[{"page":"677 - 687","external_id":{"isi":["000433237300003"],"pmid":["29784917"]},"date_published":"2018-05-21T00:00:00Z","scopus_import":"1","day":"21","oa_version":"Submitted Version","type":"journal_article","date_updated":"2023-09-11T12:44:08Z","user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","article_processing_charge":"No","department":[{"_id":"EdHa"}],"language":[{"iso":"eng"}],"doi":"10.1038/s41556-018-0108-1","article_type":"original","publisher":"Nature Publishing Group","volume":20,"issue":"6","status":"public","month":"05","date_created":"2018-12-11T11:45:38Z","isi":1,"publist_id":"7594","intvolume":"        20","year":"2018","author":[{"first_name":"Anna","last_name":"Lilja","full_name":"Lilja, Anna"},{"full_name":"Rodilla, Veronica","first_name":"Veronica","last_name":"Rodilla"},{"last_name":"Huyghe","first_name":"Mathilde","full_name":"Huyghe, Mathilde"},{"id":"3A9DB764-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0001-6005-1561","full_name":"Hannezo, Edouard B","first_name":"Edouard B","last_name":"Hannezo"},{"full_name":"Landragin, Camille","first_name":"Camille","last_name":"Landragin"},{"last_name":"Renaud","first_name":"Olivier","full_name":"Renaud, Olivier"},{"last_name":"Leroy","first_name":"Olivier","full_name":"Leroy, Olivier"},{"last_name":"Rulands","first_name":"Steffen","full_name":"Rulands, Steffen"},{"last_name":"Simons","first_name":"Benjamin","full_name":"Simons, Benjamin"},{"first_name":"Silvia","last_name":"Fré","full_name":"Fré, Silvia"}],"quality_controlled":"1","main_file_link":[{"url":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6984964","open_access":"1"}],"citation":{"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>.","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.","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>","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>.","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.","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."},"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."}],"publication_status":"published","_id":"288","oa":1,"pmid":1,"title":"Clonal analysis of Notch1-expressing cells reveals the existence of unipotent stem cells that retain long-term plasticity in the embryonic mammary gland","publication":"Nature Cell Biology"},{"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."}],"publication_status":"published","project":[{"_id":"254BA948-B435-11E9-9278-68D0E5697425","name":"Probing development and reversibility of autism spectrum disorders","grant_number":"401299"}],"_id":"3","related_material":{"record":[{"status":"public","relation":"popular_science","id":"6074"},{"status":"public","relation":"dissertation_contains","id":"12364"}],"link":[{"description":"News on IST Homepage","relation":"press_release","url":"https://ist.ac.at/en/news/mutation-that-causes-autism-and-intellectual-disability-makes-brain-less-flexible/"}]},"ddc":["570"],"oa":1,"title":"Haploinsufficiency of the intellectual disability gene SETD5 disturbs developmental gene expression and cognition","publication":"Nature Neuroscience","year":"2018","quality_controlled":"1","author":[{"first_name":"Elena","last_name":"Deliu","id":"37A40D7E-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-7370-5293","full_name":"Deliu, Elena"},{"last_name":"Arecco","first_name":"Niccoló","full_name":"Arecco, Niccoló"},{"first_name":"Jasmin","last_name":"Morandell","id":"4739D480-F248-11E8-B48F-1D18A9856A87","full_name":"Morandell, Jasmin"},{"last_name":"Dotter","first_name":"Christoph","id":"4C66542E-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-9033-9096","full_name":"Dotter, Christoph"},{"id":"475990FE-F248-11E8-B48F-1D18A9856A87","full_name":"Contreras, Ximena","first_name":"Ximena","last_name":"Contreras"},{"last_name":"Girardot","first_name":"Charles","full_name":"Girardot, Charles"},{"first_name":"Eva","last_name":"Käsper","full_name":"Käsper, Eva"},{"full_name":"Kozlova, Alena","id":"C50A9596-02D0-11E9-976E-E38CFE5CBC1D","first_name":"Alena","last_name":"Kozlova"},{"last_name":"Kishi","first_name":"Kasumi","id":"3065DFC4-F248-11E8-B48F-1D18A9856A87","full_name":"Kishi, Kasumi"},{"full_name":"Chiaradia, Ilaria","orcid":"0000-0002-9529-4464","id":"B6467F20-02D0-11E9-BDA5-E960C241894A","first_name":"Ilaria","last_name":"Chiaradia"},{"full_name":"Noh, Kyung","last_name":"Noh","first_name":"Kyung"},{"id":"3E57A680-F248-11E8-B48F-1D18A9856A87","full_name":"Novarino, Gaia","orcid":"0000-0002-7673-7178","first_name":"Gaia","last_name":"Novarino"}],"citation":{"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>.","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>","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.","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>","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.","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>.","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."},"status":"public","month":"11","date_created":"2018-12-11T11:44:05Z","isi":1,"publist_id":"8054","intvolume":"        21","publisher":"Nature Publishing Group","article_type":"original","file_date_updated":"2020-07-14T12:45:58Z","pubrep_id":"1071","issue":"12","volume":21,"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.","has_accepted_license":"1","department":[{"_id":"GaNo"},{"_id":"EdHa"}],"doi":"10.1038/s41593-018-0266-2","language":[{"iso":"eng"}],"acknowledged_ssus":[{"_id":"M-Shop"},{"_id":"PreCl"}],"day":"19","oa_version":"Submitted Version","date_updated":"2024-03-25T23:30:25Z","type":"journal_article","user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","article_processing_charge":"No","scopus_import":"1","page":"1717 - 1727","external_id":{"isi":["000451324700010"]},"file":[{"creator":"dernst","content_type":"application/pdf","file_size":8167169,"date_created":"2019-04-09T07:41:57Z","relation":"main_file","access_level":"open_access","checksum":"60abd0f05b7cdc08a6b0ec460884084f","file_name":"2017_NatureNeuroscience_Deliu.pdf","file_id":"6255","date_updated":"2020-07-14T12:45:58Z"}],"date_published":"2018-11-19T00:00:00Z"},{"file":[{"relation":"main_file","date_created":"2018-12-12T10:11:45Z","creator":"system","content_type":"application/pdf","file_size":3780491,"date_updated":"2020-07-14T12:46:22Z","file_id":"4902","file_name":"IST-2018-996-v1+1_2018_Hannezo_A-biochemical.pdf","checksum":"87a427bc2e8724be3dd22a4efdd21a33","access_level":"open_access"}],"external_id":{"isi":["000428165400009"]},"date_published":"2018-03-23T00:00:00Z","scopus_import":"1","oa_version":"Published Version","date_updated":"2023-09-08T11:41:45Z","type":"journal_article","day":"23","article_processing_charge":"No","user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","has_accepted_license":"1","department":[{"_id":"EdHa"}],"doi":"10.1038/s41467-018-03574-5","language":[{"iso":"eng"}],"file_date_updated":"2020-07-14T12:46:22Z","publisher":"Nature Publishing Group","pubrep_id":"996","volume":9,"issue":"1","month":"03","date_created":"2018-12-11T11:46:16Z","status":"public","article_number":"1210","intvolume":"         9","isi":1,"publist_id":"7427","tmp":{"image":"/images/cc_by.png","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","short":"CC BY (4.0)","legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode"},"year":"2018","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>.","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>","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.","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>.","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."},"quality_controlled":"1","author":[{"first_name":"Xiang","last_name":"Qin","full_name":"Qin, Xiang"},{"id":"3A9DB764-F248-11E8-B48F-1D18A9856A87","full_name":"Hannezo, Edouard B","orcid":"0000-0001-6005-1561","first_name":"Edouard B","last_name":"Hannezo"},{"full_name":"Mangeat, Thomas","last_name":"Mangeat","first_name":"Thomas"},{"first_name":"Chang","last_name":"Liu","full_name":"Liu, Chang"},{"first_name":"Pralay","last_name":"Majumder","full_name":"Majumder, Pralay"},{"full_name":"Liu, Jjiaying","last_name":"Liu","first_name":"Jjiaying"},{"full_name":"Choesmel Cadamuro, Valerie","last_name":"Choesmel Cadamuro","first_name":"Valerie"},{"first_name":"Jocelyn","last_name":"Mcdonald","full_name":"Mcdonald, Jocelyn"},{"last_name":"Liu","first_name":"Yinyao","full_name":"Liu, Yinyao"},{"full_name":"Yi, Bin","first_name":"Bin","last_name":"Yi"},{"last_name":"Wang","first_name":"Xiaobo","full_name":"Wang, Xiaobo"}],"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"}],"publication_status":"published","publication":"Nature Communications","title":"A biochemical network controlling basal myosin oscillation","_id":"401","ddc":["539","570"],"oa":1},{"intvolume":"       114","isi":1,"publist_id":"7403","month":"02","date_created":"2018-12-11T11:46:23Z","status":"public","issue":"4","volume":114,"publisher":"Biophysical Society","title":"Theory of eppithelial cell shape transitions induced by mechanoactive chemical gradients","publication":"Biophysical Journal","_id":"421","oa":1,"abstract":[{"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.","lang":"eng"}],"publication_status":"published","main_file_link":[{"url":"https://arxiv.org/abs/1709.01486","open_access":"1"}],"citation":{"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>.","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.","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.","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>","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>.","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>"},"quality_controlled":"1","author":[{"full_name":"Dasbiswas, Kinjal","last_name":"Dasbiswas","first_name":"Kinjal"},{"full_name":"Hannezo, Claude-Edouard B","orcid":"0000-0001-6005-1561","id":"3A9DB764-F248-11E8-B48F-1D18A9856A87","first_name":"Claude-Edouard B","last_name":"Hannezo"},{"full_name":"Gov, Nir","last_name":"Gov","first_name":"Nir"}],"year":"2018","scopus_import":"1","arxiv":1,"external_id":{"isi":["000428016700021"],"arxiv":["1709.01486"]},"date_published":"2018-02-27T00:00:00Z","page":"968 - 977","department":[{"_id":"EdHa"}],"doi":"10.1016/j.bpj.2017.12.022","language":[{"iso":"eng"}],"user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","article_processing_charge":"No","oa_version":"Submitted Version","type":"journal_article","date_updated":"2023-09-19T10:13:55Z","day":"27"},{"oa_version":"Published Version","date_updated":"2023-09-28T11:34:17Z","type":"journal_article","day":"21","user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","article_processing_charge":"No","department":[{"_id":"EdHa"}],"has_accepted_license":"1","doi":"10.1016/j.cell.2017.08.026","language":[{"iso":"eng"}],"file":[{"content_type":"application/pdf","creator":"system","file_size":12670204,"date_created":"2018-12-12T10:11:17Z","relation":"main_file","access_level":"open_access","checksum":"7a036d93a9e2e597af9bb504d6133aca","file_name":"IST-2017-883-v1+1_PIIS0092867417309510.pdf","date_updated":"2020-07-14T12:47:55Z","file_id":"4870"}],"external_id":{"isi":["000411331800024"]},"date_published":"2017-09-21T00:00:00Z","page":"242 - 255","scopus_import":"1","publication_identifier":{"issn":["00928674"]},"tmp":{"image":"/images/cc_by.png","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","short":"CC BY (4.0)","legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode"},"year":"2017","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>","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>.","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.","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>","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>.","short":"E.B. Hannezo, C. Scheele, M. Moad, N. Drogo, R. Heer, R. Sampogna, J. Van Rheenen, B. Simons, Cell 171 (2017) 242–255.","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."},"author":[{"full_name":"Hannezo, Edouard B","orcid":"0000-0001-6005-1561","id":"3A9DB764-F248-11E8-B48F-1D18A9856A87","first_name":"Edouard B","last_name":"Hannezo"},{"last_name":"Scheele","first_name":"Colinda","full_name":"Scheele, Colinda"},{"first_name":"Mohammad","last_name":"Moad","full_name":"Moad, Mohammad"},{"full_name":"Drogo, Nicholas","first_name":"Nicholas","last_name":"Drogo"},{"full_name":"Heer, Rakesh","first_name":"Rakesh","last_name":"Heer"},{"first_name":"Rosemary","last_name":"Sampogna","full_name":"Sampogna, Rosemary"},{"full_name":"Van Rheenen, Jacco","last_name":"Van Rheenen","first_name":"Jacco"},{"last_name":"Simons","first_name":"Benjamin","full_name":"Simons, Benjamin"}],"quality_controlled":"1","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"}],"publication_status":"published","publication":"Cell","title":"A unifying theory of branching morphogenesis","_id":"726","ddc":["539"],"oa":1,"file_date_updated":"2020-07-14T12:47:55Z","publisher":"Cell Press","pubrep_id":"883","volume":171,"issue":"1","month":"09","date_created":"2018-12-11T11:48:10Z","status":"public","intvolume":"       171","isi":1,"publist_id":"6952"}]