle periods independently of other cells. We demonstrate that reducing cell autonomy reshapes these waves, emphasizing the instructive role of geometry-derived volume patterns in setting the intrinsic period of the cell cycle oscillator. In addition to organizing cell cycles, early embryo geometry spatially patterns zygotic genome activation at the midblastula transition, a key step in establishing embryonic autonomy. Disrupting the embryo shape alters the zygotic genome activation pattern and causes ectopic germ layer specification, underscoring the developmental significance of geometry. Together, our findings reveal a symmetry-breaking function of early embryo geometry in coordinating cell cycle and transcriptional patterning.","lang":"eng"}],"month":"01","type":"journal_article","file_date_updated":"2026-01-21T08:21:11Z","article_processing_charge":"Yes (via OA deal)","doi":"10.1038/s41567-025-03122-1","date_created":"2026-01-20T10:12:19Z","oa_version":"Published Version","title":"Geometry-driven asymmetric cell divisions pattern cell cycles and zygotic genome activation in the zebrafish embryo","department":[{"_id":"EdHa"},{"_id":"CaHe"}],"citation":{"apa":"Mishra, N., Li, Y. I., Hannezo, E. B., &#38; Heisenberg, C.-P. J. (2026). Geometry-driven asymmetric cell divisions pattern cell cycles and zygotic genome activation in the zebrafish embryo. <i>Nature Physics</i>. Springer Nature. <a href=\"https://doi.org/10.1038/s41567-025-03122-1\">https://doi.org/10.1038/s41567-025-03122-1</a>","ama":"Mishra N, Li YI, Hannezo EB, Heisenberg C-PJ. Geometry-driven asymmetric cell divisions pattern cell cycles and zygotic genome activation in the zebrafish embryo. <i>Nature Physics</i>. 2026;22:139-150. doi:<a href=\"https://doi.org/10.1038/s41567-025-03122-1\">10.1038/s41567-025-03122-1</a>","mla":"Mishra, Nikhil, et al. “Geometry-Driven Asymmetric Cell Divisions Pattern Cell Cycles and Zygotic Genome Activation in the Zebrafish Embryo.” <i>Nature Physics</i>, vol. 22, Springer Nature, 2026, pp. 139–50, doi:<a href=\"https://doi.org/10.1038/s41567-025-03122-1\">10.1038/s41567-025-03122-1</a>.","ieee":"N. Mishra, Y. I. Li, E. B. Hannezo, and C.-P. J. Heisenberg, “Geometry-driven asymmetric cell divisions pattern cell cycles and zygotic genome activation in the zebrafish embryo,” <i>Nature Physics</i>, vol. 22. Springer Nature, pp. 139–150, 2026.","ista":"Mishra N, Li YI, Hannezo EB, Heisenberg C-PJ. 2026. Geometry-driven asymmetric cell divisions pattern cell cycles and zygotic genome activation in the zebrafish embryo. Nature Physics. 22, 139–150.","short":"N. Mishra, Y.I. Li, E.B. Hannezo, C.-P.J. Heisenberg, Nature Physics 22 (2026) 139–150.","chicago":"Mishra, Nikhil, Yuting I Li, Edouard B Hannezo, and Carl-Philipp J Heisenberg. “Geometry-Driven Asymmetric Cell Divisions Pattern Cell Cycles and Zygotic Genome Activation in the Zebrafish Embryo.” <i>Nature Physics</i>. Springer Nature, 2026. <a href=\"https://doi.org/10.1038/s41567-025-03122-1\">https://doi.org/10.1038/s41567-025-03122-1</a>."},"page":"139-150","OA_type":"hybrid","ddc":["570"],"status":"public","publication":"Nature Physics","ec_funded":1,"scopus_import":"1","has_accepted_license":"1","file":[{"content_type":"application/pdf","file_size":7335694,"checksum":"0ab7ac2fbcb61a364dba57152db64ed7","success":1,"date_created":"2026-01-21T08:21:11Z","date_updated":"2026-01-21T08:21:11Z","access_level":"open_access","relation":"main_file","file_id":"21026","creator":"dernst","file_name":"2026_NaturePhysics_Mishra.pdf"}],"publisher":"Springer Nature","acknowledged_ssus":[{"_id":"PreCl"},{"_id":"Bio"},{"_id":"ScienComp"},{"_id":"LifeSc"}],"date_updated":"2026-04-28T12:55:30Z","year":"2026","author":[{"id":"C4D70E82-1081-11EA-B3ED-9A4C3DDC885E","orcid":"0000-0002-6425-5788","full_name":"Mishra, Nikhil","first_name":"Nikhil","last_name":"Mishra"},{"id":"ee7a5ca8-8b71-11ed-b662-b3341c05b7eb","full_name":"Li, Yuting I","first_name":"Yuting I","last_name":"Li"},{"last_name":"Hannezo","first_name":"Edouard B","full_name":"Hannezo, Edouard B","orcid":"0000-0001-6005-1561","id":"3A9DB764-F248-11E8-B48F-1D18A9856A87"},{"full_name":"Heisenberg, Carl-Philipp J","first_name":"Carl-Philipp J","last_name":"Heisenberg","id":"39427864-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-0912-4566"}],"tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","image":"/images/cc_by.png","short":"CC BY (4.0)","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)"},"oa":1,"quality_controlled":"1","article_type":"original","volume":22,"PlanS_conform":"1","OA_place":"publisher","user_id":"ba8df636-2132-11f1-aed0-ed93e2281fdd","day":"05"},{"department":[{"_id":"CaHe"}],"oa_version":"Published Version","doi":"10.1038/s41467-025-62484-5","date_created":"2025-08-17T22:01:35Z","article_processing_charge":"Yes","title":"Unequal segregation of mitochondria during asymmetric cell division contributes to cell fate divergence in sister cells in vivo","external_id":{"pmid":["40759648"]},"month":"08","type":"journal_article","file_date_updated":"2025-09-01T09:46:44Z","abstract":[{"lang":"eng","text":"The unequal segregation of organelles has been proposed to be an intrinsic mechanism that contributes to cell fate divergence during asymmetric cell division; however, in vivo evidence is sparse. Using super-resolution microscopy, we analysed the segregation of organelles during the division of the neuroblast QL.p in C. elegans larvae. QL.p divides to generate a daughter that survives, QL.pa, and a daughter that dies, QL.pp. We found that mitochondria segregate unequally by density and morphology and that this is dependent on mitochondrial dynamics. Furthermore, we found that mitochondrial density in QL.pp correlates with the time it takes QL.pp to die. We propose that low mitochondrial density in QL.pp promotes the cell death fate and ensures that QL.pp dies in a highly reproducible and timely manner. Our results provide in vivo evidence that the unequal segregation of mitochondria can contribute to cell fate divergence during asymmetric cell division in a developing animal."}],"acknowledgement":"We thank members of the Conradt lab, the Center for Cell and Molecular Dynamics (https://www.uclccmd.co.uk/) and T. Schedl for discussions and comments on the manuscript. We thank L. McGuinness for excellent technical support. Some strains were provided by the Caenorhabditis Genetics Center (CGC), which is funded by NIH Office of Research Infrastructure Programs (P40 OD010440). We thank Alex Hajnal (University of Zurich, Switzerland) and Andrew deMello (ETH Zurich, Switzerland) for their support of S.B. This work was supported by a predoctoral fellowship from the Studienstiftung des deutschen Volkes to NM, funds from UCL (Division of Biosciences, UCL LSM Capital Equipment Fund) to B.C., and a Wolfson Fellowship from the Royal Society (https://royalsociety.org/) to B.C. (RSWF\\R1\\180008), and the Biotechnology and Biological Sciences Research Council (https://bbsrc.ukri.org/) (BB/V007572/1 and BB/V015648/1to B.C.).","publication_identifier":{"eissn":["2041-1723"]},"_id":"20183","date_published":"2025-08-04T00:00:00Z","language":[{"iso":"eng"}],"pmid":1,"intvolume":"        16","publication_status":"published","DOAJ_listed":"1","OA_place":"publisher","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","day":"04","PlanS_conform":"1","volume":16,"oa":1,"article_type":"original","quality_controlled":"1","tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","image":"/images/cc_by.png","short":"CC BY (4.0)","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)"},"author":[{"last_name":"Segos","first_name":"Ioannis","full_name":"Segos, Ioannis"},{"last_name":"Van Eeckhoven","first_name":"Jens","full_name":"Van Eeckhoven, Jens"},{"last_name":"Berger","first_name":"Simon","full_name":"Berger, Simon"},{"first_name":"Nikhil","last_name":"Mishra","full_name":"Mishra, Nikhil","id":"C4D70E82-1081-11EA-B3ED-9A4C3DDC885E","orcid":"0000-0002-6425-5788"},{"last_name":"Lambie","first_name":"Eric J.","full_name":"Lambie, Eric J."},{"first_name":"Barbara","last_name":"Conradt","full_name":"Conradt, Barbara"}],"year":"2025","date_updated":"2025-09-01T09:47:29Z","file":[{"file_id":"20261","relation":"main_file","file_name":"2025_NatureComm_Segos.pdf","creator":"dernst","content_type":"application/pdf","checksum":"f28e73963ea1f55876d0d1afca0f706a","file_size":3775190,"date_created":"2025-09-01T09:46:44Z","success":1,"date_updated":"2025-09-01T09:46:44Z","access_level":"open_access"}],"publisher":"Springer Nature","scopus_import":"1","has_accepted_license":"1","ddc":["570"],"article_number":"7174","citation":{"chicago":"Segos, Ioannis, Jens Van Eeckhoven, Simon Berger, Nikhil Mishra, Eric J. Lambie, and Barbara Conradt. “Unequal Segregation of Mitochondria during Asymmetric Cell Division Contributes to Cell Fate Divergence in Sister Cells in Vivo.” <i>Nature Communications</i>. Springer Nature, 2025. <a href=\"https://doi.org/10.1038/s41467-025-62484-5\">https://doi.org/10.1038/s41467-025-62484-5</a>.","short":"I. Segos, J. Van Eeckhoven, S. Berger, N. Mishra, E.J. Lambie, B. Conradt, Nature Communications 16 (2025).","ista":"Segos I, Van Eeckhoven J, Berger S, Mishra N, Lambie EJ, Conradt B. 2025. Unequal segregation of mitochondria during asymmetric cell division contributes to cell fate divergence in sister cells in vivo. Nature Communications. 16, 7174.","ieee":"I. Segos, J. Van Eeckhoven, S. Berger, N. Mishra, E. J. Lambie, and B. Conradt, “Unequal segregation of mitochondria during asymmetric cell division contributes to cell fate divergence in sister cells in vivo,” <i>Nature Communications</i>, vol. 16. Springer Nature, 2025.","mla":"Segos, Ioannis, et al. “Unequal Segregation of Mitochondria during Asymmetric Cell Division Contributes to Cell Fate Divergence in Sister Cells in Vivo.” <i>Nature Communications</i>, vol. 16, 7174, Springer Nature, 2025, doi:<a href=\"https://doi.org/10.1038/s41467-025-62484-5\">10.1038/s41467-025-62484-5</a>.","apa":"Segos, I., Van Eeckhoven, J., Berger, S., Mishra, N., Lambie, E. J., &#38; Conradt, B. (2025). Unequal segregation of mitochondria during asymmetric cell division contributes to cell fate divergence in sister cells in vivo. <i>Nature Communications</i>. Springer Nature. <a href=\"https://doi.org/10.1038/s41467-025-62484-5\">https://doi.org/10.1038/s41467-025-62484-5</a>","ama":"Segos I, Van Eeckhoven J, Berger S, Mishra N, Lambie EJ, Conradt B. Unequal segregation of mitochondria during asymmetric cell division contributes to cell fate divergence in sister cells in vivo. <i>Nature Communications</i>. 2025;16. doi:<a href=\"https://doi.org/10.1038/s41467-025-62484-5\">10.1038/s41467-025-62484-5</a>"},"OA_type":"gold","publication":"Nature Communications","status":"public"},{"issue":"10","volume":20,"user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","day":"06","tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","image":"/images/cc_by.png","short":"CC BY (4.0)","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)"},"oa":1,"article_type":"original","quality_controlled":"1","date_updated":"2024-08-06T07:08:54Z","author":[{"last_name":"Sethi","first_name":"Aditya","full_name":"Sethi, Aditya"},{"first_name":"Hai","last_name":"Wei","full_name":"Wei, Hai"},{"first_name":"Nikhil","last_name":"Mishra","full_name":"Mishra, Nikhil","orcid":"0000-0002-6425-5788","id":"C4D70E82-1081-11EA-B3ED-9A4C3DDC885E"},{"full_name":"Segos, Ioannis","first_name":"Ioannis","last_name":"Segos"},{"full_name":"Lambie, Eric J.","last_name":"Lambie","first_name":"Eric J."},{"full_name":"Zanin, Esther","last_name":"Zanin","first_name":"Esther"},{"last_name":"Conradt","first_name":"Barbara","full_name":"Conradt, Barbara"}],"year":"2022","citation":{"short":"A. Sethi, H. Wei, N. Mishra, I. Segos, E.J. Lambie, E. Zanin, B. Conradt, PLOS Biology 20 (2022).","ista":"Sethi A, Wei H, Mishra N, Segos I, Lambie EJ, Zanin E, Conradt B. 2022. A caspase–RhoGEF axis contributes to the cell size threshold for apoptotic death in developing Caenorhabditis elegans. PLOS Biology. 20(10), e3001786.","chicago":"Sethi, Aditya, Hai Wei, Nikhil Mishra, Ioannis Segos, Eric J. Lambie, Esther Zanin, and Barbara Conradt. “A Caspase–RhoGEF Axis Contributes to the Cell Size Threshold for Apoptotic Death in Developing Caenorhabditis Elegans.” <i>PLOS Biology</i>. Public Library of Science, 2022. <a href=\"https://doi.org/10.1371/journal.pbio.3001786\">https://doi.org/10.1371/journal.pbio.3001786</a>.","mla":"Sethi, Aditya, et al. “A Caspase–RhoGEF Axis Contributes to the Cell Size Threshold for Apoptotic Death in Developing Caenorhabditis Elegans.” <i>PLOS Biology</i>, vol. 20, no. 10, e3001786, Public Library of Science, 2022, doi:<a href=\"https://doi.org/10.1371/journal.pbio.3001786\">10.1371/journal.pbio.3001786</a>.","ieee":"A. Sethi <i>et al.</i>, “A caspase–RhoGEF axis contributes to the cell size threshold for apoptotic death in developing Caenorhabditis elegans,” <i>PLOS Biology</i>, vol. 20, no. 10. Public Library of Science, 2022.","ama":"Sethi A, Wei H, Mishra N, et al. A caspase–RhoGEF axis contributes to the cell size threshold for apoptotic death in developing Caenorhabditis elegans. <i>PLOS Biology</i>. 2022;20(10). doi:<a href=\"https://doi.org/10.1371/journal.pbio.3001786\">10.1371/journal.pbio.3001786</a>","apa":"Sethi, A., Wei, H., Mishra, N., Segos, I., Lambie, E. J., Zanin, E., &#38; Conradt, B. (2022). A caspase–RhoGEF axis contributes to the cell size threshold for apoptotic death in developing Caenorhabditis elegans. <i>PLOS Biology</i>. Public Library of Science. <a href=\"https://doi.org/10.1371/journal.pbio.3001786\">https://doi.org/10.1371/journal.pbio.3001786</a>"},"ddc":["570"],"article_number":"e3001786","status":"public","publication":"PLOS Biology","publisher":"Public Library of Science","file":[{"file_id":"17399","relation":"main_file","file_name":"2022_PlosBio_Sethi.pdf","creator":"dernst","content_type":"application/pdf","file_size":2515388,"checksum":"a7b46460b7819c196028481cc18a7c85","date_created":"2024-08-06T07:07:52Z","success":1,"date_updated":"2024-08-06T07:07:52Z","access_level":"open_access"}],"scopus_import":"1","has_accepted_license":"1","date_created":"2024-05-29T06:09:34Z","oa_version":"Published Version","doi":"10.1371/journal.pbio.3001786","article_processing_charge":"Yes","title":"A caspase–RhoGEF axis contributes to the cell size threshold for apoptotic death in developing Caenorhabditis elegans","department":[{"_id":"CaHe"}],"acknowledgement":"We thank members of the Conradt, Lambie, and Hajnal labs for discussions and comments on the manuscript. We thank M. Bauer, L. Jocham, N. Lebedeva, and L. McGuinness for excellent technical support; A. Hajnal and T. Kohlbrenner (University of Zurich, Switzerland) for allele zh135; and H.R. Horvitz (Massachusetts of Technology, USA) for plasmid pET-CED-3.\r\nSome strains were provided by the Caenorhabditis Genetics Center (CGC), which is funded by NIH Office of Research Infrastructure Programs (https://orip.nih.gov/) (P40 OD010440). This work was supported by UCL (Capital Equipment Fund, CEF2), a predoctoral fellowship from the China Scholarship Council (https://www.csc.edu.cn/) to HW, a predoctoral fellowship from the Studienstiftung des Deutschen Volkes (https://www.studienstiftung.de/) to NM, a Wolfson Fellowship from the Royal Society (https://royalsociety.org/) to BC (RSWF\\R1\\180008), the Deutsche Forschungsgemeinschaft (https://www.dfg.de/en/index.jsp) (ZA619/3-1 and ZA619/3-2 to EZ; C0204/10-1 and EXC114 to BC), and the Biotechnology and Biological Sciences Research Council (https://bbsrc.ukri.org/) (BB/V007572/1 to BC). ","publication_identifier":{"issn":["1545-7885"]},"external_id":{"pmid":["36201522"]},"month":"10","type":"journal_article","file_date_updated":"2024-08-06T07:07:52Z","abstract":[{"text":"A cell’s size affects the likelihood that it will die. But how is cell size controlled in this context and how does cell size impact commitment to the cell death fate? We present evidence that the caspase CED-3 interacts with the RhoGEF ECT-2 in Caenorhabditis elegans neuroblasts that generate “unwanted” cells. We propose that this interaction promotes polar actomyosin contractility, which leads to unequal neuroblast division and the generation of a daughter cell that is below the critical “lethal” size threshold. Furthermore, we find that hyperactivation of ECT-2 RhoGEF reduces the sizes of unwanted cells. Importantly, this suppresses the “cell death abnormal” phenotype caused by the partial loss of ced-3 caspase and therefore increases the likelihood that unwanted cells die. A putative null mutation of ced-3 caspase, however, is not suppressed, which indicates that cell size affects CED-3 caspase activation and/or activity. Therefore, we have uncovered novel sequential and reciprocal interactions between the apoptosis pathway and cell size that impact a cell’s commitment to the cell death fate.","lang":"eng"}],"date_published":"2022-10-06T00:00:00Z","_id":"17066","pmid":1,"intvolume":"        20","publication_status":"published","language":[{"iso":"eng"}]},{"publication":"Annual Review of Genetics","status":"public","OA_type":"free access","page":"209-233","citation":{"mla":"Mishra, Nikhil, and Carl-Philipp J. Heisenberg. “Dissecting Organismal Morphogenesis by Bridging Genetics and Biophysics.” <i>Annual Review of Genetics</i>, vol. 55, Annual Reviews, 2021, pp. 209–33, doi:<a href=\"https://doi.org/10.1146/annurev-genet-071819-103748\">10.1146/annurev-genet-071819-103748</a>.","ieee":"N. Mishra and C.-P. J. Heisenberg, “Dissecting organismal morphogenesis by bridging genetics and biophysics,” <i>Annual Review of Genetics</i>, vol. 55. Annual Reviews, pp. 209–233, 2021.","apa":"Mishra, N., &#38; Heisenberg, C.-P. J. (2021). Dissecting organismal morphogenesis by bridging genetics and biophysics. <i>Annual Review of Genetics</i>. Annual Reviews. <a href=\"https://doi.org/10.1146/annurev-genet-071819-103748\">https://doi.org/10.1146/annurev-genet-071819-103748</a>","ama":"Mishra N, Heisenberg C-PJ. Dissecting organismal morphogenesis by bridging genetics and biophysics. <i>Annual Review of Genetics</i>. 2021;55:209-233. doi:<a href=\"https://doi.org/10.1146/annurev-genet-071819-103748\">10.1146/annurev-genet-071819-103748</a>","ista":"Mishra N, Heisenberg C-PJ. 2021. Dissecting organismal morphogenesis by bridging genetics and biophysics. Annual Review of Genetics. 55, 209–233.","chicago":"Mishra, Nikhil, and Carl-Philipp J Heisenberg. “Dissecting Organismal Morphogenesis by Bridging Genetics and Biophysics.” <i>Annual Review of Genetics</i>. Annual Reviews, 2021. <a href=\"https://doi.org/10.1146/annurev-genet-071819-103748\">https://doi.org/10.1146/annurev-genet-071819-103748</a>.","short":"N. Mishra, C.-P.J. Heisenberg, Annual Review of Genetics 55 (2021) 209–233."},"publisher":"Annual Reviews","scopus_import":"1","ec_funded":1,"date_updated":"2025-06-25T09:03:21Z","author":[{"id":"C4D70E82-1081-11EA-B3ED-9A4C3DDC885E","orcid":"0000-0002-6425-5788","full_name":"Mishra, Nikhil","last_name":"Mishra","first_name":"Nikhil"},{"last_name":"Heisenberg","first_name":"Carl-Philipp J","full_name":"Heisenberg, Carl-Philipp J","orcid":"0000-0002-0912-4566","id":"39427864-F248-11E8-B48F-1D18A9856A87"}],"year":"2021","article_type":"original","quality_controlled":"1","oa":1,"volume":55,"day":"30","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","OA_place":"publisher","intvolume":"        55","publication_status":"published","pmid":1,"language":[{"iso":"eng"}],"date_published":"2021-08-30T00:00:00Z","isi":1,"_id":"10406","keyword":["morphogenesis","forward genetics","high-resolution microscopy","biophysics","biochemistry","patterning"],"publication_identifier":{"eissn":["1545-2948"],"issn":["0066-4197"]},"acknowledgement":"The authors would like to thank Feyza Nur Arslan, Suyash Naik, Diana Pinheiro, Alexandra Schauer, and Shayan Shamipour for their comments on the draft. N.M. is supported by an ISTplus postdoctoral fellowship (H2020 Marie-Sklodowska-Curie COFUND Action).","corr_author":"1","month":"08","type":"journal_article","abstract":[{"lang":"eng","text":"Multicellular organisms develop complex shapes from much simpler, single-celled zygotes through a process commonly called morphogenesis. Morphogenesis involves an interplay between several factors, ranging from the gene regulatory networks determining cell fate and differentiation to the mechanical processes underlying cell and tissue shape changes. Thus, the study of morphogenesis has historically been based on multidisciplinary approaches at the interface of biology with physics and mathematics. Recent technological advances have further improved our ability to study morphogenesis by bridging the gap between the genetic and biophysical factors through the development of new tools for visualizing, analyzing, and perturbing these factors and their biochemical intermediaries. Here, we review how a combination of genetic, microscopic, biophysical, and biochemical approaches has aided our attempts to understand morphogenesis and discuss potential approaches that may be beneficial to such an inquiry in the future."}],"external_id":{"isi":["000747220900010"],"pmid":["34460295"]},"project":[{"_id":"260C2330-B435-11E9-9278-68D0E5697425","grant_number":"754411","name":"ISTplus - Postdoctoral Fellowships","call_identifier":"H2020"}],"title":"Dissecting organismal morphogenesis by bridging genetics and biophysics","date_created":"2021-12-05T23:01:41Z","oa_version":"Published Version","doi":"10.1146/annurev-genet-071819-103748","article_processing_charge":"No","main_file_link":[{"open_access":"1","url":"https://doi.org/10.1146/annurev-genet-071819-103748"}],"department":[{"_id":"CaHe"}]}]