[{"isi":1,"page":"107-111","article_type":"original","type":"journal_article","article_processing_charge":"No","doi":"10.1038/s41586-019-1212-5","oa_version":"Submitted Version","fulldoi":"https://doi.org/10.1038/s41586-019-1212-5","language":[{"iso":"eng"}],"day":"06","_id":"6513","citation":{"chicago":"Guiu, Jordi, Edouard B Hannezo, Shiro Yui, Samuel Demharter, Svetlana Ulyanchenko, Martti Maimets, Anne Jørgensen, et al. “Tracing the Origin of Adult Intestinal Stem Cells.” <i>Nature</i>. Springer Nature, 2019. <a href=\"https://doi.org/10.1038/s41586-019-1212-5\">https://doi.org/10.1038/s41586-019-1212-5</a>.","ista":"Guiu J, Hannezo EB, Yui S, Demharter S, Ulyanchenko S, Maimets M, Jørgensen A, Perlman S, Lundvall L, Mamsen LS, Larsen A, Olesen RH, Andersen CY, Thuesen LL, Hare KJ, Pers TH, Khodosevich K, Simons BD, Jensen KB. 2019. Tracing the origin of adult intestinal stem cells. Nature. 570, 107–111.","ama":"Guiu J, Hannezo EB, Yui S, et al. Tracing the origin of adult intestinal stem cells. <i>Nature</i>. 2019;570:107-111. doi:<a href=\"https://doi.org/10.1038/s41586-019-1212-5\">10.1038/s41586-019-1212-5</a>","short":"J. Guiu, E.B. Hannezo, S. Yui, S. Demharter, S. Ulyanchenko, M. Maimets, A. Jørgensen, S. Perlman, L. Lundvall, L.S. Mamsen, A. Larsen, R.H. Olesen, C.Y. Andersen, L.L. Thuesen, K.J. Hare, T.H. Pers, K. Khodosevich, B.D. Simons, K.B. Jensen, Nature 570 (2019) 107–111.","ieee":"J. Guiu <i>et al.</i>, “Tracing the origin of adult intestinal stem cells,” <i>Nature</i>, vol. 570. Springer Nature, pp. 107–111, 2019.","mla":"Guiu, Jordi, et al. “Tracing the Origin of Adult Intestinal Stem Cells.” <i>Nature</i>, vol. 570, Springer Nature, 2019, pp. 107–11, doi:<a href=\"https://doi.org/10.1038/s41586-019-1212-5\">10.1038/s41586-019-1212-5</a>.","apa":"Guiu, J., Hannezo, E. B., Yui, S., Demharter, S., Ulyanchenko, S., Maimets, M., … Jensen, K. B. (2019). Tracing the origin of adult intestinal stem cells. <i>Nature</i>. Springer Nature. <a href=\"https://doi.org/10.1038/s41586-019-1212-5\">https://doi.org/10.1038/s41586-019-1212-5</a>"},"main_file_link":[{"open_access":"1","url":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6986928"}],"user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","publication_status":"published","publication_identifier":{"issn":["0028-0836"],"eissn":["1476-4687"]},"external_id":{"pmid":["31092921"],"isi":["000470149000048"]},"title":"Tracing the origin of adult intestinal stem cells","publisher":"Springer Nature","abstract":[{"text":"Adult intestinal stem cells are located at the bottom of crypts of Lieberkühn, where they express markers such as LGR5 1,2 and fuel the constant replenishment of the intestinal epithelium1. Although fetal LGR5-expressing cells can give rise to adult intestinal stem cells3,4, it remains unclear whether this population in the patterned epithelium represents unique intestinal stem-cell precursors. Here we show, using unbiased quantitative lineage-tracing approaches, biophysical modelling and intestinal transplantation, that all cells of the mouse intestinal epithelium—irrespective of their location and pattern of LGR5 expression in the fetal gut tube—contribute actively to the adult intestinal stem cell pool. Using 3D imaging, we find that during fetal development the villus undergoes gross remodelling and fission. This brings epithelial cells from the non-proliferative villus into the proliferative intervillus region, which enables them to contribute to the adult stem-cell niche. Our results demonstrate that large-scale remodelling of the intestinal wall and cell-fate specification are closely linked. Moreover, these findings provide a direct link between the observed plasticity and cellular reprogramming of differentiating cells in adult tissues following damage5,6,7,8,9, revealing that stem-cell identity is an induced rather than a hardwired property.","lang":"eng"}],"author":[{"first_name":"Jordi","full_name":"Guiu, Jordi","last_name":"Guiu"},{"last_name":"Hannezo","first_name":"Edouard B","id":"3A9DB764-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0001-6005-1561","full_name":"Hannezo, Edouard B"},{"full_name":"Yui, Shiro","first_name":"Shiro","last_name":"Yui"},{"last_name":"Demharter","first_name":"Samuel","full_name":"Demharter, Samuel"},{"last_name":"Ulyanchenko","full_name":"Ulyanchenko, Svetlana","first_name":"Svetlana"},{"first_name":"Martti","full_name":"Maimets, Martti","last_name":"Maimets"},{"full_name":"Jørgensen, Anne","first_name":"Anne","last_name":"Jørgensen"},{"last_name":"Perlman","full_name":"Perlman, Signe","first_name":"Signe"},{"last_name":"Lundvall","full_name":"Lundvall, Lene","first_name":"Lene"},{"last_name":"Mamsen","full_name":"Mamsen, Linn Salto","first_name":"Linn Salto"},{"last_name":"Larsen","full_name":"Larsen, Agnete","first_name":"Agnete"},{"first_name":"Rasmus H.","full_name":"Olesen, Rasmus H.","last_name":"Olesen"},{"last_name":"Andersen","full_name":"Andersen, Claus Yding","first_name":"Claus Yding"},{"last_name":"Thuesen","full_name":"Thuesen, Lea Langhoff","first_name":"Lea Langhoff"},{"full_name":"Hare, Kristine Juul","first_name":"Kristine Juul","last_name":"Hare"},{"full_name":"Pers, Tune H.","first_name":"Tune H.","last_name":"Pers"},{"full_name":"Khodosevich, Konstantin","first_name":"Konstantin","last_name":"Khodosevich"},{"full_name":"Simons, Benjamin D.","first_name":"Benjamin D.","last_name":"Simons"},{"last_name":"Jensen","full_name":"Jensen, Kim B.","first_name":"Kim B."}],"oa":1,"intvolume":"       570","status":"public","quality_controlled":"1","pmid":1,"scopus_import":"1","publication":"Nature","volume":570,"year":"2019","date_updated":"2025-07-10T11:53:29Z","date_created":"2019-06-02T21:59:14Z","department":[{"_id":"EdHa"}],"date_published":"2019-06-06T00:00:00Z","month":"06"},{"month":"10","date_published":"2019-10-01T00:00:00Z","department":[{"_id":"EdHa"}],"date_created":"2019-06-16T21:59:12Z","date_updated":"2026-04-03T09:38:46Z","publication":"Current Opinion in Cell Biology","year":"2019","volume":60,"status":"public","quality_controlled":"1","scopus_import":"1","pmid":1,"intvolume":"        60","author":[{"last_name":"Hannezo","orcid":"0000-0001-6005-1561","first_name":"Edouard B","id":"3A9DB764-F248-11E8-B48F-1D18A9856A87","full_name":"Hannezo, Edouard B"},{"last_name":"Simons","full_name":"Simons, Benjamin D.","first_name":"Benjamin D."}],"abstract":[{"text":"Branching morphogenesis is a prototypical example of complex three-dimensional organ sculpting, required in multiple developmental settings to maximize the area of exchange surfaces. It requires, in particular, the coordinated growth of different cell types together with complex patterning to lead to robust macroscopic outputs. In recent years, novel multiscale quantitative biology approaches, together with biophysical modelling, have begun to shed new light of this topic. Here, we wish to review some of these recent developments, highlighting the generic design principles that can be abstracted across different branched organs, as well as the implications for the broader fields of stem cell, developmental and systems biology.","lang":"eng"}],"publisher":"Elsevier","title":"Multiscale dynamics of branching morphogenesis","publication_status":"published","publication_identifier":{"issn":["0955-0674"],"eissn":["1879-0410"]},"external_id":{"isi":["000486545800014"],"pmid":["31181348"]},"user_id":"ba8df636-2132-11f1-aed0-ed93e2281fdd","citation":{"chicago":"Hannezo, Edouard B, and Benjamin D. Simons. “Multiscale Dynamics of Branching Morphogenesis.” <i>Current Opinion in Cell Biology</i>. Elsevier, 2019. <a href=\"https://doi.org/10.1016/j.ceb.2019.04.008\">https://doi.org/10.1016/j.ceb.2019.04.008</a>.","ista":"Hannezo EB, Simons BD. 2019. Multiscale dynamics of branching morphogenesis. Current Opinion in Cell Biology. 60, 99–105.","apa":"Hannezo, E. B., &#38; Simons, B. D. (2019). Multiscale dynamics of branching morphogenesis. <i>Current Opinion in Cell Biology</i>. Elsevier. <a href=\"https://doi.org/10.1016/j.ceb.2019.04.008\">https://doi.org/10.1016/j.ceb.2019.04.008</a>","short":"E.B. Hannezo, B.D. Simons, Current Opinion in Cell Biology 60 (2019) 99–105.","ama":"Hannezo EB, Simons BD. Multiscale dynamics of branching morphogenesis. <i>Current Opinion in Cell Biology</i>. 2019;60:99-105. doi:<a href=\"https://doi.org/10.1016/j.ceb.2019.04.008\">10.1016/j.ceb.2019.04.008</a>","mla":"Hannezo, Edouard B., and Benjamin D. Simons. “Multiscale Dynamics of Branching Morphogenesis.” <i>Current Opinion in Cell Biology</i>, vol. 60, Elsevier, 2019, pp. 99–105, doi:<a href=\"https://doi.org/10.1016/j.ceb.2019.04.008\">10.1016/j.ceb.2019.04.008</a>.","ieee":"E. B. Hannezo and B. D. Simons, “Multiscale dynamics of branching morphogenesis,” <i>Current Opinion in Cell Biology</i>, vol. 60. Elsevier, pp. 99–105, 2019."},"oa_version":"None","fulldoi":"https://doi.org/10.1016/j.ceb.2019.04.008","language":[{"iso":"eng"}],"day":"01","_id":"6559","doi":"10.1016/j.ceb.2019.04.008","article_processing_charge":"No","type":"journal_article","page":"99-105","article_type":"original","isi":1},{"volume":178,"year":"2019","publication":"Cell","pmid":1,"scopus_import":"1","status":"public","ddc":["570"],"quality_controlled":"1","intvolume":"       178","oa":1,"author":[{"last_name":"Hannezo","full_name":"Hannezo, Edouard B","first_name":"Edouard B","id":"3A9DB764-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0001-6005-1561"},{"full_name":"Heisenberg, Carl-Philipp J","orcid":"0000-0002-0912-4566","first_name":"Carl-Philipp J","id":"39427864-F248-11E8-B48F-1D18A9856A87","last_name":"Heisenberg"}],"abstract":[{"lang":"eng","text":"There is increasing evidence that both mechanical and biochemical signals play important roles in development and disease. The development of complex organisms, in particular, has been proposed to rely on the feedback between mechanical and biochemical patterning events. This feedback occurs at the molecular level via mechanosensation but can also arise as an emergent property of the system at the cellular and tissue level. In recent years, dynamic changes in tissue geometry, flow, rheology, and cell fate specification have emerged as key platforms of mechanochemical feedback loops in multiple processes. Here, we review recent experimental and theoretical advances in understanding how these feedbacks function in development and disease."}],"publisher":"Elsevier","month":"07","date_published":"2019-07-27T00:00:00Z","department":[{"_id":"CaHe"},{"_id":"EdHa"}],"ec_funded":1,"date_created":"2019-06-30T21:59:11Z","date_updated":"2026-06-18T19:09:33Z","day":"27","_id":"6601","fulldoi":"https://doi.org/10.1016/j.cell.2019.05.052","oa_version":"Published Version","language":[{"iso":"eng"}],"doi":"10.1016/j.cell.2019.05.052","article_processing_charge":"No","type":"journal_article","project":[{"grant_number":"742573","name":"Interaction and feedback between cell mechanics and fate specification in vertebrate gastrulation","_id":"260F1432-B435-11E9-9278-68D0E5697425","call_identifier":"H2020"},{"call_identifier":"FWF","_id":"268294B6-B435-11E9-9278-68D0E5697425","name":"Active mechano-chemical description of the cell cytoskeleton","grant_number":"P31639"}],"article_type":"review","page":"12-25","isi":1,"issue":"1","title":"Mechanochemical feedback loops in development and disease","external_id":{"isi":["000473002700005"],"pmid":["31251912"]},"publication_status":"published","publication_identifier":{"issn":["0092-8674"]},"user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","main_file_link":[{"url":"https://doi.org/10.1016/j.cell.2019.05.052","open_access":"1"}],"citation":{"ista":"Hannezo EB, Heisenberg C-PJ. 2019. Mechanochemical feedback loops in development and disease. Cell. 178(1), 12–25.","chicago":"Hannezo, Edouard B, and Carl-Philipp J Heisenberg. “Mechanochemical Feedback Loops in Development and Disease.” <i>Cell</i>. Elsevier, 2019. <a href=\"https://doi.org/10.1016/j.cell.2019.05.052\">https://doi.org/10.1016/j.cell.2019.05.052</a>.","ieee":"E. B. Hannezo and C.-P. J. Heisenberg, “Mechanochemical feedback loops in development and disease,” <i>Cell</i>, vol. 178, no. 1. Elsevier, pp. 12–25, 2019.","mla":"Hannezo, Edouard B., and Carl-Philipp J. Heisenberg. “Mechanochemical Feedback Loops in Development and Disease.” <i>Cell</i>, vol. 178, no. 1, Elsevier, 2019, pp. 12–25, doi:<a href=\"https://doi.org/10.1016/j.cell.2019.05.052\">10.1016/j.cell.2019.05.052</a>.","ama":"Hannezo EB, Heisenberg C-PJ. Mechanochemical feedback loops in development and disease. <i>Cell</i>. 2019;178(1):12-25. doi:<a href=\"https://doi.org/10.1016/j.cell.2019.05.052\">10.1016/j.cell.2019.05.052</a>","short":"E.B. Hannezo, C.-P.J. Heisenberg, Cell 178 (2019) 12–25.","apa":"Hannezo, E. B., &#38; Heisenberg, C.-P. J. (2019). Mechanochemical feedback loops in development and disease. <i>Cell</i>. Elsevier. <a href=\"https://doi.org/10.1016/j.cell.2019.05.052\">https://doi.org/10.1016/j.cell.2019.05.052</a>"}},{"user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","title":"Active cell migration is critical for steady-state epithelial turnover in the gut","publication_status":"published","external_id":{"isi":["000481688700050"],"pmid":["31416964"]},"citation":{"apa":"Krndija, D., Marjou, F. E., Guirao, B., Richon, S., Leroy, O., Bellaiche, Y., … Vignjevic, D. M. (2019). Active cell migration is critical for steady-state epithelial turnover in the gut. <i>Science</i>. American Association for the Advancement of Science. <a href=\"https://doi.org/10.1126/science.aau3429\">https://doi.org/10.1126/science.aau3429</a>","ieee":"D. Krndija <i>et al.</i>, “Active cell migration is critical for steady-state epithelial turnover in the gut,” <i>Science</i>, vol. 365, no. 6454. American Association for the Advancement of Science, pp. 705–710, 2019.","mla":"Krndija, Denis, et al. “Active Cell Migration Is Critical for Steady-State Epithelial Turnover in the Gut.” <i>Science</i>, vol. 365, no. 6454, American Association for the Advancement of Science, 2019, pp. 705–10, doi:<a href=\"https://doi.org/10.1126/science.aau3429\">10.1126/science.aau3429</a>.","short":"D. Krndija, F.E. Marjou, B. Guirao, S. Richon, O. Leroy, Y. Bellaiche, E.B. Hannezo, D.M. Vignjevic, Science 365 (2019) 705–710.","ama":"Krndija D, Marjou FE, Guirao B, et al. Active cell migration is critical for steady-state epithelial turnover in the gut. <i>Science</i>. 2019;365(6454):705-710. doi:<a href=\"https://doi.org/10.1126/science.aau3429\">10.1126/science.aau3429</a>","ista":"Krndija D, Marjou FE, Guirao B, Richon S, Leroy O, Bellaiche Y, Hannezo EB, Vignjevic DM. 2019. Active cell migration is critical for steady-state epithelial turnover in the gut. Science. 365(6454), 705–710.","chicago":"Krndija, Denis, Fatima El Marjou, Boris Guirao, Sophie Richon, Olivier Leroy, Yohanns Bellaiche, Edouard B Hannezo, and Danijela Matic Vignjevic. “Active Cell Migration Is Critical for Steady-State Epithelial Turnover in the Gut.” <i>Science</i>. American Association for the Advancement of Science, 2019. <a href=\"https://doi.org/10.1126/science.aau3429\">https://doi.org/10.1126/science.aau3429</a>."},"article_processing_charge":"No","fulldoi":"https://doi.org/10.1126/science.aau3429","language":[{"iso":"eng"}],"oa_version":"None","_id":"6832","day":"16","doi":"10.1126/science.aau3429","page":"705-710","issue":"6454","isi":1,"type":"journal_article","date_published":"2019-08-16T00:00:00Z","month":"08","date_updated":"2023-08-29T07:16:40Z","department":[{"_id":"EdHa"}],"date_created":"2019-08-25T22:00:51Z","quality_controlled":"1","status":"public","pmid":1,"scopus_import":"1","intvolume":"       365","publication":"Science","volume":365,"year":"2019","publisher":"American Association for the Advancement of Science","author":[{"first_name":"Denis","full_name":"Krndija, Denis","last_name":"Krndija"},{"last_name":"Marjou","first_name":"Fatima El","full_name":"Marjou, Fatima El"},{"last_name":"Guirao","full_name":"Guirao, Boris","first_name":"Boris"},{"last_name":"Richon","first_name":"Sophie","full_name":"Richon, Sophie"},{"full_name":"Leroy, Olivier","first_name":"Olivier","last_name":"Leroy"},{"full_name":"Bellaiche, Yohanns","first_name":"Yohanns","last_name":"Bellaiche"},{"full_name":"Hannezo, Edouard B","first_name":"Edouard B","id":"3A9DB764-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0001-6005-1561","last_name":"Hannezo"},{"last_name":"Vignjevic","full_name":"Vignjevic, Danijela Matic","first_name":"Danijela Matic"}],"abstract":[{"text":"Steady-state turnover is a hallmark of epithelial tissues throughout adult life. Intestinal epithelial turnover is marked by continuous cell migration, which is assumed to be driven by mitotic pressure from the crypts. However, the balance of forces in renewal remains ill-defined. Combining biophysical modeling and quantitative three-dimensional tissue imaging with genetic and physical manipulations, we revealed the existence of an actin-related protein 2/3 complex–dependent active migratory force, which explains quantitatively the profiles of cell speed, density, and tissue tension along the villi. Cells migrate collectively with minimal rearrangements while displaying dual—apicobasal and front-back—polarity characterized by actin-rich basal protrusions oriented in the direction of migration. We propose that active migration is a critical component of gut epithelial turnover.","lang":"eng"}]},{"related_material":{"record":[{"status":"public","relation":"used_in_publication","id":"7166"}]},"publisher":"American Chemical Society","type":"research_data_reference","author":[{"orcid":"0000-0003-0506-4217","id":"50B2A802-6007-11E9-A42B-EB23E6697425","first_name":"Mehmet C","full_name":"Ucar, Mehmet C","last_name":"Ucar"},{"full_name":"Lipowsky, Reinhard","first_name":"Reinhard","last_name":"Lipowsky"}],"abstract":[{"text":"A detailed description of the two stochastic models, table of parameters, supplementary data for Figures 4 and 5, parameter dependence of the results, and an analysis on motors with different force–velocity functions (PDF)","lang":"eng"}],"status":"public","article_processing_charge":"No","day":"19","_id":"9726","year":"2019","fulldoi":"https://doi.org/10.1021/acs.nanolett.9b04445.s001","oa_version":"Published Version","doi":"10.1021/acs.nanolett.9b04445.s001","citation":{"chicago":"Ucar, Mehmet C, and Reinhard Lipowsky. “Supplementary Information - Collective Force Generation by Molecular Motors Is Determined by Strain-Induced Unbinding.” American Chemical Society, 2019. <a href=\"https://doi.org/10.1021/acs.nanolett.9b04445.s001\">https://doi.org/10.1021/acs.nanolett.9b04445.s001</a>.","ista":"Ucar MC, Lipowsky R. 2019. Supplementary information - Collective force generation by molecular motors is determined by strain-induced unbinding, American Chemical Society, <a href=\"https://doi.org/10.1021/acs.nanolett.9b04445.s001\">10.1021/acs.nanolett.9b04445.s001</a>.","short":"M.C. Ucar, R. Lipowsky, (2019).","ama":"Ucar MC, Lipowsky R. Supplementary information - Collective force generation by molecular motors is determined by strain-induced unbinding. 2019. doi:<a href=\"https://doi.org/10.1021/acs.nanolett.9b04445.s001\">10.1021/acs.nanolett.9b04445.s001</a>","ieee":"M. C. Ucar and R. Lipowsky, “Supplementary information - Collective force generation by molecular motors is determined by strain-induced unbinding.” American Chemical Society, 2019.","mla":"Ucar, Mehmet C., and Reinhard Lipowsky. <i>Supplementary Information - Collective Force Generation by Molecular Motors Is Determined by Strain-Induced Unbinding</i>. American Chemical Society, 2019, doi:<a href=\"https://doi.org/10.1021/acs.nanolett.9b04445.s001\">10.1021/acs.nanolett.9b04445.s001</a>.","apa":"Ucar, M. C., &#38; Lipowsky, R. (2019). Supplementary information - Collective force generation by molecular motors is determined by strain-induced unbinding. American Chemical Society. <a href=\"https://doi.org/10.1021/acs.nanolett.9b04445.s001\">https://doi.org/10.1021/acs.nanolett.9b04445.s001</a>"},"date_updated":"2026-07-06T12:13:40Z","department":[{"_id":"EdHa"}],"date_created":"2021-07-27T09:51:46Z","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","date_published":"2019-12-19T00:00:00Z","month":"12","title":"Supplementary information - Collective force generation by molecular motors is determined by strain-induced unbinding"},{"main_file_link":[{"url":"https://doi.org/10.1016/j.cell.2019.04.030","open_access":"1"}],"citation":{"apa":"Shamipour, S., Kardos, R., Xue, S., Hof, B., Hannezo, E. B., &#38; Heisenberg, C.-P. J. (2019). Bulk actin dynamics drive phase segregation in zebrafish oocytes. <i>Cell</i>. Elsevier. <a href=\"https://doi.org/10.1016/j.cell.2019.04.030\">https://doi.org/10.1016/j.cell.2019.04.030</a>","ieee":"S. Shamipour, R. Kardos, S. Xue, B. Hof, E. B. Hannezo, and C.-P. J. Heisenberg, “Bulk actin dynamics drive phase segregation in zebrafish oocytes,” <i>Cell</i>, vol. 177, no. 6. Elsevier, p. 1463–1479.e18, 2019.","mla":"Shamipour, Shayan, et al. “Bulk Actin Dynamics Drive Phase Segregation in Zebrafish Oocytes.” <i>Cell</i>, vol. 177, no. 6, Elsevier, 2019, p. 1463–1479.e18, doi:<a href=\"https://doi.org/10.1016/j.cell.2019.04.030\">10.1016/j.cell.2019.04.030</a>.","ama":"Shamipour S, Kardos R, Xue S, Hof B, Hannezo EB, Heisenberg C-PJ. Bulk actin dynamics drive phase segregation in zebrafish oocytes. <i>Cell</i>. 2019;177(6):1463-1479.e18. doi:<a href=\"https://doi.org/10.1016/j.cell.2019.04.030\">10.1016/j.cell.2019.04.030</a>","short":"S. Shamipour, R. Kardos, S. Xue, B. Hof, E.B. Hannezo, C.-P.J. Heisenberg, Cell 177 (2019) 1463–1479.e18.","ista":"Shamipour S, Kardos R, Xue S, Hof B, Hannezo EB, Heisenberg C-PJ. 2019. Bulk actin dynamics drive phase segregation in zebrafish oocytes. Cell. 177(6), 1463–1479.e18.","chicago":"Shamipour, Shayan, Roland Kardos, Shi-lei Xue, Björn Hof, Edouard B Hannezo, and Carl-Philipp J Heisenberg. “Bulk Actin Dynamics Drive Phase Segregation in Zebrafish Oocytes.” <i>Cell</i>. Elsevier, 2019. <a href=\"https://doi.org/10.1016/j.cell.2019.04.030\">https://doi.org/10.1016/j.cell.2019.04.030</a>."},"acknowledged_ssus":[{"_id":"Bio"},{"_id":"PreCl"}],"user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","title":"Bulk actin dynamics drive phase segregation in zebrafish oocytes","publication_status":"published","publication_identifier":{"issn":["0092-8674"],"eissn":["1097-4172"]},"external_id":{"isi":["000469415100013"],"pmid":["31080065"]},"page":"1463-1479.e18","article_type":"original","related_material":{"record":[{"id":"8350","status":"public","relation":"dissertation_contains"}],"link":[{"url":"https://ist.ac.at/en/news/how-the-cytoplasm-separates-from-the-yolk/","description":"News on IST Homepage","relation":"press_release"}]},"issue":"6","isi":1,"has_accepted_license":"1","project":[{"_id":"260F1432-B435-11E9-9278-68D0E5697425","call_identifier":"H2020","grant_number":"742573","name":"Interaction and feedback between cell mechanics and fate specification in vertebrate gastrulation"},{"name":"Active mechano-chemical description of the cell cytoskeleton","grant_number":"P31639","_id":"268294B6-B435-11E9-9278-68D0E5697425","call_identifier":"FWF"}],"type":"journal_article","article_processing_charge":"No","language":[{"iso":"eng"}],"fulldoi":"https://doi.org/10.1016/j.cell.2019.04.030","oa_version":"Published Version","day":"30","_id":"6508","doi":"10.1016/j.cell.2019.04.030","file":[{"file_size":3356292,"file_id":"8686","relation":"main_file","content_type":"application/pdf","checksum":"aea43726d80e35ce3885073a5f05c3e3","success":1,"file_name":"2019_Cell_Shamipour_accepted.pdf","date_created":"2020-10-21T07:22:34Z","creator":"dernst","access_level":"open_access","date_updated":"2020-10-21T07:22:34Z"}],"date_updated":"2026-10-21T22:30:24Z","department":[{"_id":"CaHe"},{"_id":"EdHa"},{"_id":"BjHo"}],"acknowledgement":"We would like to thank Pierre Recho, Guillaume Salbreux, and Silvia Grigolon for advice on the theory, Lila Solnica-Krezel for kindly providing us with zebrafish dachsous mutants, members of the Heisenberg and Hannezo groups for fruitful discussions, and the Bioimaging and zebrafish facilities at IST Austria for their continuous support. This project has received funding from the European Union (European Research Council Advanced Grant 742573 to C.P.H.) and from the Austrian Science Fund (FWF) (P 31639 to E.H.).","date_created":"2019-06-02T21:59:12Z","ec_funded":1,"date_published":"2019-05-30T00:00:00Z","month":"05","publisher":"Elsevier","author":[{"full_name":"Shamipour, Shayan","id":"40B34FE2-F248-11E8-B48F-1D18A9856A87","first_name":"Shayan","last_name":"Shamipour"},{"last_name":"Kardos","id":"4039350E-F248-11E8-B48F-1D18A9856A87","first_name":"Roland","full_name":"Kardos, Roland"},{"full_name":"Xue, Shi-lei","id":"31D2C804-F248-11E8-B48F-1D18A9856A87","first_name":"Shi-lei","last_name":"Xue"},{"id":"3A374330-F248-11E8-B48F-1D18A9856A87","first_name":"Björn","orcid":"0000-0003-2057-2754","full_name":"Hof, Björn","last_name":"Hof"},{"last_name":"Hannezo","full_name":"Hannezo, Edouard B","orcid":"0000-0001-6005-1561","first_name":"Edouard B","id":"3A9DB764-F248-11E8-B48F-1D18A9856A87"},{"full_name":"Heisenberg, Carl-Philipp J","orcid":"0000-0002-0912-4566","id":"39427864-F248-11E8-B48F-1D18A9856A87","first_name":"Carl-Philipp J","last_name":"Heisenberg"}],"file_date_updated":"2020-10-21T07:22:34Z","oa":1,"abstract":[{"text":"Segregation of maternal determinants within the oocyte constitutes the first step in embryo patterning. In zebrafish oocytes, extensive ooplasmic streaming leads to the segregation of ooplasm from yolk granules along the animal-vegetal axis of the oocyte. Here, we show that this process does not rely on cortical actin reorganization, as previously thought, but instead on a cell-cycle-dependent bulk actin polymerization wave traveling from the animal to the vegetal pole of the oocyte. This wave functions in segregation by both pulling ooplasm animally and pushing yolk granules vegetally. Using biophysical experimentation and theory, we show that ooplasm pulling is mediated by bulk actin network flows exerting friction forces on the ooplasm, while yolk granule pushing is achieved by a mechanism closely resembling actin comet formation on yolk granules. Our study defines a novel role of cell-cycle-controlled bulk actin polymerization waves in oocyte polarization via ooplasmic segregation.","lang":"eng"}],"ddc":["570"],"status":"public","quality_controlled":"1","scopus_import":"1","pmid":1,"intvolume":"       177","publication":"Cell","volume":177,"year":"2019"},{"issue":"6","isi":1,"page":"677 - 687","article_type":"original","publist_id":"7594","type":"journal_article","article_processing_charge":"No","doi":"10.1038/s41556-018-0108-1","oa_version":"Submitted Version","fulldoi":"https://doi.org/10.1038/s41556-018-0108-1","language":[{"iso":"eng"}],"day":"21","_id":"288","citation":{"ista":"Lilja A, Rodilla V, Huyghe M, Hannezo EB, Landragin C, Renaud O, Leroy O, Rulands S, Simons B, Fré S. 2018. Clonal analysis of Notch1-expressing cells reveals the existence of unipotent stem cells that retain long-term plasticity in the embryonic mammary gland. Nature Cell Biology. 20(6), 677–687.","chicago":"Lilja, Anna, Veronica Rodilla, Mathilde Huyghe, Edouard B Hannezo, Camille Landragin, Olivier Renaud, Olivier Leroy, Steffen Rulands, Benjamin Simons, and Silvia Fré. “Clonal Analysis of Notch1-Expressing Cells Reveals the Existence of Unipotent Stem Cells That Retain Long-Term Plasticity in the Embryonic Mammary Gland.” <i>Nature Cell Biology</i>. Nature Publishing Group, 2018. <a href=\"https://doi.org/10.1038/s41556-018-0108-1\">https://doi.org/10.1038/s41556-018-0108-1</a>.","apa":"Lilja, A., Rodilla, V., Huyghe, M., Hannezo, E. B., Landragin, C., Renaud, O., … Fré, S. (2018). Clonal analysis of Notch1-expressing cells reveals the existence of unipotent stem cells that retain long-term plasticity in the embryonic mammary gland. <i>Nature Cell Biology</i>. Nature Publishing Group. <a href=\"https://doi.org/10.1038/s41556-018-0108-1\">https://doi.org/10.1038/s41556-018-0108-1</a>","ieee":"A. Lilja <i>et al.</i>, “Clonal analysis of Notch1-expressing cells reveals the existence of unipotent stem cells that retain long-term plasticity in the embryonic mammary gland,” <i>Nature Cell Biology</i>, vol. 20, no. 6. Nature Publishing Group, pp. 677–687, 2018.","mla":"Lilja, Anna, et al. “Clonal Analysis of Notch1-Expressing Cells Reveals the Existence of Unipotent Stem Cells That Retain Long-Term Plasticity in the Embryonic Mammary Gland.” <i>Nature Cell Biology</i>, vol. 20, no. 6, Nature Publishing Group, 2018, pp. 677–87, doi:<a href=\"https://doi.org/10.1038/s41556-018-0108-1\">10.1038/s41556-018-0108-1</a>.","short":"A. Lilja, V. Rodilla, M. Huyghe, E.B. Hannezo, C. Landragin, O. Renaud, O. Leroy, S. Rulands, B. Simons, S. Fré, Nature Cell Biology 20 (2018) 677–687.","ama":"Lilja A, Rodilla V, Huyghe M, et al. Clonal analysis of Notch1-expressing cells reveals the existence of unipotent stem cells that retain long-term plasticity in the embryonic mammary gland. <i>Nature Cell Biology</i>. 2018;20(6):677-687. doi:<a href=\"https://doi.org/10.1038/s41556-018-0108-1\">10.1038/s41556-018-0108-1</a>"},"main_file_link":[{"open_access":"1","url":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6984964"}],"user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","publication_status":"published","external_id":{"isi":["000433237300003"],"pmid":["29784917"]},"title":"Clonal analysis of Notch1-expressing cells reveals the existence of unipotent stem cells that retain long-term plasticity in the embryonic mammary gland","publisher":"Nature Publishing Group","abstract":[{"lang":"eng","text":"Recent lineage tracing studies have revealed that mammary gland homeostasis relies on unipotent stem cells. However, whether and when lineage restriction occurs during embryonic mammary development, and which signals orchestrate cell fate specification, remain unknown. Using a combination of in vivo clonal analysis with whole mount immunofluorescence and mathematical modelling of clonal dynamics, we found that embryonic multipotent mammary cells become lineage-restricted surprisingly early in development, with evidence for unipotency as early as E12.5 and no statistically discernable bipotency after E15.5. To gain insights into the mechanisms governing the switch from multipotency to unipotency, we used gain-of-function Notch1 mice and demonstrated that Notch activation cell autonomously dictates luminal cell fate specification to both embryonic and basally committed mammary cells. These functional studies have important implications for understanding the signals underlying cell plasticity and serve to clarify how reactivation of embryonic programs in adult cells can lead to cancer."}],"author":[{"first_name":"Anna","full_name":"Lilja, Anna","last_name":"Lilja"},{"last_name":"Rodilla","first_name":"Veronica","full_name":"Rodilla, Veronica"},{"full_name":"Huyghe, Mathilde","first_name":"Mathilde","last_name":"Huyghe"},{"full_name":"Hannezo, Edouard B","id":"3A9DB764-F248-11E8-B48F-1D18A9856A87","first_name":"Edouard B","orcid":"0000-0001-6005-1561","last_name":"Hannezo"},{"last_name":"Landragin","first_name":"Camille","full_name":"Landragin, Camille"},{"last_name":"Renaud","first_name":"Olivier","full_name":"Renaud, Olivier"},{"last_name":"Leroy","full_name":"Leroy, Olivier","first_name":"Olivier"},{"first_name":"Steffen","full_name":"Rulands, Steffen","last_name":"Rulands"},{"full_name":"Simons, Benjamin","first_name":"Benjamin","last_name":"Simons"},{"full_name":"Fré, Silvia","first_name":"Silvia","last_name":"Fré"}],"oa":1,"intvolume":"        20","status":"public","quality_controlled":"1","scopus_import":"1","pmid":1,"publication":"Nature Cell Biology","year":"2018","volume":20,"date_updated":"2023-09-11T12:44:08Z","date_created":"2018-12-11T11:45:38Z","department":[{"_id":"EdHa"}],"date_published":"2018-05-21T00:00:00Z","month":"05"},{"status":"public","quality_controlled":"1","ddc":["570"],"scopus_import":"1","intvolume":"        46","publication":"Developmental Cell","year":"2018","volume":46,"publisher":"Cell Press","author":[{"first_name":"Magdalena","full_name":"Sznurkowska, Magdalena","last_name":"Sznurkowska"},{"full_name":"Hannezo, Edouard B","first_name":"Edouard B","id":"3A9DB764-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0001-6005-1561","last_name":"Hannezo"},{"first_name":"Roberta","full_name":"Azzarelli, Roberta","last_name":"Azzarelli"},{"last_name":"Rulands","first_name":"Steffen","full_name":"Rulands, Steffen"},{"last_name":"Nestorowa","first_name":"Sonia","full_name":"Nestorowa, Sonia"},{"last_name":"Hindley","first_name":"Christopher","full_name":"Hindley, Christopher"},{"last_name":"Nichols","full_name":"Nichols, Jennifer","first_name":"Jennifer"},{"full_name":"Göttgens, Berthold","first_name":"Berthold","last_name":"Göttgens"},{"full_name":"Huch, Meritxell","first_name":"Meritxell","last_name":"Huch"},{"full_name":"Philpott, Anna","first_name":"Anna","last_name":"Philpott"},{"last_name":"Simons","first_name":"Benjamin","full_name":"Simons, Benjamin"}],"file_date_updated":"2020-07-14T12:44:43Z","oa":1,"abstract":[{"lang":"eng","text":"Pancreas development involves a coordinated process in which an early phase of cell segregation is followed by a longer phase of lineage restriction, expansion, and tissue remodeling. By combining clonal tracing and whole-mount reconstruction with proliferation kinetics and single-cell transcriptional profiling, we define the functional basis of pancreas morphogenesis. We show that the large-scale organization of mouse pancreas can be traced to the activity of self-renewing precursors positioned at the termini of growing ducts, which act collectively to drive serial rounds of stochastic ductal bifurcation balanced by termination. During this phase of branching morphogenesis, multipotent precursors become progressively fate-restricted, giving rise to self-renewing acinar-committed precursors that are conveyed with growing ducts, as well as ductal progenitors that expand the trailing ducts and give rise to delaminating endocrine cells. These findings define quantitatively how the functional behavior and lineage progression of precursor pools determine the large-scale patterning of pancreatic sub-compartments."}],"tmp":{"name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","image":"/images/cc_by.png","legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","short":"CC BY (4.0)"},"date_published":"2018-08-06T00:00:00Z","month":"08","file":[{"date_created":"2018-12-17T10:49:49Z","file_name":"2018_DevelopmentalCell_Sznurkowska.pdf","checksum":"78d2062b9e3c3b90fe71545aeb6d2f65","date_updated":"2020-07-14T12:44:43Z","access_level":"open_access","creator":"dernst","file_id":"5694","file_size":8948384,"content_type":"application/pdf","relation":"main_file"}],"date_updated":"2023-09-11T12:52:41Z","department":[{"_id":"EdHa"}],"acknowledgement":"E.H. is funded by a Junior Research Fellowship from Trinity College, Cam-bridge, a Sir Henry Wellcome Fellowship from the Wellcome Trust, and theBettencourt-Schueller Young Researcher Prize for support.","date_created":"2018-12-11T11:44:48Z","article_processing_charge":"No","fulldoi":"https://doi.org/10.1016/j.devcel.2018.06.028","oa_version":"Published Version","language":[{"iso":"eng"}],"day":"06","_id":"132","doi":"10.1016/j.devcel.2018.06.028","page":"360 - 375","article_type":"original","issue":"3","isi":1,"has_accepted_license":"1","publist_id":"7791","type":"journal_article","user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","title":"Defining lineage potential and fate behavior of precursors during pancreas development","publication_status":"published","external_id":{"isi":["000441327300012"]},"citation":{"mla":"Sznurkowska, Magdalena, et al. “Defining Lineage Potential and Fate Behavior of Precursors during Pancreas Development.” <i>Developmental Cell</i>, vol. 46, no. 3, Cell Press, 2018, pp. 360–75, doi:<a href=\"https://doi.org/10.1016/j.devcel.2018.06.028\">10.1016/j.devcel.2018.06.028</a>.","ieee":"M. Sznurkowska <i>et al.</i>, “Defining lineage potential and fate behavior of precursors during pancreas development,” <i>Developmental Cell</i>, vol. 46, no. 3. Cell Press, pp. 360–375, 2018.","ama":"Sznurkowska M, Hannezo EB, Azzarelli R, et al. Defining lineage potential and fate behavior of precursors during pancreas development. <i>Developmental Cell</i>. 2018;46(3):360-375. doi:<a href=\"https://doi.org/10.1016/j.devcel.2018.06.028\">10.1016/j.devcel.2018.06.028</a>","short":"M. Sznurkowska, E.B. Hannezo, R. Azzarelli, S. Rulands, S. Nestorowa, C. Hindley, J. Nichols, B. Göttgens, M. Huch, A. Philpott, B. Simons, Developmental Cell 46 (2018) 360–375.","apa":"Sznurkowska, M., Hannezo, E. B., Azzarelli, R., Rulands, S., Nestorowa, S., Hindley, C., … Simons, B. (2018). Defining lineage potential and fate behavior of precursors during pancreas development. <i>Developmental Cell</i>. Cell Press. <a href=\"https://doi.org/10.1016/j.devcel.2018.06.028\">https://doi.org/10.1016/j.devcel.2018.06.028</a>","ista":"Sznurkowska M, Hannezo EB, Azzarelli R, Rulands S, Nestorowa S, Hindley C, Nichols J, Göttgens B, Huch M, Philpott A, Simons B. 2018. Defining lineage potential and fate behavior of precursors during pancreas development. Developmental Cell. 46(3), 360–375.","chicago":"Sznurkowska, Magdalena, Edouard B Hannezo, Roberta Azzarelli, Steffen Rulands, Sonia Nestorowa, Christopher Hindley, Jennifer Nichols, et al. “Defining Lineage Potential and Fate Behavior of Precursors during Pancreas Development.” <i>Developmental Cell</i>. Cell Press, 2018. <a href=\"https://doi.org/10.1016/j.devcel.2018.06.028\">https://doi.org/10.1016/j.devcel.2018.06.028</a>."}},{"citation":{"short":"E.B. Hannezo, B.D. Simons, Development Growth and Differentiation 60 (2018) 512–521.","ama":"Hannezo EB, Simons BD. Statistical theory of branching morphogenesis. <i>Development Growth and Differentiation</i>. 2018;60(9):512-521. doi:<a href=\"https://doi.org/10.1111/dgd.12570\">10.1111/dgd.12570</a>","ieee":"E. B. Hannezo and B. D. Simons, “Statistical theory of branching morphogenesis,” <i>Development Growth and Differentiation</i>, vol. 60, no. 9. Wiley, pp. 512–521, 2018.","mla":"Hannezo, Edouard B., and Benjamin D. Simons. “Statistical Theory of Branching Morphogenesis.” <i>Development Growth and Differentiation</i>, vol. 60, no. 9, Wiley, 2018, pp. 512–21, doi:<a href=\"https://doi.org/10.1111/dgd.12570\">10.1111/dgd.12570</a>.","apa":"Hannezo, E. B., &#38; Simons, B. D. (2018). Statistical theory of branching morphogenesis. <i>Development Growth and Differentiation</i>. Wiley. <a href=\"https://doi.org/10.1111/dgd.12570\">https://doi.org/10.1111/dgd.12570</a>","chicago":"Hannezo, Edouard B, and Benjamin D. Simons. “Statistical Theory of Branching Morphogenesis.” <i>Development Growth and Differentiation</i>. Wiley, 2018. <a href=\"https://doi.org/10.1111/dgd.12570\">https://doi.org/10.1111/dgd.12570</a>.","ista":"Hannezo EB, Simons BD. 2018. Statistical theory of branching morphogenesis. Development Growth and Differentiation. 60(9), 512–521."},"title":"Statistical theory of branching morphogenesis","publication_identifier":{"issn":["0012-1592"]},"external_id":{"isi":["000453555100002"]},"user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","has_accepted_license":"1","type":"journal_article","page":"512-521","issue":"9","isi":1,"fulldoi":"https://doi.org/10.1111/dgd.12570","language":[{"iso":"eng"}],"oa_version":"Published Version","_id":"5787","day":"09","doi":"10.1111/dgd.12570","article_processing_charge":"No","department":[{"_id":"EdHa"}],"date_created":"2018-12-30T22:59:14Z","file":[{"creator":"dernst","date_updated":"2020-07-14T12:47:11Z","access_level":"open_access","file_name":"2018_DevGrowh_Hannezo.pdf","date_created":"2019-02-06T10:40:46Z","checksum":"a6d30b0785db902c734a84fecb2eadd9","relation":"main_file","content_type":"application/pdf","file_id":"5933","file_size":1313606}],"date_updated":"2025-07-10T11:52:59Z","month":"12","date_published":"2018-12-09T00:00:00Z","author":[{"last_name":"Hannezo","id":"3A9DB764-F248-11E8-B48F-1D18A9856A87","first_name":"Edouard B","orcid":"0000-0001-6005-1561","full_name":"Hannezo, Edouard B"},{"first_name":"Benjamin D.","full_name":"Simons, Benjamin D.","last_name":"Simons"}],"file_date_updated":"2020-07-14T12:47:11Z","oa":1,"abstract":[{"lang":"eng","text":"Branching  morphogenesis  remains  a  subject  of  abiding  interest.  Although  much  is  \r\nknown about the gene regulatory programs and signaling pathways that operate at \r\nthe cellular scale, it has remained unclear how the macroscopic features of branched \r\norgans,  including  their  size,  network  topology  and  spatial  patterning,  are  encoded.  \r\nLately, it has been proposed that, these features can be explained quantitatively in \r\nseveral organs within a single unifying framework. Based on large-\r\nscale organ recon\r\n-\r\nstructions  and  cell  lineage  tracing,  it  has  been  argued  that  morphogenesis  follows  \r\nfrom the collective dynamics of sublineage- \r\nrestricted self- \r\nrenewing progenitor cells, \r\nlocalized at ductal tips, that act cooperatively to drive a serial process of ductal elon\r\n-\r\ngation and stochastic tip bifurcation. By correlating differentiation or cell cycle exit \r\nwith proximity to maturing ducts, this dynamic results in the specification of a com-\r\nplex  network  of  defined  density  and  statistical  organization.  These  results  suggest  \r\nthat, for several mammalian tissues, branched epithelial structures develop as a self- \r\norganized  process,  reliant  upon  a  strikingly  simple,  but  generic,  set  of  local  rules,  \r\nwithout  recourse  to  a  rigid  and  deterministic  sequence  of  genetically  programmed  \r\nevents. Here, we review the basis of these findings and discuss their implications."}],"tmp":{"name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","image":"/images/cc_by.png","legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","short":"CC BY (4.0)"},"publisher":"Wiley","publication":"Development Growth and Differentiation","year":"2018","volume":60,"quality_controlled":"1","status":"public","ddc":["570"],"scopus_import":"1","intvolume":"        60"},{"publication_identifier":{"issn":["2054-5703"]},"publication_status":"published","external_id":{"pmid":["30662738"],"isi":["000456566500027"]},"title":"Chromatic transitions in the emergence of syntax networks","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","article_number":"181286","citation":{"ista":"Corominas-Murtra B, Fibla MS, Valverde S, Solé R. 2018. Chromatic transitions in the emergence of syntax networks. Royal Society Open Science. 5(12), 181286.","chicago":"Corominas-Murtra, Bernat, Martí Sànchez Fibla, Sergi Valverde, and Ricard Solé. “Chromatic Transitions in the Emergence of Syntax Networks.” <i>Royal Society Open Science</i>. The Royal Society, 2018. <a href=\"https://doi.org/10.1098/rsos.181286\">https://doi.org/10.1098/rsos.181286</a>.","ieee":"B. Corominas-Murtra, M. S. Fibla, S. Valverde, and R. Solé, “Chromatic transitions in the emergence of syntax networks,” <i>Royal Society Open Science</i>, vol. 5, no. 12. The Royal Society, 2018.","mla":"Corominas-Murtra, Bernat, et al. “Chromatic Transitions in the Emergence of Syntax Networks.” <i>Royal Society Open Science</i>, vol. 5, no. 12, 181286, The Royal Society, 2018, doi:<a href=\"https://doi.org/10.1098/rsos.181286\">10.1098/rsos.181286</a>.","short":"B. Corominas-Murtra, M.S. Fibla, S. Valverde, R. Solé, Royal Society Open Science 5 (2018).","ama":"Corominas-Murtra B, Fibla MS, Valverde S, Solé R. Chromatic transitions in the emergence of syntax networks. <i>Royal Society Open Science</i>. 2018;5(12). doi:<a href=\"https://doi.org/10.1098/rsos.181286\">10.1098/rsos.181286</a>","apa":"Corominas-Murtra, B., Fibla, M. S., Valverde, S., &#38; Solé, R. (2018). Chromatic transitions in the emergence of syntax networks. <i>Royal Society Open Science</i>. The Royal Society. <a href=\"https://doi.org/10.1098/rsos.181286\">https://doi.org/10.1098/rsos.181286</a>"},"doi":"10.1098/rsos.181286","oa_version":"Published Version","fulldoi":"https://doi.org/10.1098/rsos.181286","language":[{"iso":"eng"}],"_id":"5859","day":"12","article_processing_charge":"No","has_accepted_license":"1","type":"journal_article","issue":"12","isi":1,"article_type":"original","month":"12","date_published":"2018-12-12T00:00:00Z","date_created":"2019-01-20T22:59:18Z","acknowledgement":"This work was supported by the James McDonnell Foundation (B.C-M., S.V. and R.S.)","department":[{"_id":"EdHa"}],"date_updated":"2023-10-18T06:41:12Z","file":[{"relation":"main_file","content_type":"application/pdf","file_size":646732,"file_id":"5924","access_level":"open_access","date_updated":"2020-07-14T12:47:13Z","creator":"dernst","checksum":"9664d4417f6b792242e31eea77ce9501","file_name":"2018_RoyalSocOS_Corominas.pdf","date_created":"2019-02-05T14:38:09Z"}],"publication":"Royal Society Open Science","volume":5,"year":"2018","intvolume":"         5","status":"public","ddc":["570"],"quality_controlled":"1","scopus_import":"1","pmid":1,"tmp":{"name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","image":"/images/cc_by.png","legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","short":"CC BY (4.0)"},"abstract":[{"lang":"eng","text":"The emergence of syntax during childhood is a remarkable example of how complex correlations unfold in nonlinear ways through development. In particular, rapid transitions seem to occur as children reach the age of two, which seems to separate a two-word, tree-like network of syntactic relations among words from the scale-free graphs associated with the adult, complex grammar. Here, we explore the evolution of syntax networks through language acquisition using the chromatic number, which captures the transition and provides a natural link to standard theories on syntactic structures. The data analysis is compared to a null model of network growth dynamics which is shown to display non-trivial and sensible differences. At a more general level, we observe that the chromatic classes define independent regions of the graph, and thus, can be interpreted as the footprints of incompatibility relations, somewhat as opposed to modularity considerations."}],"author":[{"full_name":"Corominas-Murtra, Bernat","id":"43BE2298-F248-11E8-B48F-1D18A9856A87","first_name":"Bernat","orcid":"0000-0001-9806-5643","last_name":"Corominas-Murtra"},{"last_name":"Fibla","full_name":"Fibla, Martí Sànchez","first_name":"Martí Sànchez"},{"last_name":"Valverde","full_name":"Valverde, Sergi","first_name":"Sergi"},{"full_name":"Solé, Ricard","first_name":"Ricard","last_name":"Solé"}],"oa":1,"file_date_updated":"2020-07-14T12:47:13Z","publisher":"The Royal Society"},{"publisher":"Nature Publishing Group","tmp":{"name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","image":"/images/cc_by.png","legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","short":"CC BY (4.0)"},"abstract":[{"text":"The actomyosin cytoskeleton, a key stress-producing unit in epithelial cells, oscillates spontaneously in a wide variety of systems. Although much of the signal cascade regulating myosin activity has been characterized, the origin of such oscillatory behavior is still unclear. Here, we show that basal myosin II oscillation in Drosophila ovarian epithelium is not controlled by actomyosin cortical tension, but instead relies on a biochemical oscillator involving ROCK and myosin phosphatase. Key to this oscillation is a diffusive ROCK flow, linking junctional Rho1 to medial actomyosin cortex, and dynamically maintained by a self-activation loop reliant on ROCK kinase activity. In response to the resulting myosin II recruitment, myosin phosphatase is locally enriched and shuts off ROCK and myosin II signals. Coupling Drosophila genetics, live imaging, modeling, and optogenetics, we uncover an intrinsic biochemical oscillator at the core of myosin II regulatory network, shedding light on the spatio-temporal dynamics of force generation.","lang":"eng"}],"author":[{"last_name":"Qin","first_name":"Xiang","full_name":"Qin, Xiang"},{"id":"3A9DB764-F248-11E8-B48F-1D18A9856A87","first_name":"Edouard B","orcid":"0000-0001-6005-1561","full_name":"Hannezo, Edouard B","last_name":"Hannezo"},{"last_name":"Mangeat","first_name":"Thomas","full_name":"Mangeat, Thomas"},{"last_name":"Liu","first_name":"Chang","full_name":"Liu, Chang"},{"full_name":"Majumder, Pralay","first_name":"Pralay","last_name":"Majumder"},{"last_name":"Liu","first_name":"Jjiaying","full_name":"Liu, Jjiaying"},{"last_name":"Choesmel Cadamuro","first_name":"Valerie","full_name":"Choesmel Cadamuro, Valerie"},{"full_name":"Mcdonald, Jocelyn","first_name":"Jocelyn","last_name":"Mcdonald"},{"last_name":"Liu","full_name":"Liu, Yinyao","first_name":"Yinyao"},{"full_name":"Yi, Bin","first_name":"Bin","last_name":"Yi"},{"full_name":"Wang, Xiaobo","first_name":"Xiaobo","last_name":"Wang"}],"oa":1,"file_date_updated":"2020-07-14T12:46:22Z","intvolume":"         9","status":"public","quality_controlled":"1","ddc":["539","570"],"scopus_import":"1","publication":"Nature Communications","year":"2018","volume":9,"date_updated":"2023-09-08T11:41:45Z","file":[{"access_level":"open_access","date_updated":"2020-07-14T12:46:22Z","creator":"system","checksum":"87a427bc2e8724be3dd22a4efdd21a33","file_name":"IST-2018-996-v1+1_2018_Hannezo_A-biochemical.pdf","date_created":"2018-12-12T10:11:45Z","relation":"main_file","content_type":"application/pdf","file_size":3780491,"file_id":"4902"}],"date_created":"2018-12-11T11:46:16Z","department":[{"_id":"EdHa"}],"date_published":"2018-03-23T00:00:00Z","month":"03","issue":"1","isi":1,"has_accepted_license":"1","publist_id":"7427","pubrep_id":"996","type":"journal_article","article_processing_charge":"No","doi":"10.1038/s41467-018-03574-5","fulldoi":"https://doi.org/10.1038/s41467-018-03574-5","oa_version":"Published Version","language":[{"iso":"eng"}],"day":"23","_id":"401","citation":{"apa":"Qin, X., Hannezo, E. B., Mangeat, T., Liu, C., Majumder, P., Liu, J., … Wang, X. (2018). A biochemical network controlling basal myosin oscillation. <i>Nature Communications</i>. Nature Publishing Group. <a href=\"https://doi.org/10.1038/s41467-018-03574-5\">https://doi.org/10.1038/s41467-018-03574-5</a>","mla":"Qin, Xiang, et al. “A Biochemical Network Controlling Basal Myosin Oscillation.” <i>Nature Communications</i>, vol. 9, no. 1, 1210, Nature Publishing Group, 2018, doi:<a href=\"https://doi.org/10.1038/s41467-018-03574-5\">10.1038/s41467-018-03574-5</a>.","ieee":"X. Qin <i>et al.</i>, “A biochemical network controlling basal myosin oscillation,” <i>Nature Communications</i>, vol. 9, no. 1. Nature Publishing Group, 2018.","ama":"Qin X, Hannezo EB, Mangeat T, et al. A biochemical network controlling basal myosin oscillation. <i>Nature Communications</i>. 2018;9(1). doi:<a href=\"https://doi.org/10.1038/s41467-018-03574-5\">10.1038/s41467-018-03574-5</a>","short":"X. Qin, E.B. Hannezo, T. Mangeat, C. Liu, P. Majumder, J. Liu, V. Choesmel Cadamuro, J. Mcdonald, Y. Liu, B. Yi, X. Wang, Nature Communications 9 (2018).","ista":"Qin X, Hannezo EB, Mangeat T, Liu C, Majumder P, Liu J, Choesmel Cadamuro V, Mcdonald J, Liu Y, Yi B, Wang X. 2018. A biochemical network controlling basal myosin oscillation. Nature Communications. 9(1), 1210.","chicago":"Qin, Xiang, Edouard B Hannezo, Thomas Mangeat, Chang Liu, Pralay Majumder, Jjiaying Liu, Valerie Choesmel Cadamuro, et al. “A Biochemical Network Controlling Basal Myosin Oscillation.” <i>Nature Communications</i>. Nature Publishing Group, 2018. <a href=\"https://doi.org/10.1038/s41467-018-03574-5\">https://doi.org/10.1038/s41467-018-03574-5</a>."},"user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","article_number":"1210","publication_status":"published","external_id":{"isi":["000428165400009"]},"title":"A biochemical network controlling basal myosin oscillation"},{"type":"journal_article","publist_id":"7403","page":"968 - 977","isi":1,"arxiv":1,"issue":"4","day":"27","_id":"421","fulldoi":"https://doi.org/10.1016/j.bpj.2017.12.022","language":[{"iso":"eng"}],"oa_version":"Submitted Version","doi":"10.1016/j.bpj.2017.12.022","article_processing_charge":"No","main_file_link":[{"url":"https://arxiv.org/abs/1709.01486","open_access":"1"}],"citation":{"apa":"Dasbiswas, K., Hannezo, E. B., &#38; Gov, N. (2018). Theory of eppithelial cell shape transitions induced by mechanoactive chemical gradients. <i>Biophysical Journal</i>. Biophysical Society. <a href=\"https://doi.org/10.1016/j.bpj.2017.12.022\">https://doi.org/10.1016/j.bpj.2017.12.022</a>","ieee":"K. Dasbiswas, E. B. Hannezo, and N. Gov, “Theory of eppithelial cell shape transitions induced by mechanoactive chemical gradients,” <i>Biophysical Journal</i>, vol. 114, no. 4. Biophysical Society, pp. 968–977, 2018.","mla":"Dasbiswas, Kinjal, et al. “Theory of Eppithelial Cell Shape Transitions Induced by Mechanoactive Chemical Gradients.” <i>Biophysical Journal</i>, vol. 114, no. 4, Biophysical Society, 2018, pp. 968–77, doi:<a href=\"https://doi.org/10.1016/j.bpj.2017.12.022\">10.1016/j.bpj.2017.12.022</a>.","ama":"Dasbiswas K, Hannezo EB, Gov N. Theory of eppithelial cell shape transitions induced by mechanoactive chemical gradients. <i>Biophysical Journal</i>. 2018;114(4):968-977. doi:<a href=\"https://doi.org/10.1016/j.bpj.2017.12.022\">10.1016/j.bpj.2017.12.022</a>","short":"K. Dasbiswas, E.B. Hannezo, N. Gov, Biophysical Journal 114 (2018) 968–977.","ista":"Dasbiswas K, Hannezo EB, Gov N. 2018. Theory of eppithelial cell shape transitions induced by mechanoactive chemical gradients. Biophysical Journal. 114(4), 968–977.","chicago":"Dasbiswas, Kinjal, Edouard B Hannezo, and Nir Gov. “Theory of Eppithelial Cell Shape Transitions Induced by Mechanoactive Chemical Gradients.” <i>Biophysical Journal</i>. Biophysical Society, 2018. <a href=\"https://doi.org/10.1016/j.bpj.2017.12.022\">https://doi.org/10.1016/j.bpj.2017.12.022</a>."},"title":"Theory of eppithelial cell shape transitions induced by mechanoactive chemical gradients","external_id":{"arxiv":["1709.01486"],"isi":["000428016700021"]},"publication_status":"published","user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","oa":1,"author":[{"last_name":"Dasbiswas","full_name":"Dasbiswas, Kinjal","first_name":"Kinjal"},{"full_name":"Hannezo, Claude-Edouard B","id":"3A9DB764-F248-11E8-B48F-1D18A9856A87","first_name":"Claude-Edouard B","orcid":"0000-0001-6005-1561","last_name":"Hannezo"},{"first_name":"Nir","full_name":"Gov, Nir","last_name":"Gov"}],"abstract":[{"lang":"eng","text":"Cell shape is determined by a balance of intrinsic properties of the cell as well as its mechanochemical environment. Inhomogeneous shape changes underlie many morphogenetic events and involve spatial gradients in active cellular forces induced by complex chemical signaling. Here, we introduce a mechanochemical model based on the notion that cell shape changes may be induced by external diffusible biomolecules that influence cellular contractility (or equivalently, adhesions) in a concentration-dependent manner—and whose spatial profile in turn is affected by cell shape. We map out theoretically the possible interplay between chemical concentration and cellular structure. Besides providing a direct route to spatial gradients in cell shape profiles in tissues, we show that the dependence on cell shape helps create robust mechanochemical gradients."}],"publisher":"Biophysical Society","year":"2018","volume":114,"publication":"Biophysical Journal","scopus_import":"1","quality_controlled":"1","status":"public","intvolume":"       114","department":[{"_id":"EdHa"}],"date_created":"2018-12-11T11:46:23Z","date_updated":"2023-09-19T10:13:55Z","month":"02","date_published":"2018-02-27T00:00:00Z"},{"abstract":[{"text":"A major problem for evolutionary theory is understanding the so-called open-ended nature of evolutionary change, from its definition to its origins. Open-ended evolution (OEE) refers to the unbounded increase in complexity that seems to characterize evolution on multiple scales. This property seems to be a characteristic feature of biological and technological evolution and is strongly tied to the generative potential associated with combinatorics, which allows the system to grow and expand their available state spaces. Interestingly, many complex systems presumably displaying OEE, from language to proteins, share a common statistical property: the presence of Zipf's Law. Given an inventory of basic items (such as words or protein domains) required to build more complex structures (sentences or proteins) Zipf's Law tells us that most of these elements are rare whereas a few of them are extremely common. Using algorithmic information theory, in this paper we provide a fundamental definition for open-endedness, which can be understood as postulates. Its statistical counterpart, based on standard Shannon information theory, has the structure of a variational problem which is shown to lead to Zipf's Law as the expected consequence of an evolutionary process displaying OEE. We further explore the problem of information conservation through an OEE process and we conclude that statistical information (standard Shannon information) is not conserved, resulting in the paradoxical situation in which the increase of information content has the effect of erasing itself. We prove that this paradox is solved if we consider non-statistical forms of information. This last result implies that standard information theory may not be a suitable theoretical framework to explore the persistence and increase of the information content in OEE systems.","lang":"eng"}],"author":[{"last_name":"Corominas-Murtra","orcid":"0000-0001-9806-5643","id":"43BE2298-F248-11E8-B48F-1D18A9856A87","first_name":"Bernat","full_name":"Corominas-Murtra, Bernat"},{"full_name":"Seoane, Luís F.","first_name":"Luís F.","last_name":"Seoane"},{"first_name":"Ricard","full_name":"Solé, Ricard","last_name":"Solé"}],"oa":1,"publisher":"Royal Society","publication":"Journal of the Royal Society Interface","volume":15,"year":"2018","intvolume":"        15","status":"public","quality_controlled":"1","scopus_import":"1","date_created":"2019-01-20T22:59:19Z","department":[{"_id":"EdHa"}],"date_updated":"2026-08-12T06:28:34Z","month":"12","date_published":"2018-12-12T00:00:00Z","type":"journal_article","issue":"149","isi":1,"arxiv":1,"doi":"10.1098/rsif.2018.0395","language":[{"iso":"eng"}],"fulldoi":"https://doi.org/10.1098/rsif.2018.0395","oa_version":"Preprint","day":"12","_id":"5860","article_processing_charge":"No","citation":{"mla":"Corominas-Murtra, Bernat, et al. “Zipf’s Law, Unbounded Complexity and Open-Ended Evolution.” <i>Journal of the Royal Society Interface</i>, vol. 15, no. 149, 20180395, Royal Society, 2018, doi:<a href=\"https://doi.org/10.1098/rsif.2018.0395\">10.1098/rsif.2018.0395</a>.","ieee":"B. Corominas-Murtra, L. F. Seoane, and R. Solé, “Zipf’s Law, unbounded complexity and open-ended evolution,” <i>Journal of the Royal Society Interface</i>, vol. 15, no. 149. Royal Society, 2018.","ama":"Corominas-Murtra B, Seoane LF, Solé R. Zipf’s Law, unbounded complexity and open-ended evolution. <i>Journal of the Royal Society Interface</i>. 2018;15(149). doi:<a href=\"https://doi.org/10.1098/rsif.2018.0395\">10.1098/rsif.2018.0395</a>","short":"B. Corominas-Murtra, L.F. Seoane, R. Solé, Journal of the Royal Society Interface 15 (2018).","apa":"Corominas-Murtra, B., Seoane, L. F., &#38; Solé, R. (2018). Zipf’s Law, unbounded complexity and open-ended evolution. <i>Journal of the Royal Society Interface</i>. Royal Society. <a href=\"https://doi.org/10.1098/rsif.2018.0395\">https://doi.org/10.1098/rsif.2018.0395</a>","ista":"Corominas-Murtra B, Seoane LF, Solé R. 2018. Zipf’s Law, unbounded complexity and open-ended evolution. Journal of the Royal Society Interface. 15(149), 20180395.","chicago":"Corominas-Murtra, Bernat, Luís F. Seoane, and Ricard Solé. “Zipf’s Law, Unbounded Complexity and Open-Ended Evolution.” <i>Journal of the Royal Society Interface</i>. Royal Society, 2018. <a href=\"https://doi.org/10.1098/rsif.2018.0395\">https://doi.org/10.1098/rsif.2018.0395</a>."},"main_file_link":[{"url":"https://arxiv.org/abs/1612.01605","open_access":"1"}],"publication_identifier":{"issn":["1742-5689"]},"publication_status":"published","external_id":{"arxiv":["1612.01605"],"isi":["000456783800002"]},"title":"Zipf's Law, unbounded complexity and open-ended evolution","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","article_number":"20180395"},{"publication":"Nature Neuroscience","volume":21,"year":"2018","status":"public","quality_controlled":"1","ddc":["570"],"scopus_import":"1","intvolume":"        21","author":[{"full_name":"Deliu, Elena","first_name":"Elena","id":"37A40D7E-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-7370-5293","last_name":"Deliu"},{"last_name":"Arecco","first_name":"Niccoló","full_name":"Arecco, Niccoló"},{"full_name":"Morandell, Jasmin","id":"4739D480-F248-11E8-B48F-1D18A9856A87","first_name":"Jasmin","last_name":"Morandell"},{"first_name":"Christoph","id":"4C66542E-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-9033-9096","full_name":"Dotter, Christoph","last_name":"Dotter"},{"last_name":"Contreras","full_name":"Contreras, Ximena","first_name":"Ximena","id":"475990FE-F248-11E8-B48F-1D18A9856A87"},{"last_name":"Girardot","first_name":"Charles","full_name":"Girardot, Charles"},{"first_name":"Eva","full_name":"Käsper, Eva","last_name":"Käsper"},{"full_name":"Kozlova, Alena","first_name":"Alena","id":"C50A9596-02D0-11E9-976E-E38CFE5CBC1D","last_name":"Kozlova"},{"last_name":"Kishi","full_name":"Kishi, Kasumi","id":"3065DFC4-F248-11E8-B48F-1D18A9856A87","first_name":"Kasumi","orcid":"0000-0001-6060-4795"},{"full_name":"Chiaradia, Ilaria","orcid":"0000-0002-9529-4464","first_name":"Ilaria","id":"B6467F20-02D0-11E9-BDA5-E960C241894A","last_name":"Chiaradia"},{"last_name":"Noh","full_name":"Noh, Kyung","first_name":"Kyung"},{"last_name":"Novarino","orcid":"0000-0002-7673-7178","id":"3E57A680-F248-11E8-B48F-1D18A9856A87","first_name":"Gaia","full_name":"Novarino, Gaia"}],"oa":1,"file_date_updated":"2020-07-14T12:45:58Z","corr_author":"1","abstract":[{"lang":"eng","text":"SETD5 gene mutations have been identified as a frequent cause of idiopathic intellectual disability. Here we show that Setd5-haploinsufficient mice present developmental defects such as abnormal brain-to-body weight ratios and neural crest defect-associated phenotypes. Furthermore, Setd5-mutant mice show impairments in cognitive tasks, enhanced long-term potentiation, delayed ontogenetic profile of ultrasonic vocalization, and behavioral inflexibility. Behavioral issues are accompanied by abnormal expression of postsynaptic density proteins previously associated with cognition. Our data additionally indicate that Setd5 regulates RNA polymerase II dynamics and gene transcription via its interaction with the Hdac3 and Paf1 complexes, findings potentially explaining the gene expression defects observed in Setd5-haploinsufficient mice. Our results emphasize the decisive role of Setd5 in a biological pathway found to be disrupted in humans with intellectual disability and autism spectrum disorder."}],"publisher":"Nature Publishing Group","month":"11","date_published":"2018-11-19T00:00:00Z","department":[{"_id":"GaNo"},{"_id":"EdHa"}],"date_created":"2018-12-11T11:44:05Z","acknowledgement":"This work was supported by the Simons Foundation Autism Research Initiative (grant 401299) to G.N. and the DFG (SPP1738 grant NO 1249) to K.-M.N.","file":[{"file_size":8167169,"file_id":"6255","relation":"main_file","content_type":"application/pdf","checksum":"60abd0f05b7cdc08a6b0ec460884084f","file_name":"2017_NatureNeuroscience_Deliu.pdf","date_created":"2019-04-09T07:41:57Z","creator":"dernst","access_level":"open_access","date_updated":"2020-07-14T12:45:58Z"}],"date_updated":"2026-10-21T22:30:10Z","oa_version":"Submitted Version","fulldoi":"https://doi.org/10.1038/s41593-018-0266-2","language":[{"iso":"eng"}],"_id":"3","day":"19","doi":"10.1038/s41593-018-0266-2","article_processing_charge":"No","has_accepted_license":"1","project":[{"grant_number":"401299","name":"Probing development and reversibility of autism spectrum disorders","_id":"254BA948-B435-11E9-9278-68D0E5697425"}],"publist_id":"8054","pubrep_id":"1071","type":"journal_article","page":"1717 - 1727","article_type":"original","related_material":{"link":[{"relation":"press_release","description":"News on IST Homepage","url":"https://ist.ac.at/en/news/mutation-that-causes-autism-and-intellectual-disability-makes-brain-less-flexible/"}],"record":[{"status":"public","id":"6074","relation":"popular_science"},{"status":"public","relation":"dissertation_contains","id":"12364"}]},"issue":"12","isi":1,"title":"Haploinsufficiency of the intellectual disability gene SETD5 disturbs developmental gene expression and cognition","publication_status":"published","external_id":{"isi":["000451324700010"]},"user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","acknowledged_ssus":[{"_id":"M-Shop"},{"_id":"PreCl"}],"citation":{"ama":"Deliu E, Arecco N, Morandell J, et al. Haploinsufficiency of the intellectual disability gene SETD5 disturbs developmental gene expression and cognition. <i>Nature Neuroscience</i>. 2018;21(12):1717-1727. doi:<a href=\"https://doi.org/10.1038/s41593-018-0266-2\">10.1038/s41593-018-0266-2</a>","short":"E. Deliu, N. Arecco, J. Morandell, C. Dotter, X. Contreras, C. Girardot, E. Käsper, A. Kozlova, K. Kishi, I. Chiaradia, K. Noh, G. Novarino, Nature Neuroscience 21 (2018) 1717–1727.","mla":"Deliu, Elena, et al. “Haploinsufficiency of the Intellectual Disability Gene SETD5 Disturbs Developmental Gene Expression and Cognition.” <i>Nature Neuroscience</i>, vol. 21, no. 12, Nature Publishing Group, 2018, pp. 1717–27, doi:<a href=\"https://doi.org/10.1038/s41593-018-0266-2\">10.1038/s41593-018-0266-2</a>.","ieee":"E. Deliu <i>et al.</i>, “Haploinsufficiency of the intellectual disability gene SETD5 disturbs developmental gene expression and cognition,” <i>Nature Neuroscience</i>, vol. 21, no. 12. Nature Publishing Group, pp. 1717–1727, 2018.","apa":"Deliu, E., Arecco, N., Morandell, J., Dotter, C., Contreras, X., Girardot, C., … Novarino, G. (2018). Haploinsufficiency of the intellectual disability gene SETD5 disturbs developmental gene expression and cognition. <i>Nature Neuroscience</i>. Nature Publishing Group. <a href=\"https://doi.org/10.1038/s41593-018-0266-2\">https://doi.org/10.1038/s41593-018-0266-2</a>","chicago":"Deliu, Elena, Niccoló Arecco, Jasmin Morandell, Christoph Dotter, Ximena Contreras, Charles Girardot, Eva Käsper, et al. “Haploinsufficiency of the Intellectual Disability Gene SETD5 Disturbs Developmental Gene Expression and Cognition.” <i>Nature Neuroscience</i>. Nature Publishing Group, 2018. <a href=\"https://doi.org/10.1038/s41593-018-0266-2\">https://doi.org/10.1038/s41593-018-0266-2</a>.","ista":"Deliu E, Arecco N, Morandell J, Dotter C, Contreras X, Girardot C, Käsper E, Kozlova A, Kishi K, Chiaradia I, Noh K, Novarino G. 2018. Haploinsufficiency of the intellectual disability gene SETD5 disturbs developmental gene expression and cognition. Nature Neuroscience. 21(12), 1717–1727."}},{"user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","external_id":{"isi":["000411331800024"]},"publication_status":"published","publication_identifier":{"issn":["0092-8674"]},"title":"A unifying theory of branching morphogenesis","citation":{"apa":"Hannezo, E. B., Scheele, C., Moad, M., Drogo, N., Heer, R., Sampogna, R., … Simons, B. (2017). A unifying theory of branching morphogenesis. <i>Cell</i>. Cell Press. <a href=\"https://doi.org/10.1016/j.cell.2017.08.026\">https://doi.org/10.1016/j.cell.2017.08.026</a>","ama":"Hannezo EB, Scheele C, Moad M, et al. A unifying theory of branching morphogenesis. <i>Cell</i>. 2017;171(1):242-255. doi:<a href=\"https://doi.org/10.1016/j.cell.2017.08.026\">10.1016/j.cell.2017.08.026</a>","short":"E.B. Hannezo, C. Scheele, M. Moad, N. Drogo, R. Heer, R. Sampogna, J. Van Rheenen, B. Simons, Cell 171 (2017) 242–255.","ieee":"E. B. Hannezo <i>et al.</i>, “A unifying theory of branching morphogenesis,” <i>Cell</i>, vol. 171, no. 1. Cell Press, pp. 242–255, 2017.","mla":"Hannezo, Edouard B., et al. “A Unifying Theory of Branching Morphogenesis.” <i>Cell</i>, vol. 171, no. 1, Cell Press, 2017, pp. 242–55, doi:<a href=\"https://doi.org/10.1016/j.cell.2017.08.026\">10.1016/j.cell.2017.08.026</a>.","chicago":"Hannezo, Edouard B, Colinda Scheele, Mohammad Moad, Nicholas Drogo, Rakesh Heer, Rosemary Sampogna, Jacco Van Rheenen, and Benjamin Simons. “A Unifying Theory of Branching Morphogenesis.” <i>Cell</i>. Cell Press, 2017. <a href=\"https://doi.org/10.1016/j.cell.2017.08.026\">https://doi.org/10.1016/j.cell.2017.08.026</a>.","ista":"Hannezo EB, Scheele C, Moad M, Drogo N, Heer R, Sampogna R, Van Rheenen J, Simons B. 2017. A unifying theory of branching morphogenesis. Cell. 171(1), 242–255."},"article_processing_charge":"No","doi":"10.1016/j.cell.2017.08.026","_id":"726","day":"21","fulldoi":"https://doi.org/10.1016/j.cell.2017.08.026","language":[{"iso":"eng"}],"oa_version":"Published Version","isi":1,"issue":"1","page":"242 - 255","type":"journal_article","pubrep_id":"883","has_accepted_license":"1","publist_id":"6952","date_published":"2017-09-21T00:00:00Z","month":"09","date_updated":"2025-07-10T11:54:27Z","file":[{"content_type":"application/pdf","relation":"main_file","file_size":12670204,"file_id":"4870","creator":"system","access_level":"open_access","date_updated":"2020-07-14T12:47:55Z","checksum":"7a036d93a9e2e597af9bb504d6133aca","date_created":"2018-12-12T10:11:17Z","file_name":"IST-2017-883-v1+1_PIIS0092867417309510.pdf"}],"date_created":"2018-12-11T11:48:10Z","department":[{"_id":"EdHa"}],"intvolume":"       171","scopus_import":"1","ddc":["539"],"quality_controlled":"1","status":"public","volume":171,"year":"2017","publication":"Cell","publisher":"Cell Press","abstract":[{"text":"The morphogenesis of branched organs remains a subject of abiding interest. Although much is known about the underlying signaling pathways, it remains unclear how macroscopic features of branched organs, including their size, network topology, and spatial patterning, are encoded. Here, we show that, in mouse mammary gland, kidney, and human prostate, these features can be explained quantitatively within a single unifying framework of branching and annihilating random walks. Based on quantitative analyses of large-scale organ reconstructions and proliferation kinetics measurements, we propose that morphogenesis follows from the proliferative activity of equipotent tips that stochastically branch and randomly explore their environment but compete neutrally for space, becoming proliferatively inactive when in proximity with neighboring ducts. These results show that complex branched epithelial structures develop as a self-organized process, reliant upon a strikingly simple but generic rule, without recourse to a rigid and deterministic sequence of genetically programmed events.","lang":"eng"}],"tmp":{"name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","image":"/images/cc_by.png","legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","short":"CC BY (4.0)"},"corr_author":"1","oa":1,"file_date_updated":"2020-07-14T12:47:55Z","author":[{"last_name":"Hannezo","full_name":"Hannezo, Edouard B","id":"3A9DB764-F248-11E8-B48F-1D18A9856A87","first_name":"Edouard B","orcid":"0000-0001-6005-1561"},{"full_name":"Scheele, Colinda","first_name":"Colinda","last_name":"Scheele"},{"last_name":"Moad","full_name":"Moad, Mohammad","first_name":"Mohammad"},{"last_name":"Drogo","first_name":"Nicholas","full_name":"Drogo, Nicholas"},{"first_name":"Rakesh","full_name":"Heer, Rakesh","last_name":"Heer"},{"last_name":"Sampogna","full_name":"Sampogna, Rosemary","first_name":"Rosemary"},{"full_name":"Van Rheenen, Jacco","first_name":"Jacco","last_name":"Van Rheenen"},{"first_name":"Benjamin","full_name":"Simons, Benjamin","last_name":"Simons"}]}]