[{"related_material":{"record":[{"relation":"used_in_publication","id":"20","status":"public"}]},"citation":{"short":"J. Higareda Almaraz, M. Karbiener, M. Giroud, F. Pauler, T. Gerhalter, S. Herzig, M. Scheideler, (2018).","chicago":"Higareda Almaraz, Juan, Michael Karbiener, Maude Giroud, Florian Pauler, Teresa Gerhalter, Stephan Herzig, and Marcel Scheideler. “Additional File 3: Of Norepinephrine Triggers an Immediate-Early Regulatory Network Response in Primary Human White Adipocytes.” Springer Nature, 2018. <a href=\"https://doi.org/10.6084/m9.figshare.7295369.v1\">https://doi.org/10.6084/m9.figshare.7295369.v1</a>.","ieee":"J. Higareda Almaraz <i>et al.</i>, “Additional file 3: Of Norepinephrine triggers an immediate-early regulatory network response in primary human white adipocytes.” Springer Nature, 2018.","apa":"Higareda Almaraz, J., Karbiener, M., Giroud, M., Pauler, F., Gerhalter, T., Herzig, S., &#38; Scheideler, M. (2018). Additional file 3: Of Norepinephrine triggers an immediate-early regulatory network response in primary human white adipocytes. Springer Nature. <a href=\"https://doi.org/10.6084/m9.figshare.7295369.v1\">https://doi.org/10.6084/m9.figshare.7295369.v1</a>","mla":"Higareda Almaraz, Juan, et al. <i>Additional File 3: Of Norepinephrine Triggers an Immediate-Early Regulatory Network Response in Primary Human White Adipocytes</i>. Springer Nature, 2018, doi:<a href=\"https://doi.org/10.6084/m9.figshare.7295369.v1\">10.6084/m9.figshare.7295369.v1</a>.","ista":"Higareda Almaraz J, Karbiener M, Giroud M, Pauler F, Gerhalter T, Herzig S, Scheideler M. 2018. Additional file 3: Of Norepinephrine triggers an immediate-early regulatory network response in primary human white adipocytes, Springer Nature, <a href=\"https://doi.org/10.6084/m9.figshare.7295369.v1\">10.6084/m9.figshare.7295369.v1</a>.","ama":"Higareda Almaraz J, Karbiener M, Giroud M, et al. Additional file 3: Of Norepinephrine triggers an immediate-early regulatory network response in primary human white adipocytes. 2018. doi:<a href=\"https://doi.org/10.6084/m9.figshare.7295369.v1\">10.6084/m9.figshare.7295369.v1</a>"},"status":"public","date_published":"2018-11-03T00:00:00Z","doi":"10.6084/m9.figshare.7295369.v1","main_file_link":[{"url":"https://doi.org/10.6084/m9.figshare.7295369.v1","open_access":"1"}],"oa":1,"_id":"9808","article_processing_charge":"No","publisher":"Springer Nature","user_id":"6785fbc1-c503-11eb-8a32-93094b40e1cf","department":[{"_id":"SiHi"}],"year":"2018","title":"Additional file 3: Of Norepinephrine triggers an immediate-early regulatory network response in primary human white adipocytes","date_created":"2021-08-06T12:31:57Z","author":[{"full_name":"Higareda Almaraz, Juan","first_name":"Juan","last_name":"Higareda Almaraz"},{"first_name":"Michael","last_name":"Karbiener","full_name":"Karbiener, Michael"},{"first_name":"Maude","last_name":"Giroud","full_name":"Giroud, Maude"},{"last_name":"Pauler","first_name":"Florian","full_name":"Pauler, Florian","id":"48EA0138-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-7462-0048"},{"full_name":"Gerhalter, Teresa","last_name":"Gerhalter","first_name":"Teresa"},{"full_name":"Herzig, Stephan","last_name":"Herzig","first_name":"Stephan"},{"first_name":"Marcel","last_name":"Scheideler","full_name":"Scheideler, Marcel"}],"oa_version":"Published Version","type":"research_data_reference","month":"11","day":"03","date_updated":"2023-09-13T09:10:47Z","abstract":[{"text":"Table S4. Counts per Gene per Million Reads Mapped. (XLSX 2751 kb).","lang":"eng"}]},{"page":"3917 - 3931","author":[{"full_name":"Pfurr, Sabrina","last_name":"Pfurr","first_name":"Sabrina"},{"full_name":"Chu, Yu","first_name":"Yu","last_name":"Chu"},{"full_name":"Bohrer, Christian","first_name":"Christian","last_name":"Bohrer"},{"last_name":"Greulich","first_name":"Franziska","full_name":"Greulich, Franziska"},{"orcid":"0000-0002-8483-8753","id":"2E26DF60-F248-11E8-B48F-1D18A9856A87","full_name":"Beattie, Robert J","last_name":"Beattie","first_name":"Robert J"},{"first_name":"Könül","last_name":"Mammadzada","full_name":"Mammadzada, Könül"},{"full_name":"Hils, Miriam","last_name":"Hils","first_name":"Miriam"},{"full_name":"Arnold, Sebastian","first_name":"Sebastian","last_name":"Arnold"},{"full_name":"Taylor, Verdon","first_name":"Verdon","last_name":"Taylor"},{"full_name":"Schachtrup, Kristina","last_name":"Schachtrup","first_name":"Kristina"},{"first_name":"N Henriette","last_name":"Uhlenhaut","full_name":"Uhlenhaut, N Henriette"},{"first_name":"Christian","last_name":"Schachtrup","full_name":"Schachtrup, Christian"}],"day":"31","date_updated":"2023-09-26T16:20:09Z","abstract":[{"text":"During corticogenesis, distinct classes of neurons are born from progenitor cells located in the ventricular and subventricular zones, from where they migrate towards the pial surface to assemble into highly organized layer-specific circuits. However, the precise and coordinated transcriptional network activity defining neuronal identity is still not understood. Here, we show that genetic depletion of the basic helix-loop-helix (bHLH) transcription factor E2A splice variant E47 increased the number of Tbr1-positive deep layer and Satb2-positive upper layer neurons at E14.5, while depletion of the alternatively spliced E12 variant did not affect layer-specific neurogenesis. While ChIP-Seq identified a big overlap for E12- and E47-specific binding sites in embryonic NSCs, including sites at the cyclin-dependent kinase inhibitor (CDKI) Cdkn1c gene locus, RNA-Seq revealed a unique transcriptional regulation by each splice variant. E47 activated the expression of the CDKI Cdkn1c through binding to a distal enhancer. Finally, overexpression of E47 in embryonic NSCs in vitro impaired neurite outgrowth and E47 overexpression in vivo by in utero electroporation disturbed proper layer-specific neurogenesis and upregulated p57(KIP2) expression. Overall, this study identified E2A target genes in embryonic NSCs and demonstrates that E47 regulates neuronal differentiation via p57(KIP2).","lang":"eng"}],"oa_version":"None","month":"10","type":"journal_article","title":"The E2A splice variant E47 regulates the differentiation of projection neurons via p57(KIP2) during cortical development","volume":144,"date_created":"2018-12-11T11:48:36Z","publist_id":"6846","user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","publisher":"Company of Biologists","department":[{"_id":"SiHi"}],"year":"2017","publication":"Development","_id":"805","article_processing_charge":"No","scopus_import":"1","publication_status":"published","doi":"10.1242/dev.145698","date_published":"2017-10-31T00:00:00Z","quality_controlled":"1","external_id":{"isi":["000414025600007"]},"status":"public","intvolume":"       144","isi":1,"citation":{"ieee":"S. Pfurr <i>et al.</i>, “The E2A splice variant E47 regulates the differentiation of projection neurons via p57(KIP2) during cortical development,” <i>Development</i>, vol. 144. Company of Biologists, pp. 3917–3931, 2017.","chicago":"Pfurr, Sabrina, Yu Chu, Christian Bohrer, Franziska Greulich, Robert J Beattie, Könül Mammadzada, Miriam Hils, et al. “The E2A Splice Variant E47 Regulates the Differentiation of Projection Neurons via P57(KIP2) during Cortical Development.” <i>Development</i>. Company of Biologists, 2017. <a href=\"https://doi.org/10.1242/dev.145698\">https://doi.org/10.1242/dev.145698</a>.","short":"S. Pfurr, Y. Chu, C. Bohrer, F. Greulich, R.J. Beattie, K. Mammadzada, M. Hils, S. Arnold, V. Taylor, K. Schachtrup, N.H. Uhlenhaut, C. Schachtrup, Development 144 (2017) 3917–3931.","ama":"Pfurr S, Chu Y, Bohrer C, et al. The E2A splice variant E47 regulates the differentiation of projection neurons via p57(KIP2) during cortical development. <i>Development</i>. 2017;144:3917-3931. doi:<a href=\"https://doi.org/10.1242/dev.145698\">10.1242/dev.145698</a>","mla":"Pfurr, Sabrina, et al. “The E2A Splice Variant E47 Regulates the Differentiation of Projection Neurons via P57(KIP2) during Cortical Development.” <i>Development</i>, vol. 144, Company of Biologists, 2017, pp. 3917–31, doi:<a href=\"https://doi.org/10.1242/dev.145698\">10.1242/dev.145698</a>.","ista":"Pfurr S, Chu Y, Bohrer C, Greulich F, Beattie RJ, Mammadzada K, Hils M, Arnold S, Taylor V, Schachtrup K, Uhlenhaut NH, Schachtrup C. 2017. The E2A splice variant E47 regulates the differentiation of projection neurons via p57(KIP2) during cortical development. Development. 144, 3917–3931.","apa":"Pfurr, S., Chu, Y., Bohrer, C., Greulich, F., Beattie, R. J., Mammadzada, K., … Schachtrup, C. (2017). The E2A splice variant E47 regulates the differentiation of projection neurons via p57(KIP2) during cortical development. <i>Development</i>. Company of Biologists. <a href=\"https://doi.org/10.1242/dev.145698\">https://doi.org/10.1242/dev.145698</a>"},"language":[{"iso":"eng"}]},{"date_published":"2017-08-14T00:00:00Z","ddc":["576"],"has_accepted_license":"1","oa":1,"publication_status":"published","citation":{"ieee":"D. Andergassen <i>et al.</i>, “Mapping the mouse Allelome reveals tissue specific regulation of allelic expression,” <i>eLife</i>, vol. 6. eLife Sciences Publications, 2017.","chicago":"Andergassen, Daniel, Christoph Dotter, Dyniel Wenzel, Verena Sigl, Philipp Bammer, Markus Muckenhuber, Daniela Mayer, et al. “Mapping the Mouse Allelome Reveals Tissue Specific Regulation of Allelic Expression.” <i>ELife</i>. eLife Sciences Publications, 2017. <a href=\"https://doi.org/10.7554/eLife.25125\">https://doi.org/10.7554/eLife.25125</a>.","short":"D. Andergassen, C. Dotter, D. Wenzel, V. Sigl, P. Bammer, M. Muckenhuber, D. Mayer, T. Kulinski, H. Theussl, J. Penninger, C. Bock, D. Barlow, F. Pauler, Q. Hudson, ELife 6 (2017).","ama":"Andergassen D, Dotter C, Wenzel D, et al. Mapping the mouse Allelome reveals tissue specific regulation of allelic expression. <i>eLife</i>. 2017;6. doi:<a href=\"https://doi.org/10.7554/eLife.25125\">10.7554/eLife.25125</a>","mla":"Andergassen, Daniel, et al. “Mapping the Mouse Allelome Reveals Tissue Specific Regulation of Allelic Expression.” <i>ELife</i>, vol. 6, e25125, eLife Sciences Publications, 2017, doi:<a href=\"https://doi.org/10.7554/eLife.25125\">10.7554/eLife.25125</a>.","ista":"Andergassen D, Dotter C, Wenzel D, Sigl V, Bammer P, Muckenhuber M, Mayer D, Kulinski T, Theussl H, Penninger J, Bock C, Barlow D, Pauler F, Hudson Q. 2017. Mapping the mouse Allelome reveals tissue specific regulation of allelic expression. eLife. 6, e25125.","apa":"Andergassen, D., Dotter, C., Wenzel, D., Sigl, V., Bammer, P., Muckenhuber, M., … Hudson, Q. (2017). Mapping the mouse Allelome reveals tissue specific regulation of allelic expression. <i>ELife</i>. eLife Sciences Publications. <a href=\"https://doi.org/10.7554/eLife.25125\">https://doi.org/10.7554/eLife.25125</a>"},"intvolume":"         6","status":"public","file_date_updated":"2020-07-14T12:47:50Z","date_created":"2018-12-11T11:48:05Z","volume":6,"month":"08","type":"journal_article","oa_version":"Published Version","date_updated":"2021-01-12T08:11:57Z","abstract":[{"lang":"eng","text":"To determine the dynamics of allelic-specific expression during mouse development, we analyzed RNA-seq data from 23 F1 tissues from different developmental stages, including 19 female tissues allowing X chromosome inactivation (XCI) escapers to also be detected. We demonstrate that allelic expression arising from genetic or epigenetic differences is highly tissue-specific. We find that tissue-specific strain-biased gene expression may be regulated by tissue-specific enhancers or by post-transcriptional differences in stability between the alleles. We also find that escape from X-inactivation is tissue-specific, with leg muscle showing an unexpectedly high rate of XCI escapers. By surveying a range of tissues during development, and performing extensive validation, we are able to provide a high confidence list of mouse imprinted genes including 18 novel genes. This shows that cluster size varies dynamically during development and can be substantially larger than previously thought, with the Igf2r cluster extending over 10 Mb in placenta."}],"_id":"713","year":"2017","quality_controlled":"1","doi":"10.7554/eLife.25125","pubrep_id":"885","publication_identifier":{"issn":["2050084X"]},"language":[{"iso":"eng"}],"project":[{"_id":"25E9AF9E-B435-11E9-9278-68D0E5697425","call_identifier":"FWF","name":"Revealing the mechanisms underlying drug interactions","grant_number":"P27201-B22"}],"publist_id":"6971","article_number":"e25125","title":"Mapping the mouse Allelome reveals tissue specific regulation of allelic expression","day":"14","license":"https://creativecommons.org/licenses/by/4.0/","file":[{"date_updated":"2020-07-14T12:47:50Z","file_id":"5020","checksum":"1ace3462e64a971b9ead896091829549","date_created":"2018-12-12T10:13:36Z","access_level":"open_access","file_name":"IST-2017-885-v1+1_elife-25125-figures-v2.pdf","content_type":"application/pdf","relation":"main_file","file_size":6399510,"creator":"system"},{"file_name":"IST-2017-885-v1+2_elife-25125-v2.pdf","relation":"main_file","content_type":"application/pdf","file_size":4264398,"creator":"system","date_updated":"2020-07-14T12:47:50Z","file_id":"5021","checksum":"6241dc31eeb87b03facadec3a53a6827","date_created":"2018-12-12T10:13:36Z","access_level":"open_access"}],"author":[{"full_name":"Andergassen, Daniel","first_name":"Daniel","last_name":"Andergassen"},{"last_name":"Dotter","first_name":"Christoph","id":"4C66542E-F248-11E8-B48F-1D18A9856A87","full_name":"Dotter, Christoph"},{"first_name":"Dyniel","last_name":"Wenzel","full_name":"Wenzel, Dyniel"},{"full_name":"Sigl, Verena","first_name":"Verena","last_name":"Sigl"},{"full_name":"Bammer, Philipp","first_name":"Philipp","last_name":"Bammer"},{"full_name":"Muckenhuber, Markus","first_name":"Markus","last_name":"Muckenhuber"},{"last_name":"Mayer","first_name":"Daniela","full_name":"Mayer, Daniela"},{"last_name":"Kulinski","first_name":"Tomasz","full_name":"Kulinski, Tomasz"},{"full_name":"Theussl, Hans","first_name":"Hans","last_name":"Theussl"},{"first_name":"Josef","last_name":"Penninger","full_name":"Penninger, Josef"},{"first_name":"Christoph","last_name":"Bock","full_name":"Bock, Christoph"},{"last_name":"Barlow","first_name":"Denise","full_name":"Barlow, Denise"},{"full_name":"Pauler, Florian","id":"48EA0138-F248-11E8-B48F-1D18A9856A87","first_name":"Florian","last_name":"Pauler"},{"last_name":"Hudson","first_name":"Quanah","full_name":"Hudson, Quanah"}],"tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","image":"/images/cc_by.png","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","short":"CC BY (4.0)"},"scopus_import":1,"publication":"eLife","department":[{"_id":"GaNo"},{"_id":"SiHi"}],"user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","publisher":"eLife Sciences Publications"},{"project":[{"_id":"25D7962E-B435-11E9-9278-68D0E5697425","name":"Quantitative Structure-Function Analysis of Cerebral Cortex Assembly at Clonal Level","grant_number":"RGP0053/2014"},{"_id":"25D61E48-B435-11E9-9278-68D0E5697425","call_identifier":"FP7","name":"Molecular Mechanisms of Cerebral Cortex Development","grant_number":"618444"}],"language":[{"iso":"eng"}],"issue":"24","publication_identifier":{"issn":["00145793"]},"pubrep_id":"928","doi":"10.1002/1873-3468.12906","quality_controlled":"1","publisher":"Wiley-Blackwell","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","pmid":1,"department":[{"_id":"SiHi"}],"publication":"FEBS letters","article_processing_charge":"Yes (in subscription journal)","scopus_import":"1","ec_funded":1,"tmp":{"name":"Creative Commons Attribution-NonCommercial 4.0 International (CC BY-NC 4.0)","short":"CC BY-NC (4.0)","image":"/images/cc_by_nc.png","legal_code_url":"https://creativecommons.org/licenses/by-nc/4.0/legalcode"},"author":[{"id":"2E26DF60-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-8483-8753","full_name":"Beattie, Robert J","last_name":"Beattie","first_name":"Robert J"},{"last_name":"Hippenmeyer","first_name":"Simon","full_name":"Hippenmeyer, Simon","id":"37B36620-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0003-2279-1061"}],"license":"https://creativecommons.org/licenses/by-nc/4.0/","file":[{"access_level":"open_access","date_created":"2018-12-12T10:16:24Z","checksum":"a46dadc84e0c28d389dd3e9e954464db","file_id":"5211","date_updated":"2020-07-14T12:47:24Z","creator":"system","file_size":644149,"relation":"main_file","content_type":"application/pdf","file_name":"IST-2018-928-v1+1_Beattie_et_al-2017-FEBS_Letters.pdf"}],"day":"01","title":"Mechanisms of radial glia progenitor cell lineage progression","publist_id":"7183","external_id":{"pmid":["29121403"]},"status":"public","intvolume":"       591","citation":{"chicago":"Beattie, Robert J, and Simon Hippenmeyer. “Mechanisms of Radial Glia Progenitor Cell Lineage Progression.” <i>FEBS Letters</i>. Wiley-Blackwell, 2017. <a href=\"https://doi.org/10.1002/1873-3468.12906\">https://doi.org/10.1002/1873-3468.12906</a>.","ieee":"R. J. Beattie and S. Hippenmeyer, “Mechanisms of radial glia progenitor cell lineage progression,” <i>FEBS letters</i>, vol. 591, no. 24. Wiley-Blackwell, pp. 3993–4008, 2017.","short":"R.J. Beattie, S. Hippenmeyer, FEBS Letters 591 (2017) 3993–4008.","ama":"Beattie RJ, Hippenmeyer S. Mechanisms of radial glia progenitor cell lineage progression. <i>FEBS letters</i>. 2017;591(24):3993-4008. doi:<a href=\"https://doi.org/10.1002/1873-3468.12906\">10.1002/1873-3468.12906</a>","apa":"Beattie, R. J., &#38; Hippenmeyer, S. (2017). Mechanisms of radial glia progenitor cell lineage progression. <i>FEBS Letters</i>. Wiley-Blackwell. <a href=\"https://doi.org/10.1002/1873-3468.12906\">https://doi.org/10.1002/1873-3468.12906</a>","ista":"Beattie RJ, Hippenmeyer S. 2017. Mechanisms of radial glia progenitor cell lineage progression. FEBS letters. 591(24), 3993–4008.","mla":"Beattie, Robert J., and Simon Hippenmeyer. “Mechanisms of Radial Glia Progenitor Cell Lineage Progression.” <i>FEBS Letters</i>, vol. 591, no. 24, Wiley-Blackwell, 2017, pp. 3993–4008, doi:<a href=\"https://doi.org/10.1002/1873-3468.12906\">10.1002/1873-3468.12906</a>."},"oa":1,"publication_status":"published","has_accepted_license":"1","ddc":["571","610"],"date_published":"2017-12-01T00:00:00Z","year":"2017","_id":"621","page":"3993  - 4008","abstract":[{"lang":"eng","text":"The mammalian cerebral cortex is responsible for higher cognitive functions such as perception, consciousness, and acquiring and processing information. The neocortex is organized into six distinct laminae, each composed of a rich diversity of cell types which assemble into highly complex cortical circuits. Radial glia progenitors (RGPs) are responsible for producing all neocortical neurons and certain glia lineages. Here, we discuss recent discoveries emerging from clonal lineage analysis at the single RGP cell level that provide us with an inaugural quantitative framework of RGP lineage progression. We further discuss the importance of the relative contribution of intrinsic gene functions and non-cell-autonomous or community effects in regulating RGP proliferation behavior and lineage progression."}],"date_updated":"2024-02-14T12:02:08Z","month":"12","oa_version":"Published Version","type":"journal_article","volume":591,"file_date_updated":"2020-07-14T12:47:24Z","date_created":"2018-12-11T11:47:32Z"},{"isi":1,"language":[{"iso":"eng"}],"issue":"3","project":[{"grant_number":"618444","name":"Molecular Mechanisms of Cerebral Cortex Development","_id":"25D61E48-B435-11E9-9278-68D0E5697425","call_identifier":"FP7"},{"_id":"25D7962E-B435-11E9-9278-68D0E5697425","name":"Quantitative Structure-Function Analysis of Cerebral Cortex Assembly at Clonal Level","grant_number":"RGP0053/2014"}],"doi":"10.1016/j.neuron.2017.04.012","quality_controlled":"1","publication_identifier":{"issn":["08966273"]},"publication":"Neuron","scopus_import":"1","article_processing_charge":"No","ec_funded":1,"user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","publisher":"Cell Press","department":[{"_id":"SiHi"},{"_id":"MaJö"}],"title":"Mosaic analysis with double markers reveals distinct sequential functions of Lgl1 in neural stem cells","publist_id":"6473","author":[{"full_name":"Beattie, Robert J","orcid":"0000-0002-8483-8753","id":"2E26DF60-F248-11E8-B48F-1D18A9856A87","last_name":"Beattie","first_name":"Robert J"},{"id":"2C67902A-F248-11E8-B48F-1D18A9856A87","full_name":"Postiglione, Maria P","last_name":"Postiglione","first_name":"Maria P"},{"full_name":"Burnett, Laura","id":"3B717F68-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-8937-410X","last_name":"Burnett","first_name":"Laura"},{"last_name":"Laukoter","first_name":"Susanne","full_name":"Laukoter, Susanne","orcid":"0000-0002-7903-3010","id":"2D6B7A9A-F248-11E8-B48F-1D18A9856A87"},{"full_name":"Streicher, Carmen","id":"36BCB99C-F248-11E8-B48F-1D18A9856A87","last_name":"Streicher","first_name":"Carmen"},{"orcid":"0000-0002-7462-0048","id":"48EA0138-F248-11E8-B48F-1D18A9856A87","full_name":"Pauler, Florian","last_name":"Pauler","first_name":"Florian"},{"last_name":"Xiao","first_name":"Guanxi","full_name":"Xiao, Guanxi"},{"full_name":"Klezovitch, Olga","first_name":"Olga","last_name":"Klezovitch"},{"full_name":"Vasioukhin, Valeri","last_name":"Vasioukhin","first_name":"Valeri"},{"last_name":"Ghashghaei","first_name":"Troy","full_name":"Ghashghaei, Troy"},{"orcid":"0000-0003-2279-1061","id":"37B36620-F248-11E8-B48F-1D18A9856A87","full_name":"Hippenmeyer, Simon","last_name":"Hippenmeyer","first_name":"Simon"}],"day":"03","intvolume":"        94","citation":{"mla":"Beattie, Robert J., et al. “Mosaic Analysis with Double Markers Reveals Distinct Sequential Functions of Lgl1 in Neural Stem Cells.” <i>Neuron</i>, vol. 94, no. 3, Cell Press, 2017, p. 517–533.e3, doi:<a href=\"https://doi.org/10.1016/j.neuron.2017.04.012\">10.1016/j.neuron.2017.04.012</a>.","ista":"Beattie RJ, Postiglione MP, Burnett L, Laukoter S, Streicher C, Pauler F, Xiao G, Klezovitch O, Vasioukhin V, Ghashghaei T, Hippenmeyer S. 2017. Mosaic analysis with double markers reveals distinct sequential functions of Lgl1 in neural stem cells. Neuron. 94(3), 517–533.e3.","apa":"Beattie, R. J., Postiglione, M. P., Burnett, L., Laukoter, S., Streicher, C., Pauler, F., … Hippenmeyer, S. (2017). Mosaic analysis with double markers reveals distinct sequential functions of Lgl1 in neural stem cells. <i>Neuron</i>. Cell Press. <a href=\"https://doi.org/10.1016/j.neuron.2017.04.012\">https://doi.org/10.1016/j.neuron.2017.04.012</a>","ama":"Beattie RJ, Postiglione MP, Burnett L, et al. Mosaic analysis with double markers reveals distinct sequential functions of Lgl1 in neural stem cells. <i>Neuron</i>. 2017;94(3):517-533.e3. doi:<a href=\"https://doi.org/10.1016/j.neuron.2017.04.012\">10.1016/j.neuron.2017.04.012</a>","short":"R.J. Beattie, M.P. Postiglione, L. Burnett, S. Laukoter, C. Streicher, F. Pauler, G. Xiao, O. Klezovitch, V. Vasioukhin, T. Ghashghaei, S. Hippenmeyer, Neuron 94 (2017) 517–533.e3.","ieee":"R. J. Beattie <i>et al.</i>, “Mosaic analysis with double markers reveals distinct sequential functions of Lgl1 in neural stem cells,” <i>Neuron</i>, vol. 94, no. 3. Cell Press, p. 517–533.e3, 2017.","chicago":"Beattie, Robert J, Maria P Postiglione, Laura Burnett, Susanne Laukoter, Carmen Streicher, Florian Pauler, Guanxi Xiao, et al. “Mosaic Analysis with Double Markers Reveals Distinct Sequential Functions of Lgl1 in Neural Stem Cells.” <i>Neuron</i>. Cell Press, 2017. <a href=\"https://doi.org/10.1016/j.neuron.2017.04.012\">https://doi.org/10.1016/j.neuron.2017.04.012</a>."},"status":"public","external_id":{"isi":["000400466700011"]},"date_published":"2017-05-03T00:00:00Z","acknowledged_ssus":[{"_id":"Bio"},{"_id":"PreCl"}],"publication_status":"published","_id":"944","year":"2017","volume":94,"date_created":"2018-12-11T11:49:20Z","page":"517 - 533.e3","date_updated":"2023-09-26T15:37:02Z","abstract":[{"text":"The concerted production of neurons and glia by neural stem cells (NSCs) is essential for neural circuit assembly. In the developing cerebral cortex, radial glia progenitors (RGPs) generate nearly all neocortical neurons and certain glia lineages. RGP proliferation behavior shows a high degree of non-stochasticity, thus a deterministic characteristic of neuron and glia production. However, the cellular and molecular mechanisms controlling RGP behavior and proliferation dynamics in neurogenesis and glia generation remain unknown. By using mosaic analysis with double markers (MADM)-based genetic paradigms enabling the sparse and global knockout with unprecedented single-cell resolution, we identified Lgl1 as a critical regulatory component. We uncover Lgl1-dependent tissue-wide community effects required for embryonic cortical neurogenesis and novel cell-autonomous Lgl1 functions controlling RGP-mediated glia genesis and postnatal NSC behavior. These results suggest that NSC-mediated neuron and glia production is tightly regulated through the concerted interplay of sequential Lgl1-dependent global and cell intrinsic mechanisms.","lang":"eng"}],"oa_version":"None","type":"journal_article","month":"05"},{"project":[{"call_identifier":"FP7","_id":"25D61E48-B435-11E9-9278-68D0E5697425","name":"Molecular Mechanisms of Cerebral Cortex Development","grant_number":"618444"},{"_id":"25D7962E-B435-11E9-9278-68D0E5697425","name":"Quantitative Structure-Function Analysis of Cerebral Cortex Assembly at Clonal Level","grant_number":"RGP0053/2014"},{"grant_number":"291734","name":"International IST Postdoc Fellowship Programme","call_identifier":"FP7","_id":"25681D80-B435-11E9-9278-68D0E5697425"},{"grant_number":"T00817-B21","name":"The biochemical basis of PAR polarization","_id":"25985A36-B435-11E9-9278-68D0E5697425","call_identifier":"FWF"}],"language":[{"iso":"eng"}],"isi":1,"pubrep_id":"830","publication_identifier":{"issn":["16625102"]},"quality_controlled":"1","doi":"10.3389/fncel.2017.00176","department":[{"_id":"SiHi"},{"_id":"MaLo"}],"user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","publisher":"Frontiers Research Foundation","scopus_import":"1","ec_funded":1,"article_processing_charge":"Yes","tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","image":"/images/cc_by.png","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","short":"CC BY (4.0)"},"publication":"Frontiers in Cellular Neuroscience","day":"28","file":[{"checksum":"dc1f5a475b918d09a0f9f587400b1626","file_id":"4764","date_updated":"2020-07-14T12:48:16Z","access_level":"open_access","date_created":"2018-12-12T10:09:40Z","file_name":"IST-2017-830-v1+1_2017_Hansen_CellPolarity.pdf","creator":"system","file_size":2153858,"content_type":"application/pdf","relation":"main_file"}],"author":[{"id":"38853E16-F248-11E8-B48F-1D18A9856A87","full_name":"Hansen, Andi H","first_name":"Andi H","last_name":"Hansen"},{"first_name":"Christian F","last_name":"Düllberg","orcid":"0000-0001-6335-9748","id":"459064DC-F248-11E8-B48F-1D18A9856A87","full_name":"Düllberg, Christian F"},{"id":"34CAE85C-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0003-1919-7416","full_name":"Mieck, Christine","last_name":"Mieck","first_name":"Christine"},{"last_name":"Loose","first_name":"Martin","id":"462D4284-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0001-7309-9724","full_name":"Loose, Martin"},{"full_name":"Hippenmeyer, Simon","id":"37B36620-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0003-2279-1061","last_name":"Hippenmeyer","first_name":"Simon"}],"publist_id":"6445","title":"Cell polarity in cerebral cortex development - cellular architecture shaped by biochemical networks","article_number":"176","external_id":{"isi":["000404486700001"]},"status":"public","citation":{"mla":"Hansen, Andi H., et al. “Cell Polarity in Cerebral Cortex Development - Cellular Architecture Shaped by Biochemical Networks.” <i>Frontiers in Cellular Neuroscience</i>, vol. 11, 176, Frontiers Research Foundation, 2017, doi:<a href=\"https://doi.org/10.3389/fncel.2017.00176\">10.3389/fncel.2017.00176</a>.","ista":"Hansen AH, Düllberg CF, Mieck C, Loose M, Hippenmeyer S. 2017. Cell polarity in cerebral cortex development - cellular architecture shaped by biochemical networks. Frontiers in Cellular Neuroscience. 11, 176.","apa":"Hansen, A. H., Düllberg, C. F., Mieck, C., Loose, M., &#38; Hippenmeyer, S. (2017). Cell polarity in cerebral cortex development - cellular architecture shaped by biochemical networks. <i>Frontiers in Cellular Neuroscience</i>. Frontiers Research Foundation. <a href=\"https://doi.org/10.3389/fncel.2017.00176\">https://doi.org/10.3389/fncel.2017.00176</a>","ama":"Hansen AH, Düllberg CF, Mieck C, Loose M, Hippenmeyer S. Cell polarity in cerebral cortex development - cellular architecture shaped by biochemical networks. <i>Frontiers in Cellular Neuroscience</i>. 2017;11. doi:<a href=\"https://doi.org/10.3389/fncel.2017.00176\">10.3389/fncel.2017.00176</a>","short":"A.H. Hansen, C.F. Düllberg, C. Mieck, M. Loose, S. Hippenmeyer, Frontiers in Cellular Neuroscience 11 (2017).","ieee":"A. H. Hansen, C. F. Düllberg, C. Mieck, M. Loose, and S. Hippenmeyer, “Cell polarity in cerebral cortex development - cellular architecture shaped by biochemical networks,” <i>Frontiers in Cellular Neuroscience</i>, vol. 11. Frontiers Research Foundation, 2017.","chicago":"Hansen, Andi H, Christian F Düllberg, Christine Mieck, Martin Loose, and Simon Hippenmeyer. “Cell Polarity in Cerebral Cortex Development - Cellular Architecture Shaped by Biochemical Networks.” <i>Frontiers in Cellular Neuroscience</i>. Frontiers Research Foundation, 2017. <a href=\"https://doi.org/10.3389/fncel.2017.00176\">https://doi.org/10.3389/fncel.2017.00176</a>."},"intvolume":"        11","related_material":{"record":[{"relation":"dissertation_contains","status":"public","id":"9962"}]},"has_accepted_license":"1","publication_status":"published","oa":1,"date_published":"2017-06-28T00:00:00Z","ddc":["570"],"year":"2017","_id":"960","abstract":[{"text":"The human cerebral cortex is the seat of our cognitive abilities and composed of an extraordinary number of neurons, organized in six distinct layers. The establishment of specific morphological and physiological features in individual neurons needs to be regulated with high precision. Impairments in the sequential developmental programs instructing corticogenesis lead to alterations in the cortical cytoarchitecture which is thought to represent the major underlying cause for several neurological disorders including neurodevelopmental and psychiatric diseases. In this review we discuss the role of cell polarity at sequential stages during cortex development. We first provide an overview of morphological cell polarity features in cortical neural stem cells and newly-born postmitotic neurons. We then synthesize a conceptual molecular and biochemical framework how cell polarity is established at the cellular level through a break in symmetry in nascent cortical projection neurons. Lastly we provide a perspective how the molecular mechanisms applying to single cells could be probed and integrated in an in vivo and tissue-wide context.","lang":"eng"}],"date_updated":"2024-03-25T23:30:23Z","oa_version":"Published Version","month":"06","type":"journal_article","date_created":"2018-12-11T11:49:25Z","file_date_updated":"2020-07-14T12:48:16Z","volume":11},{"publication_identifier":{"issn":["09646906"]},"doi":"10.1093/hmg/ddw383","quality_controlled":"1","isi":1,"language":[{"iso":"eng"}],"issue":"2","author":[{"full_name":"Breuss, Martin","first_name":"Martin","last_name":"Breuss"},{"full_name":"Nguyen, Thai","last_name":"Nguyen","first_name":"Thai"},{"full_name":"Srivatsan, Anjana","last_name":"Srivatsan","first_name":"Anjana"},{"full_name":"Leca, Ines","first_name":"Ines","last_name":"Leca"},{"first_name":"Guoling","last_name":"Tian","full_name":"Tian, Guoling"},{"first_name":"Tanja","last_name":"Fritz","full_name":"Fritz, Tanja"},{"full_name":"Hansen, Andi H","id":"38853E16-F248-11E8-B48F-1D18A9856A87","first_name":"Andi H","last_name":"Hansen"},{"full_name":"Musaev, Damir","first_name":"Damir","last_name":"Musaev"},{"full_name":"Mcevoy Venneri, Jennifer","first_name":"Jennifer","last_name":"Mcevoy Venneri"},{"last_name":"Kiely","first_name":"James","full_name":"Kiely, James"},{"full_name":"Rosti, Rasim","first_name":"Rasim","last_name":"Rosti"},{"full_name":"Scott, Eric","last_name":"Scott","first_name":"Eric"},{"full_name":"Tan, Uner","last_name":"Tan","first_name":"Uner"},{"full_name":"Kolodner, Richard","first_name":"Richard","last_name":"Kolodner"},{"full_name":"Cowan, Nicholas","last_name":"Cowan","first_name":"Nicholas"},{"last_name":"Keays","first_name":"David","full_name":"Keays, David"},{"first_name":"Joseph","last_name":"Gleeson","full_name":"Gleeson, Joseph"}],"day":"01","title":"Uner Tan syndrome caused by a homozygous TUBB2B mutation affecting microtubule stability","publist_id":"6379","publisher":"Oxford University Press","user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","department":[{"_id":"SiHi"}],"publication":"Human Molecular Genetics","article_processing_charge":"No","scopus_import":"1","publication_status":"published","date_published":"2017-01-01T00:00:00Z","external_id":{"isi":["000397066400002"]},"status":"public","intvolume":"        26","citation":{"ieee":"M. Breuss <i>et al.</i>, “Uner Tan syndrome caused by a homozygous TUBB2B mutation affecting microtubule stability,” <i>Human Molecular Genetics</i>, vol. 26, no. 2. Oxford University Press, pp. 258–269, 2017.","chicago":"Breuss, Martin, Thai Nguyen, Anjana Srivatsan, Ines Leca, Guoling Tian, Tanja Fritz, Andi H Hansen, et al. “Uner Tan Syndrome Caused by a Homozygous TUBB2B Mutation Affecting Microtubule Stability.” <i>Human Molecular Genetics</i>. Oxford University Press, 2017. <a href=\"https://doi.org/10.1093/hmg/ddw383\">https://doi.org/10.1093/hmg/ddw383</a>.","short":"M. Breuss, T. Nguyen, A. Srivatsan, I. Leca, G. Tian, T. Fritz, A.H. Hansen, D. Musaev, J. Mcevoy Venneri, J. Kiely, R. Rosti, E. Scott, U. Tan, R. Kolodner, N. Cowan, D. Keays, J. Gleeson, Human Molecular Genetics 26 (2017) 258–269.","ama":"Breuss M, Nguyen T, Srivatsan A, et al. Uner Tan syndrome caused by a homozygous TUBB2B mutation affecting microtubule stability. <i>Human Molecular Genetics</i>. 2017;26(2):258-269. doi:<a href=\"https://doi.org/10.1093/hmg/ddw383\">10.1093/hmg/ddw383</a>","mla":"Breuss, Martin, et al. “Uner Tan Syndrome Caused by a Homozygous TUBB2B Mutation Affecting Microtubule Stability.” <i>Human Molecular Genetics</i>, vol. 26, no. 2, Oxford University Press, 2017, pp. 258–69, doi:<a href=\"https://doi.org/10.1093/hmg/ddw383\">10.1093/hmg/ddw383</a>.","ista":"Breuss M, Nguyen T, Srivatsan A, Leca I, Tian G, Fritz T, Hansen AH, Musaev D, Mcevoy Venneri J, Kiely J, Rosti R, Scott E, Tan U, Kolodner R, Cowan N, Keays D, Gleeson J. 2017. Uner Tan syndrome caused by a homozygous TUBB2B mutation affecting microtubule stability. Human Molecular Genetics. 26(2), 258–269.","apa":"Breuss, M., Nguyen, T., Srivatsan, A., Leca, I., Tian, G., Fritz, T., … Gleeson, J. (2017). Uner Tan syndrome caused by a homozygous TUBB2B mutation affecting microtubule stability. <i>Human Molecular Genetics</i>. Oxford University Press. <a href=\"https://doi.org/10.1093/hmg/ddw383\">https://doi.org/10.1093/hmg/ddw383</a>"},"page":"258 - 269","abstract":[{"lang":"eng","text":"The integrity and dynamic properties of the microtubule cytoskeleton are indispensable for the development of the mammalian brain. Consequently, mutations in the genes that encode the structural component (the α/β-tubulin heterodimer) can give rise to severe, sporadic neurodevelopmental disorders. These are commonly referred to as the tubulinopathies. Here we report the addition of recessive quadrupedalism, also known as Uner Tan syndrome (UTS), to the growing list of diseases caused by tubulin variants. Analysis of a consanguineous UTS family identified a biallelic TUBB2B mutation, resulting in a p.R390Q amino acid substitution. In addition to the identifying quadrupedal locomotion, all three patients showed severe cerebellar hypoplasia. None, however, displayed the basal ganglia malformations typically associated with TUBB2B mutations. Functional analysis of the R390Q substitution revealed that it did not affect the ability of β-tubulin to fold or become assembled into the α/β-heterodimer, nor did it influence the incorporation of mutant-containing heterodimers into microtubule polymers. The 390Q mutation in S. cerevisiae TUB2 did not affect growth under basal conditions, but did result in increased sensitivity to microtubule-depolymerizing drugs, indicative of a mild impact of this mutation on microtubule function. The TUBB2B mutation described here represents an unusual recessive mode of inheritance for missense-mediated tubulinopathies and reinforces the sensitivity of the developing cerebellum to microtubule defects."}],"date_updated":"2023-09-22T09:42:42Z","type":"journal_article","oa_version":"None","month":"01","volume":26,"date_created":"2018-12-11T11:49:42Z","year":"2017","_id":"1016"},{"external_id":{"isi":["000415140700007"]},"status":"public","citation":{"short":"M. Breuss, I. Leca, T. Gstrein, A.H. Hansen, D. Keays, Molecular and Cellular Neuroscience 84 (2017) 58–67.","ieee":"M. Breuss, I. Leca, T. Gstrein, A. H. Hansen, and D. Keays, “Tubulins and brain development: The origins of functional specification,” <i>Molecular and Cellular Neuroscience</i>, vol. 84. Academic Press, pp. 58–67, 2017.","chicago":"Breuss, Martin, Ines Leca, Thomas Gstrein, Andi H Hansen, and David Keays. “Tubulins and Brain Development: The Origins of Functional Specification.” <i>Molecular and Cellular Neuroscience</i>. Academic Press, 2017. <a href=\"https://doi.org/10.1016/j.mcn.2017.03.002\">https://doi.org/10.1016/j.mcn.2017.03.002</a>.","ista":"Breuss M, Leca I, Gstrein T, Hansen AH, Keays D. 2017. Tubulins and brain development: The origins of functional specification. Molecular and Cellular Neuroscience. 84, 58–67.","mla":"Breuss, Martin, et al. “Tubulins and Brain Development: The Origins of Functional Specification.” <i>Molecular and Cellular Neuroscience</i>, vol. 84, Academic Press, 2017, pp. 58–67, doi:<a href=\"https://doi.org/10.1016/j.mcn.2017.03.002\">10.1016/j.mcn.2017.03.002</a>.","apa":"Breuss, M., Leca, I., Gstrein, T., Hansen, A. H., &#38; Keays, D. (2017). Tubulins and brain development: The origins of functional specification. <i>Molecular and Cellular Neuroscience</i>. Academic Press. <a href=\"https://doi.org/10.1016/j.mcn.2017.03.002\">https://doi.org/10.1016/j.mcn.2017.03.002</a>","ama":"Breuss M, Leca I, Gstrein T, Hansen AH, Keays D. Tubulins and brain development: The origins of functional specification. <i>Molecular and Cellular Neuroscience</i>. 2017;84:58-67. doi:<a href=\"https://doi.org/10.1016/j.mcn.2017.03.002\">10.1016/j.mcn.2017.03.002</a>"},"intvolume":"        84","has_accepted_license":"1","oa":1,"publication_status":"published","ddc":["571"],"date_published":"2017-10-01T00:00:00Z","year":"2017","_id":"1017","date_updated":"2023-09-22T09:42:15Z","abstract":[{"text":"The development of the vertebrate central nervous system is reliant on a complex cascade of biological processes that include mitotic division, relocation of migrating neurons, and the extension of dendritic and axonal processes. Each of these cellular events requires the diverse functional repertoire of the microtubule cytoskeleton for the generation of forces, assembly of macromolecular complexes and transport of molecules and organelles. The tubulins are a multi-gene family that encode for the constituents of microtubules, and have been implicated in a spectrum of neurological disorders. Evidence is building that different tubulins tune the functional properties of the microtubule cytoskeleton dependent on the cell type, developmental profile and subcellular localisation. Here we review of the origins of the functional specification of the tubulin gene family in the developing brain at a transcriptional, translational, and post-transcriptional level. We remind the reader that tubulins are not just loading controls for your average Western blot.","lang":"eng"}],"month":"10","type":"journal_article","oa_version":"Published Version","page":"58 - 67","date_created":"2018-12-11T11:49:42Z","file_date_updated":"2018-12-12T10:09:19Z","volume":84,"language":[{"iso":"eng"}],"isi":1,"pubrep_id":"806","publication_identifier":{"issn":["10447431"]},"quality_controlled":"1","doi":"10.1016/j.mcn.2017.03.002","department":[{"_id":"SiHi"}],"publisher":"Academic Press","user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","article_processing_charge":"No","scopus_import":"1","tmp":{"name":"Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0)","short":"CC BY-NC-ND (4.0)","image":"/images/cc_by_nc_nd.png","legal_code_url":"https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode"},"publication":"Molecular and Cellular Neuroscience","file":[{"date_updated":"2018-12-12T10:09:19Z","file_id":"4742","date_created":"2018-12-12T10:09:19Z","access_level":"open_access","file_name":"IST-2017-806-v1+2_1-s2.0-S1044743116302500-main_1_.pdf","content_type":"application/pdf","relation":"main_file","file_size":1436377,"creator":"system"}],"license":"https://creativecommons.org/licenses/by-nc-nd/4.0/","day":"01","author":[{"full_name":"Breuss, Martin","last_name":"Breuss","first_name":"Martin"},{"full_name":"Leca, Ines","last_name":"Leca","first_name":"Ines"},{"first_name":"Thomas","last_name":"Gstrein","full_name":"Gstrein, Thomas"},{"first_name":"Andi H","last_name":"Hansen","full_name":"Hansen, Andi H","id":"38853E16-F248-11E8-B48F-1D18A9856A87"},{"first_name":"David","last_name":"Keays","full_name":"Keays, David"}],"publist_id":"6377","title":"Tubulins and brain development: The origins of functional specification"},{"citation":{"ama":"Riccio P, Cebrián C, Zong H, Hippenmeyer S, Costantini F. Data from: Ret and Etv4 promote directed movements of progenitor cells during renal branching morphogenesis. 2017. doi:<a href=\"https://doi.org/10.5061/dryad.pk16b\">10.5061/dryad.pk16b</a>","mla":"Riccio, Paul, et al. <i>Data from: Ret and Etv4 Promote Directed Movements of Progenitor Cells during Renal Branching Morphogenesis</i>. Dryad, 2017, doi:<a href=\"https://doi.org/10.5061/dryad.pk16b\">10.5061/dryad.pk16b</a>.","ista":"Riccio P, Cebrián C, Zong H, Hippenmeyer S, Costantini F. 2017. Data from: Ret and Etv4 promote directed movements of progenitor cells during renal branching morphogenesis, Dryad, <a href=\"https://doi.org/10.5061/dryad.pk16b\">10.5061/dryad.pk16b</a>.","apa":"Riccio, P., Cebrián, C., Zong, H., Hippenmeyer, S., &#38; Costantini, F. (2017). Data from: Ret and Etv4 promote directed movements of progenitor cells during renal branching morphogenesis. Dryad. <a href=\"https://doi.org/10.5061/dryad.pk16b\">https://doi.org/10.5061/dryad.pk16b</a>","ieee":"P. Riccio, C. Cebrián, H. Zong, S. Hippenmeyer, and F. Costantini, “Data from: Ret and Etv4 promote directed movements of progenitor cells during renal branching morphogenesis.” Dryad, 2017.","chicago":"Riccio, Paul, Christina Cebrián, Hui Zong, Simon Hippenmeyer, and Frank Costantini. “Data from: Ret and Etv4 Promote Directed Movements of Progenitor Cells during Renal Branching Morphogenesis.” Dryad, 2017. <a href=\"https://doi.org/10.5061/dryad.pk16b\">https://doi.org/10.5061/dryad.pk16b</a>.","short":"P. Riccio, C. Cebrián, H. Zong, S. Hippenmeyer, F. Costantini, (2017)."},"related_material":{"record":[{"relation":"used_in_publication","id":"9702","status":"deleted"}]},"status":"public","main_file_link":[{"url":"https://doi.org/10.5061/dryad.pk16b","open_access":"1"}],"date_published":"2017-01-14T00:00:00Z","doi":"10.5061/dryad.pk16b","oa":1,"article_processing_charge":"No","_id":"9707","year":"2017","department":[{"_id":"SiHi"}],"publisher":"Dryad","user_id":"6785fbc1-c503-11eb-8a32-93094b40e1cf","date_created":"2021-07-23T09:39:34Z","title":"Data from: Ret and Etv4 promote directed movements of progenitor cells during renal branching morphogenesis","month":"01","type":"research_data_reference","oa_version":"Published Version","day":"14","abstract":[{"lang":"eng","text":"Branching morphogenesis of the epithelial ureteric bud forms the renal collecting duct system and is critical for normal nephron number, while low nephron number is implicated in hypertension and renal disease. Ureteric bud growth and branching requires GDNF signaling from the surrounding mesenchyme to cells at the ureteric bud tips, via the Ret receptor tyrosine kinase and coreceptor Gfrα1; Ret signaling up-regulates transcription factors Etv4 and Etv5, which are also critical for branching. Despite extensive knowledge of the genetic control of these events, it is not understood, at the cellular level, how renal branching morphogenesis is achieved or how Ret signaling influences epithelial cell behaviors to promote this process. Analysis of chimeric embryos previously suggested a role for Ret signaling in promoting cell rearrangements in the nephric duct, but this method was unsuited to study individual cell behaviors during ureteric bud branching. Here, we use Mosaic Analysis with Double Markers (MADM), combined with organ culture and time-lapse imaging, to trace the movements and divisions of individual ureteric bud tip cells. We first examine wild-type clones and then Ret or Etv4 mutant/wild-type clones in which the mutant and wild-type sister cells are differentially and heritably marked by green and red fluorescent proteins. We find that, in normal kidneys, most individual tip cells behave as self-renewing progenitors, some of whose progeny remain at the tips while others populate the growing UB trunks. In Ret or Etv4 MADM clones, the wild-type cells generated at a UB tip are much more likely to remain at, or move to, the new tips during branching and elongation, while their Ret−/− or Etv4−/− sister cells tend to lag behind and contribute only to the trunks. By tracking successive mitoses in a cell lineage, we find that Ret signaling has little effect on proliferation, in contrast to its effects on cell movement. Our results show that Ret/Etv4 signaling promotes directed cell movements in the ureteric bud tips, and suggest a model in which these cell movements mediate branching morphogenesis."}],"date_updated":"2022-08-25T13:34:55Z","author":[{"first_name":"Paul","last_name":"Riccio","full_name":"Riccio, Paul"},{"full_name":"Cebrián, Christina","first_name":"Christina","last_name":"Cebrián"},{"full_name":"Zong, Hui","first_name":"Hui","last_name":"Zong"},{"last_name":"Hippenmeyer","first_name":"Simon","full_name":"Hippenmeyer, Simon","orcid":"0000-0003-2279-1061","id":"37B36620-F248-11E8-B48F-1D18A9856A87"},{"last_name":"Costantini","first_name":"Frank","full_name":"Costantini, Frank"}]},{"volume":14,"file_date_updated":"2020-07-14T12:44:57Z","date_created":"2018-12-11T11:52:19Z","date_updated":"2023-02-23T10:01:08Z","abstract":[{"lang":"eng","text":"Branching morphogenesis of the epithelial ureteric bud forms the renal collecting duct system and is critical for normal nephron number, while low nephron number is implicated in hypertension and renal disease. Ureteric bud growth and branching requires GDNF signaling from the surrounding mesenchyme to cells at the ureteric bud tips, via the Ret receptor tyrosine kinase and coreceptor Gfrα1; Ret signaling up-regulates transcription factors Etv4 and Etv5, which are also critical for branching. Despite extensive knowledge of the genetic control of these events, it is not understood, at the cellular level, how renal branching morphogenesis is achieved or how Ret signaling influences epithelial cell behaviors to promote this process. Analysis of chimeric embryos previously suggested a role for Ret signaling in promoting cell rearrangements in the nephric duct, but this method was unsuited to study individual cell behaviors during ureteric bud branching. Here, we use Mosaic Analysis with Double Markers (MADM), combined with organ culture and time-lapse imaging, to trace the movements and divisions of individual ureteric bud tip cells. We first examine wild-type clones and then Ret or Etv4 mutant/wild-type clones in which the mutant and wild-type sister cells are differentially and heritably marked by green and red fluorescent proteins. We find that, in normal kidneys, most individual tip cells behave as self-renewing progenitors, some of whose progeny remain at the tips while others populate the growing UB trunks. In Ret or Etv4 MADM clones, the wild-type cells generated at a UB tip are much more likely to remain at, or move to, the new tips during branching and elongation, while their Ret−/− or Etv4−/− sister cells tend to lag behind and contribute only to the trunks. By tracking successive mitoses in a cell lineage, we find that Ret signaling has little effect on proliferation, in contrast to its effects on cell movement. Our results show that Ret/Etv4 signaling promotes directed cell movements in the ureteric bud tips, and suggest a model in which these cell movements mediate branching morphogenesis."}],"month":"02","oa_version":"Published Version","type":"journal_article","_id":"1488","acknowledgement":"We thank Silvia Arber, Thomas Jessell, Kenneth M. Murphy, Carlton Bates, Hideki Enomoto, Liqun Luo and Andrew McMahon for mouse strains; Thomas Jessell for antibodies; and Laura Martinez Prat for experimental assistance.","year":"2016","ddc":["570"],"date_published":"2016-02-19T00:00:00Z","publication_status":"published","oa":1,"has_accepted_license":"1","intvolume":"        14","related_material":{"record":[{"relation":"research_data","id":"9703","status":"deleted"}]},"citation":{"ama":"Riccio P, Cebrián C, Zong H, Hippenmeyer S, Costantini F. Ret and Etv4 promote directed movements of progenitor cells during renal branching morphogenesis. <i>PLoS Biology</i>. 2016;14(2). doi:<a href=\"https://doi.org/10.1371/journal.pbio.1002382\">10.1371/journal.pbio.1002382</a>","apa":"Riccio, P., Cebrián, C., Zong, H., Hippenmeyer, S., &#38; Costantini, F. (2016). Ret and Etv4 promote directed movements of progenitor cells during renal branching morphogenesis. <i>PLoS Biology</i>. Public Library of Science. <a href=\"https://doi.org/10.1371/journal.pbio.1002382\">https://doi.org/10.1371/journal.pbio.1002382</a>","ista":"Riccio P, Cebrián C, Zong H, Hippenmeyer S, Costantini F. 2016. Ret and Etv4 promote directed movements of progenitor cells during renal branching morphogenesis. PLoS Biology. 14(2), e1002382.","mla":"Riccio, Paul, et al. “Ret and Etv4 Promote Directed Movements of Progenitor Cells during Renal Branching Morphogenesis.” <i>PLoS Biology</i>, vol. 14, no. 2, e1002382, Public Library of Science, 2016, doi:<a href=\"https://doi.org/10.1371/journal.pbio.1002382\">10.1371/journal.pbio.1002382</a>.","chicago":"Riccio, Paul, Cristina Cebrián, Hui Zong, Simon Hippenmeyer, and Frank Costantini. “Ret and Etv4 Promote Directed Movements of Progenitor Cells during Renal Branching Morphogenesis.” <i>PLoS Biology</i>. Public Library of Science, 2016. <a href=\"https://doi.org/10.1371/journal.pbio.1002382\">https://doi.org/10.1371/journal.pbio.1002382</a>.","ieee":"P. Riccio, C. Cebrián, H. Zong, S. Hippenmeyer, and F. Costantini, “Ret and Etv4 promote directed movements of progenitor cells during renal branching morphogenesis,” <i>PLoS Biology</i>, vol. 14, no. 2. Public Library of Science, 2016.","short":"P. Riccio, C. Cebrián, H. Zong, S. Hippenmeyer, F. Costantini, PLoS Biology 14 (2016)."},"status":"public","title":"Ret and Etv4 promote directed movements of progenitor cells during renal branching morphogenesis","article_number":"e1002382","publist_id":"5699","author":[{"full_name":"Riccio, Paul","first_name":"Paul","last_name":"Riccio"},{"full_name":"Cebrián, Cristina","first_name":"Cristina","last_name":"Cebrián"},{"last_name":"Zong","first_name":"Hui","full_name":"Zong, Hui"},{"full_name":"Hippenmeyer, Simon","orcid":"0000-0003-2279-1061","id":"37B36620-F248-11E8-B48F-1D18A9856A87","last_name":"Hippenmeyer","first_name":"Simon"},{"full_name":"Costantini, Frank","last_name":"Costantini","first_name":"Frank"}],"file":[{"date_created":"2018-12-12T10:13:42Z","access_level":"open_access","date_updated":"2020-07-14T12:44:57Z","file_id":"5027","checksum":"7f8fa1b3a29f94c0a14dd4465278cdbc","relation":"main_file","content_type":"application/pdf","file_size":5904773,"creator":"system","file_name":"IST-2016-517-v1+1_journal.pbio.1002382_1_.PDF"}],"day":"19","publication":"PLoS Biology","scopus_import":1,"tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","image":"/images/cc_by.png","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","short":"CC BY (4.0)"},"user_id":"3E5EF7F0-F248-11E8-B48F-1D18A9856A87","publisher":"Public Library of Science","department":[{"_id":"SiHi"}],"doi":"10.1371/journal.pbio.1002382","quality_controlled":"1","pubrep_id":"517","language":[{"iso":"eng"}],"issue":"2"},{"date_created":"2018-12-11T11:50:35Z","publist_id":"6172","volume":36,"title":"Neural stem cells to cerebral cortex: Emerging mechanisms regulating progenitor behavior and productivity","day":"09","abstract":[{"text":"This review accompanies a 2016 SFN mini-symposium presenting examples of current studies that address a central question: How do neural stem cells (NSCs) divide in different ways to produce heterogeneous daughter types at the right time and in proper numbers to build a cerebral cortex with the appropriate size and structure? We will focus on four aspects of corticogenesis: cytokinesis events that follow apical mitoses of NSCs; coordinating abscission with delamination from the apical membrane; timing of neurogenesis and its indirect regulation through emergence of intermediate progenitors; and capacity of single NSCs to generate the correct number and laminar fate of cortical neurons. Defects in these mechanisms can cause microcephaly and other brain malformations, and understanding them is critical to designing diagnostic tools and preventive and corrective therapies.","lang":"eng"}],"date_updated":"2021-01-12T06:48:54Z","oa_version":"None","type":"journal_article","month":"11","page":"11394 - 11401","author":[{"last_name":"Dwyer","first_name":"Noelle","full_name":"Dwyer, Noelle"},{"last_name":"Chen","first_name":"Bin","full_name":"Chen, Bin"},{"full_name":"Chou, Shen","first_name":"Shen","last_name":"Chou"},{"full_name":"Hippenmeyer, Simon","orcid":"0000-0003-2279-1061","id":"37B36620-F248-11E8-B48F-1D18A9856A87","last_name":"Hippenmeyer","first_name":"Simon"},{"last_name":"Nguyen","first_name":"Laurent","full_name":"Nguyen, Laurent"},{"full_name":"Ghashghaei, Troy","last_name":"Ghashghaei","first_name":"Troy"}],"scopus_import":1,"publication":"Journal of Neuroscience","_id":"1181","department":[{"_id":"SiHi"}],"year":"2016","user_id":"3E5EF7F0-F248-11E8-B48F-1D18A9856A87","publisher":"Society for Neuroscience","acknowledgement":"This work was supported by National Institutes of Health Grants R01NS089795 and R01NS098370 to H.T.G., R01NS076640 to N.D.D., and R01MH094589 and R01NS089777 to B.C., Academia Sinica AS-104-TPB09-2 to S.-J.C, European Union FP7-CIG618444 and Human Frontiers Science Program RGP0053 to S.H., and Fonds Léon Fredericq, from the Fondation Médicale Reine Elisabeth, and from the Fonation Simone et Pierre Clerdent to L.N. The authors apologize to colleagues whose work could not be cited due to space limitations.","quality_controlled":"1","doi":"10.1523/JNEUROSCI.2359-16.2016","date_published":"2016-11-09T00:00:00Z","publication_status":"published","citation":{"ama":"Dwyer N, Chen B, Chou S, Hippenmeyer S, Nguyen L, Ghashghaei T. Neural stem cells to cerebral cortex: Emerging mechanisms regulating progenitor behavior and productivity. <i>Journal of Neuroscience</i>. 2016;36(45):11394-11401. doi:<a href=\"https://doi.org/10.1523/JNEUROSCI.2359-16.2016\">10.1523/JNEUROSCI.2359-16.2016</a>","mla":"Dwyer, Noelle, et al. “Neural Stem Cells to Cerebral Cortex: Emerging Mechanisms Regulating Progenitor Behavior and Productivity.” <i>Journal of Neuroscience</i>, vol. 36, no. 45, Society for Neuroscience, 2016, pp. 11394–401, doi:<a href=\"https://doi.org/10.1523/JNEUROSCI.2359-16.2016\">10.1523/JNEUROSCI.2359-16.2016</a>.","ista":"Dwyer N, Chen B, Chou S, Hippenmeyer S, Nguyen L, Ghashghaei T. 2016. Neural stem cells to cerebral cortex: Emerging mechanisms regulating progenitor behavior and productivity. Journal of Neuroscience. 36(45), 11394–11401.","apa":"Dwyer, N., Chen, B., Chou, S., Hippenmeyer, S., Nguyen, L., &#38; Ghashghaei, T. (2016). Neural stem cells to cerebral cortex: Emerging mechanisms regulating progenitor behavior and productivity. <i>Journal of Neuroscience</i>. Society for Neuroscience. <a href=\"https://doi.org/10.1523/JNEUROSCI.2359-16.2016\">https://doi.org/10.1523/JNEUROSCI.2359-16.2016</a>","ieee":"N. Dwyer, B. Chen, S. Chou, S. Hippenmeyer, L. Nguyen, and T. Ghashghaei, “Neural stem cells to cerebral cortex: Emerging mechanisms regulating progenitor behavior and productivity,” <i>Journal of Neuroscience</i>, vol. 36, no. 45. Society for Neuroscience, pp. 11394–11401, 2016.","chicago":"Dwyer, Noelle, Bin Chen, Shen Chou, Simon Hippenmeyer, Laurent Nguyen, and Troy Ghashghaei. “Neural Stem Cells to Cerebral Cortex: Emerging Mechanisms Regulating Progenitor Behavior and Productivity.” <i>Journal of Neuroscience</i>. Society for Neuroscience, 2016. <a href=\"https://doi.org/10.1523/JNEUROSCI.2359-16.2016\">https://doi.org/10.1523/JNEUROSCI.2359-16.2016</a>.","short":"N. Dwyer, B. Chen, S. Chou, S. Hippenmeyer, L. Nguyen, T. Ghashghaei, Journal of Neuroscience 36 (2016) 11394–11401."},"language":[{"iso":"eng"}],"issue":"45","intvolume":"        36","status":"public","project":[{"grant_number":"RGP0053/2014","_id":"25D7962E-B435-11E9-9278-68D0E5697425","name":"Quantitative Structure-Function Analysis of Cerebral Cortex Assembly at Clonal Level"}]},{"publication_status":"published","oa":1,"date_published":"2015-09-02T00:00:00Z","main_file_link":[{"open_access":"1","url":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4560602/"}],"external_id":{"pmid":["26299473"]},"status":"public","intvolume":"        87","citation":{"mla":"Mayer, Christian, et al. “Clonally Related Forebrain Interneurons Disperse Broadly across Both Functional Areas and Structural Boundaries.” <i>Neuron</i>, vol. 87, no. 5, Elsevier, 2015, pp. 989–98, doi:<a href=\"https://doi.org/10.1016/j.neuron.2015.07.011\">10.1016/j.neuron.2015.07.011</a>.","ista":"Mayer C, Jaglin X, Cobbs L, Bandler R, Streicher C, Cepko C, Hippenmeyer S, Fishell G. 2015. Clonally related forebrain interneurons disperse broadly across both functional areas and structural boundaries. Neuron. 87(5), 989–998.","apa":"Mayer, C., Jaglin, X., Cobbs, L., Bandler, R., Streicher, C., Cepko, C., … Fishell, G. (2015). Clonally related forebrain interneurons disperse broadly across both functional areas and structural boundaries. <i>Neuron</i>. Elsevier. <a href=\"https://doi.org/10.1016/j.neuron.2015.07.011\">https://doi.org/10.1016/j.neuron.2015.07.011</a>","ama":"Mayer C, Jaglin X, Cobbs L, et al. Clonally related forebrain interneurons disperse broadly across both functional areas and structural boundaries. <i>Neuron</i>. 2015;87(5):989-998. doi:<a href=\"https://doi.org/10.1016/j.neuron.2015.07.011\">10.1016/j.neuron.2015.07.011</a>","short":"C. Mayer, X. Jaglin, L. Cobbs, R. Bandler, C. Streicher, C. Cepko, S. Hippenmeyer, G. Fishell, Neuron 87 (2015) 989–998.","ieee":"C. Mayer <i>et al.</i>, “Clonally related forebrain interneurons disperse broadly across both functional areas and structural boundaries,” <i>Neuron</i>, vol. 87, no. 5. Elsevier, pp. 989–998, 2015.","chicago":"Mayer, Christian, Xavier Jaglin, Lucy Cobbs, Rachel Bandler, Carmen Streicher, Constance Cepko, Simon Hippenmeyer, and Gord Fishell. “Clonally Related Forebrain Interneurons Disperse Broadly across Both Functional Areas and Structural Boundaries.” <i>Neuron</i>. Elsevier, 2015. <a href=\"https://doi.org/10.1016/j.neuron.2015.07.011\">https://doi.org/10.1016/j.neuron.2015.07.011</a>."},"page":"989 - 998","abstract":[{"lang":"eng","text":"The medial ganglionic eminence (MGE) gives rise to the majority of mouse forebrain interneurons. Here, we examine the lineage relationship among MGE-derived interneurons using a replication-defective retroviral library containing a highly diverse set of DNA barcodes. Recovering the barcodes from the mature progeny of infected progenitor cells enabled us to unambiguously determine their respective lineal relationship. We found that clonal dispersion occurs across large areas of the brain and is not restricted by anatomical divisions. As such, sibling interneurons can populate the cortex, hippocampus striatum, and globus pallidus. The majority of interneurons appeared to be generated from asymmetric divisions of MGE progenitor cells, followed by symmetric divisions within the subventricular zone. Altogether, our findings uncover that lineage relationships do not appear to determine interneuron allocation to particular regions. As such, it is likely that clonally related interneurons have considerable flexibility as to the particular forebrain circuits to which they can contribute."}],"date_updated":"2021-01-12T06:51:32Z","type":"journal_article","oa_version":"Submitted Version","month":"09","volume":87,"date_created":"2018-12-11T11:52:40Z","acknowledgement":"Research in the G.F. laboratory is supported by NIH (NS 081297, MH095147, and P01NS074972) and the Simons Foundation. Research in the S.H. laboratory is supported by the European Union (FP7-CIG618444). C.M. is supported by EMBO ALTF (1295-2012). X.H.J. is supported by EMBO (ALTF 303-2010) and HFSP (LT000078/2011-L).\r\n\r\n","year":"2015","_id":"1550","doi":"10.1016/j.neuron.2015.07.011","quality_controlled":"1","language":[{"iso":"eng"}],"issue":"5","author":[{"full_name":"Mayer, Christian","last_name":"Mayer","first_name":"Christian"},{"first_name":"Xavier","last_name":"Jaglin","full_name":"Jaglin, Xavier"},{"first_name":"Lucy","last_name":"Cobbs","full_name":"Cobbs, Lucy"},{"first_name":"Rachel","last_name":"Bandler","full_name":"Bandler, Rachel"},{"id":"36BCB99C-F248-11E8-B48F-1D18A9856A87","full_name":"Streicher, Carmen","first_name":"Carmen","last_name":"Streicher"},{"first_name":"Constance","last_name":"Cepko","full_name":"Cepko, Constance"},{"orcid":"0000-0003-2279-1061","id":"37B36620-F248-11E8-B48F-1D18A9856A87","full_name":"Hippenmeyer, Simon","first_name":"Simon","last_name":"Hippenmeyer"},{"full_name":"Fishell, Gord","first_name":"Gord","last_name":"Fishell"}],"day":"02","title":"Clonally related forebrain interneurons disperse broadly across both functional areas and structural boundaries","publist_id":"5621","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","publisher":"Elsevier","pmid":1,"department":[{"_id":"SiHi"}],"publication":"Neuron","scopus_import":1},{"issue":"8","language":[{"iso":"eng"}],"doi":"10.1038/ncb3001","quality_controlled":"1","publisher":"Nature Publishing Group","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","department":[{"_id":"SiHi"}],"pmid":1,"publication":"Nature Cell Biology","article_type":"original","article_processing_charge":"No","scopus_import":1,"author":[{"full_name":"Williams, Scott","last_name":"Williams","first_name":"Scott"},{"full_name":"Ratliff, Lyndsay","first_name":"Lyndsay","last_name":"Ratliff"},{"full_name":"Postiglione, Maria P","id":"2C67902A-F248-11E8-B48F-1D18A9856A87","first_name":"Maria P","last_name":"Postiglione"},{"full_name":"Knoblich, Juergen","last_name":"Knoblich","first_name":"Juergen"},{"last_name":"Fuchs","first_name":"Elaine","full_name":"Fuchs, Elaine"}],"day":"13","title":"Par3-mInsc and Gα i3 cooperate to promote oriented epidermal cell divisions through LGN","publist_id":"5196","status":"public","external_id":{"pmid":["25016959"]},"intvolume":"        16","citation":{"apa":"Williams, S., Ratliff, L., Postiglione, M. P., Knoblich, J., &#38; Fuchs, E. (2014). Par3-mInsc and Gα i3 cooperate to promote oriented epidermal cell divisions through LGN. <i>Nature Cell Biology</i>. Nature Publishing Group. <a href=\"https://doi.org/10.1038/ncb3001\">https://doi.org/10.1038/ncb3001</a>","ista":"Williams S, Ratliff L, Postiglione MP, Knoblich J, Fuchs E. 2014. Par3-mInsc and Gα i3 cooperate to promote oriented epidermal cell divisions through LGN. Nature Cell Biology. 16(8), 758–769.","mla":"Williams, Scott, et al. “Par3-MInsc and Gα I3 Cooperate to Promote Oriented Epidermal Cell Divisions through LGN.” <i>Nature Cell Biology</i>, vol. 16, no. 8, Nature Publishing Group, 2014, pp. 758–69, doi:<a href=\"https://doi.org/10.1038/ncb3001\">10.1038/ncb3001</a>.","ama":"Williams S, Ratliff L, Postiglione MP, Knoblich J, Fuchs E. Par3-mInsc and Gα i3 cooperate to promote oriented epidermal cell divisions through LGN. <i>Nature Cell Biology</i>. 2014;16(8):758-769. doi:<a href=\"https://doi.org/10.1038/ncb3001\">10.1038/ncb3001</a>","short":"S. Williams, L. Ratliff, M.P. Postiglione, J. Knoblich, E. Fuchs, Nature Cell Biology 16 (2014) 758–769.","chicago":"Williams, Scott, Lyndsay Ratliff, Maria P Postiglione, Juergen Knoblich, and Elaine Fuchs. “Par3-MInsc and Gα I3 Cooperate to Promote Oriented Epidermal Cell Divisions through LGN.” <i>Nature Cell Biology</i>. Nature Publishing Group, 2014. <a href=\"https://doi.org/10.1038/ncb3001\">https://doi.org/10.1038/ncb3001</a>.","ieee":"S. Williams, L. Ratliff, M. P. Postiglione, J. Knoblich, and E. Fuchs, “Par3-mInsc and Gα i3 cooperate to promote oriented epidermal cell divisions through LGN,” <i>Nature Cell Biology</i>, vol. 16, no. 8. Nature Publishing Group, pp. 758–769, 2014."},"oa":1,"publication_status":"published","date_published":"2014-07-13T00:00:00Z","main_file_link":[{"url":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4159251/","open_access":"1"}],"year":"2014","_id":"1899","page":"758 - 769","month":"07","type":"journal_article","oa_version":"Submitted Version","date_updated":"2021-01-12T06:53:55Z","abstract":[{"text":"Asymmetric cell divisions allow stem cells to balance proliferation and differentiation. During embryogenesis, murine epidermis expands rapidly from a single layer of unspecified basal layer progenitors to a stratified, differentiated epithelium. Morphogenesis involves perpendicular (asymmetric) divisions and the spindle orientation protein LGN, but little is known about how the apical localization of LGN is regulated. Here, we combine conventional genetics and lentiviral-mediated in vivo RNAi to explore the functions of the LGN-interacting proteins Par3, mInsc and Gα i3. Whereas loss of each gene alone leads to randomized division angles, combined loss of Gnai3 and mInsc causes a phenotype of mostly planar divisions, akin to loss of LGN. These findings lend experimental support for the hitherto untested model that Par3-mInsc and Gα i3 act cooperatively to polarize LGN and promote perpendicular divisions. Finally, we uncover a developmental switch between delamination-driven early stratification and spindle-orientation-dependent differentiation that occurs around E15, revealing a two-step mechanism underlying epidermal maturation.","lang":"eng"}],"volume":16,"date_created":"2018-12-11T11:54:36Z"},{"publication_status":"published","quality_controlled":"1","doi":"10.1073/pnas.1408233111","date_published":"2014-06-17T00:00:00Z","status":"public","issue":"24","language":[{"iso":"eng"}],"citation":{"apa":"Ali, S., Hippenmeyer, S., Saadat, L., Luo, L., Weissman, I., &#38; Ardehali, R. (2014). Existing cardiomyocytes generate cardiomyocytes at a low rate after birth in mice. <i>PNAS</i>. National Academy of Sciences. <a href=\"https://doi.org/10.1073/pnas.1408233111\">https://doi.org/10.1073/pnas.1408233111</a>","ista":"Ali S, Hippenmeyer S, Saadat L, Luo L, Weissman I, Ardehali R. 2014. Existing cardiomyocytes generate cardiomyocytes at a low rate after birth in mice. PNAS. 111(24), 8850–8855.","mla":"Ali, Shah, et al. “Existing Cardiomyocytes Generate Cardiomyocytes at a Low Rate after Birth in Mice.” <i>PNAS</i>, vol. 111, no. 24, National Academy of Sciences, 2014, pp. 8850–55, doi:<a href=\"https://doi.org/10.1073/pnas.1408233111\">10.1073/pnas.1408233111</a>.","ama":"Ali S, Hippenmeyer S, Saadat L, Luo L, Weissman I, Ardehali R. Existing cardiomyocytes generate cardiomyocytes at a low rate after birth in mice. <i>PNAS</i>. 2014;111(24):8850-8855. doi:<a href=\"https://doi.org/10.1073/pnas.1408233111\">10.1073/pnas.1408233111</a>","short":"S. Ali, S. Hippenmeyer, L. Saadat, L. Luo, I. Weissman, R. Ardehali, PNAS 111 (2014) 8850–8855.","chicago":"Ali, Shah, Simon Hippenmeyer, Lily Saadat, Liqun Luo, Irving Weissman, and Reza Ardehali. “Existing Cardiomyocytes Generate Cardiomyocytes at a Low Rate after Birth in Mice.” <i>PNAS</i>. National Academy of Sciences, 2014. <a href=\"https://doi.org/10.1073/pnas.1408233111\">https://doi.org/10.1073/pnas.1408233111</a>.","ieee":"S. Ali, S. Hippenmeyer, L. Saadat, L. Luo, I. Weissman, and R. Ardehali, “Existing cardiomyocytes generate cardiomyocytes at a low rate after birth in mice,” <i>PNAS</i>, vol. 111, no. 24. National Academy of Sciences, pp. 8850–8855, 2014."},"intvolume":"       111","oa_version":"None","month":"06","type":"journal_article","day":"17","date_updated":"2021-01-12T06:54:46Z","abstract":[{"text":"The mammalian heart has long been considered a postmitotic organ, implying that the total number of cardiomyocytes is set at birth. Analysis of cell division in the mammalian heart is complicated by cardiomyocyte binucleation shortly after birth, which makes it challenging to interpret traditional assays of cell turnover [Laflamme MA, Murray CE (2011) Nature 473(7347):326–335; Bergmann O, et al. (2009) Science 324(5923):98–102]. An elegant multi-isotope imaging-mass spectrometry technique recently calculated the low, discrete rate of cardiomyocyte generation in mice [Senyo SE, et al. (2013) Nature 493(7432):433–436], yet our cellular-level understanding of postnatal cardiomyogenesis remains limited. Herein, we provide a new line of evidence for the differentiated α-myosin heavy chain-expressing cardiomyocyte as the cell of origin of postnatal cardiomyogenesis using the “mosaic analysis with double markers” mouse model. We show limited, life-long, symmetric division of cardiomyocytes as a rare event that is evident in utero but significantly diminishes after the first month of life in mice; daughter cardiomyocytes divide very seldom, which this study is the first to demonstrate, to our knowledge. Furthermore, ligation of the left anterior descending coronary artery, which causes a myocardial infarction in the mosaic analysis with double-marker mice, did not increase the rate of cardiomyocyte division above the basal level for up to 4 wk after the injury. The clonal analysis described here provides direct evidence of postnatal mammalian cardiomyogenesis.","lang":"eng"}],"page":"8850 - 8855","author":[{"full_name":"Ali, Shah","first_name":"Shah","last_name":"Ali"},{"id":"37B36620-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0003-2279-1061","full_name":"Hippenmeyer, Simon","first_name":"Simon","last_name":"Hippenmeyer"},{"last_name":"Saadat","first_name":"Lily","full_name":"Saadat, Lily"},{"full_name":"Luo, Liqun","first_name":"Liqun","last_name":"Luo"},{"full_name":"Weissman, Irving","last_name":"Weissman","first_name":"Irving"},{"full_name":"Ardehali, Reza","last_name":"Ardehali","first_name":"Reza"}],"date_created":"2018-12-11T11:55:15Z","publist_id":"5052","title":"Existing cardiomyocytes generate cardiomyocytes at a low rate after birth in mice","volume":111,"year":"2014","department":[{"_id":"SiHi"}],"user_id":"4435EBFC-F248-11E8-B48F-1D18A9856A87","publisher":"National Academy of Sciences","scopus_import":1,"_id":"2020","publication":"PNAS"},{"doi":"10.1126/science.1258996","date_published":"2014-10-31T00:00:00Z","quality_controlled":"1","main_file_link":[{"open_access":"1","url":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4631524/"}],"oa":1,"publication_status":"published","intvolume":"       346","issue":"6209","language":[{"iso":"eng"}],"citation":{"short":"J. William, S. Hippenmeyer, L. Luo, Science 346 (2014) 626–629.","chicago":"William, Joo, Simon Hippenmeyer, and Liqun Luo. “Dendrite Morphogenesis Depends on Relative Levels of NT-3/TrkC Signaling.” <i>Science</i>. American Association for the Advancement of Science, 2014. <a href=\"https://doi.org/10.1126/science.1258996\">https://doi.org/10.1126/science.1258996</a>.","ieee":"J. William, S. Hippenmeyer, and L. Luo, “Dendrite morphogenesis depends on relative levels of NT-3/TrkC signaling,” <i>Science</i>, vol. 346, no. 6209. American Association for the Advancement of Science, pp. 626–629, 2014.","apa":"William, J., Hippenmeyer, S., &#38; Luo, L. (2014). Dendrite morphogenesis depends on relative levels of NT-3/TrkC signaling. <i>Science</i>. American Association for the Advancement of Science. <a href=\"https://doi.org/10.1126/science.1258996\">https://doi.org/10.1126/science.1258996</a>","mla":"William, Joo, et al. “Dendrite Morphogenesis Depends on Relative Levels of NT-3/TrkC Signaling.” <i>Science</i>, vol. 346, no. 6209, American Association for the Advancement of Science, 2014, pp. 626–29, doi:<a href=\"https://doi.org/10.1126/science.1258996\">10.1126/science.1258996</a>.","ista":"William J, Hippenmeyer S, Luo L. 2014. Dendrite morphogenesis depends on relative levels of NT-3/TrkC signaling. Science. 346(6209), 626–629.","ama":"William J, Hippenmeyer S, Luo L. Dendrite morphogenesis depends on relative levels of NT-3/TrkC signaling. <i>Science</i>. 2014;346(6209):626-629. doi:<a href=\"https://doi.org/10.1126/science.1258996\">10.1126/science.1258996</a>"},"status":"public","title":"Dendrite morphogenesis depends on relative levels of NT-3/TrkC signaling","volume":346,"publist_id":"5051","date_created":"2018-12-11T11:55:15Z","page":"626 - 629","author":[{"first_name":"Joo","last_name":"William","full_name":"William, Joo"},{"first_name":"Simon","last_name":"Hippenmeyer","full_name":"Hippenmeyer, Simon","id":"37B36620-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0003-2279-1061"},{"full_name":"Luo, Liqun","last_name":"Luo","first_name":"Liqun"}],"oa_version":"Submitted Version","month":"10","type":"journal_article","day":"31","date_updated":"2021-01-12T06:54:47Z","abstract":[{"lang":"eng","text":"Neurotrophins regulate diverse aspects of neuronal development and plasticity, but their precise in vivo functions during neural circuit assembly in the central brain remain unclear. We show that the neurotrophin receptor tropomyosin-related kinase C (TrkC) is required for dendritic growth and branching of mouse cerebellar Purkinje cells. Sparse TrkC knockout reduced dendrite complexity, but global Purkinje cell knockout had no effect. Removal of the TrkC ligand neurotrophin-3 (NT-3) from cerebellar granule cells, which provide major afferent input to developing Purkinje cell dendrites, rescued the dendrite defects caused by sparse TrkC disruption in Purkinje cells. Our data demonstrate that NT-3 from presynaptic neurons (granule cells) is required for TrkC-dependent competitive dendrite morphogenesis in postsynaptic neurons (Purkinje cells)—a previously unknown mechanism of neural circuit development."}],"_id":"2021","publication":"Science","scopus_import":1,"user_id":"4435EBFC-F248-11E8-B48F-1D18A9856A87","publisher":"American Association for the Advancement of Science","year":"2014","department":[{"_id":"SiHi"}]},{"project":[{"grant_number":"618444","name":"Molecular Mechanisms of Cerebral Cortex Development","call_identifier":"FP7","_id":"25D61E48-B435-11E9-9278-68D0E5697425"},{"_id":"25D7962E-B435-11E9-9278-68D0E5697425","name":"Quantitative Structure-Function Analysis of Cerebral Cortex Assembly at Clonal Level","grant_number":"RGP0053/2014"}],"issue":"4","language":[{"iso":"eng"}],"pubrep_id":"423","doi":"10.1016/j.cell.2014.10.027","quality_controlled":"1","publisher":"Cell Press","user_id":"4435EBFC-F248-11E8-B48F-1D18A9856A87","department":[{"_id":"SiHi"},{"_id":"Bio"}],"publication":"Cell","tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","image":"/images/cc_by.png","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","short":"CC BY (4.0)"},"ec_funded":1,"scopus_import":1,"author":[{"first_name":"Peng","last_name":"Gao","full_name":"Gao, Peng"},{"full_name":"Postiglione, Maria P","id":"2C67902A-F248-11E8-B48F-1D18A9856A87","first_name":"Maria P","last_name":"Postiglione"},{"full_name":"Krieger, Teresa","first_name":"Teresa","last_name":"Krieger"},{"last_name":"Hernandez","first_name":"Luisirene","full_name":"Hernandez, Luisirene"},{"first_name":"Chao","last_name":"Wang","full_name":"Wang, Chao"},{"full_name":"Han, Zhi","first_name":"Zhi","last_name":"Han"},{"last_name":"Streicher","first_name":"Carmen","full_name":"Streicher, Carmen","id":"36BCB99C-F248-11E8-B48F-1D18A9856A87"},{"id":"41DB591E-F248-11E8-B48F-1D18A9856A87","full_name":"Papusheva, Ekaterina","last_name":"Papusheva","first_name":"Ekaterina"},{"full_name":"Insolera, Ryan","first_name":"Ryan","last_name":"Insolera"},{"first_name":"Kritika","last_name":"Chugh","full_name":"Chugh, Kritika"},{"full_name":"Kodish, Oren","last_name":"Kodish","first_name":"Oren"},{"last_name":"Huang","first_name":"Kun","full_name":"Huang, Kun"},{"full_name":"Simons, Benjamin","first_name":"Benjamin","last_name":"Simons"},{"full_name":"Luo, Liqun","last_name":"Luo","first_name":"Liqun"},{"full_name":"Hippenmeyer, Simon","id":"37B36620-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0003-2279-1061","first_name":"Simon","last_name":"Hippenmeyer"},{"last_name":"Shi","first_name":"Song","full_name":"Shi, Song"}],"day":"06","file":[{"file_name":"IST-2016-423-v1+1_1-s2.0-S0092867414013154-main.pdf","file_size":4435787,"relation":"main_file","content_type":"application/pdf","creator":"system","file_id":"4709","date_updated":"2020-07-14T12:45:25Z","checksum":"6c5de8329bb2ffa71cba9fda750f14ce","date_created":"2018-12-12T10:08:47Z","access_level":"open_access"}],"title":"Deterministic progenitor behavior and unitary production of neurons in the neocortex","publist_id":"5050","status":"public","intvolume":"       159","citation":{"chicago":"Gao, Peng, Maria P Postiglione, Teresa Krieger, Luisirene Hernandez, Chao Wang, Zhi Han, Carmen Streicher, et al. “Deterministic Progenitor Behavior and Unitary Production of Neurons in the Neocortex.” <i>Cell</i>. Cell Press, 2014. <a href=\"https://doi.org/10.1016/j.cell.2014.10.027\">https://doi.org/10.1016/j.cell.2014.10.027</a>.","ieee":"P. Gao <i>et al.</i>, “Deterministic progenitor behavior and unitary production of neurons in the neocortex,” <i>Cell</i>, vol. 159, no. 4. Cell Press, pp. 775–788, 2014.","short":"P. Gao, M.P. Postiglione, T. Krieger, L. Hernandez, C. Wang, Z. Han, C. Streicher, E. Papusheva, R. Insolera, K. Chugh, O. Kodish, K. Huang, B. Simons, L. Luo, S. Hippenmeyer, S. Shi, Cell 159 (2014) 775–788.","ama":"Gao P, Postiglione MP, Krieger T, et al. Deterministic progenitor behavior and unitary production of neurons in the neocortex. <i>Cell</i>. 2014;159(4):775-788. doi:<a href=\"https://doi.org/10.1016/j.cell.2014.10.027\">10.1016/j.cell.2014.10.027</a>","apa":"Gao, P., Postiglione, M. P., Krieger, T., Hernandez, L., Wang, C., Han, Z., … Shi, S. (2014). Deterministic progenitor behavior and unitary production of neurons in the neocortex. <i>Cell</i>. Cell Press. <a href=\"https://doi.org/10.1016/j.cell.2014.10.027\">https://doi.org/10.1016/j.cell.2014.10.027</a>","mla":"Gao, Peng, et al. “Deterministic Progenitor Behavior and Unitary Production of Neurons in the Neocortex.” <i>Cell</i>, vol. 159, no. 4, Cell Press, 2014, pp. 775–88, doi:<a href=\"https://doi.org/10.1016/j.cell.2014.10.027\">10.1016/j.cell.2014.10.027</a>.","ista":"Gao P, Postiglione MP, Krieger T, Hernandez L, Wang C, Han Z, Streicher C, Papusheva E, Insolera R, Chugh K, Kodish O, Huang K, Simons B, Luo L, Hippenmeyer S, Shi S. 2014. Deterministic progenitor behavior and unitary production of neurons in the neocortex. Cell. 159(4), 775–788."},"publication_status":"published","oa":1,"has_accepted_license":"1","ddc":["570"],"date_published":"2014-11-06T00:00:00Z","year":"2014","_id":"2022","page":"775 - 788","type":"journal_article","month":"11","oa_version":"Published Version","date_updated":"2021-01-12T06:54:47Z","abstract":[{"text":"Radial glial progenitors (RGPs) are responsible for producing nearly all neocortical neurons. To gain insight into the patterns of RGP division and neuron production, we quantitatively analyzed excitatory neuron genesis in the mouse neocortex using Mosaic Analysis with Double Markers, which provides single-cell resolution of progenitor division patterns and potential in vivo. We found that RGPs progress through a coherent program in which their proliferative potential diminishes in a predictable manner. Upon entry into the neurogenic phase, individual RGPs produce ∼8–9 neurons distributed in both deep and superficial layers, indicating a unitary output in neuronal production. Removal of OTX1, a transcription factor transiently expressed in RGPs, results in both deep- and superficial-layer neuron loss and a reduction in neuronal unit size. Moreover, ∼1/6 of neurogenic RGPs proceed to produce glia. These results suggest that progenitor behavior and histogenesis in the mammalian neocortex conform to a remarkably orderly and deterministic program.","lang":"eng"}],"volume":159,"file_date_updated":"2020-07-14T12:45:25Z","date_created":"2018-12-11T11:55:16Z"},{"project":[{"grant_number":"618444","_id":"25D61E48-B435-11E9-9278-68D0E5697425","call_identifier":"FP7","name":"Molecular Mechanisms of Cerebral Cortex Development"}],"language":[{"iso":"eng"}],"issue":"3","pubrep_id":"528","publication_identifier":{"issn":["1479-6708"],"eissn":["1748-6971"]},"quality_controlled":"1","doi":"10.2217/fnl.14.18","department":[{"_id":"SiHi"}],"publisher":"Future Science Group","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","scopus_import":"1","ec_funded":1,"article_processing_charge":"No","tmp":{"name":"Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0)","short":"CC BY-NC-ND (4.0)","image":"/images/cc_by_nc_nd.png","legal_code_url":"https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode"},"publication":"Future Neurology","file":[{"file_name":"IST-2016-528-v1+1_fnl.14.18.pdf","file_size":3848424,"content_type":"application/pdf","relation":"main_file","creator":"system","file_id":"4812","date_updated":"2020-07-14T12:45:31Z","checksum":"ba06659ecadabceec9a37dd8c4586dce","date_created":"2018-12-12T10:10:25Z","access_level":"open_access"}],"day":"01","author":[{"id":"2C67902A-F248-11E8-B48F-1D18A9856A87","full_name":"Postiglione, Maria P","last_name":"Postiglione","first_name":"Maria P"},{"first_name":"Simon","last_name":"Hippenmeyer","id":"37B36620-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0003-2279-1061","full_name":"Hippenmeyer, Simon"}],"publist_id":"4806","title":"Monitoring neurogenesis in the cerebral cortex: an update","status":"public","citation":{"chicago":"Postiglione, Maria P, and Simon Hippenmeyer. “Monitoring Neurogenesis in the Cerebral Cortex: An Update.” <i>Future Neurology</i>. Future Science Group, 2014. <a href=\"https://doi.org/10.2217/fnl.14.18\">https://doi.org/10.2217/fnl.14.18</a>.","ieee":"M. P. Postiglione and S. Hippenmeyer, “Monitoring neurogenesis in the cerebral cortex: an update,” <i>Future Neurology</i>, vol. 9, no. 3. Future Science Group, pp. 323–340, 2014.","short":"M.P. Postiglione, S. Hippenmeyer, Future Neurology 9 (2014) 323–340.","ama":"Postiglione MP, Hippenmeyer S. Monitoring neurogenesis in the cerebral cortex: an update. <i>Future Neurology</i>. 2014;9(3):323-340. doi:<a href=\"https://doi.org/10.2217/fnl.14.18\">10.2217/fnl.14.18</a>","apa":"Postiglione, M. P., &#38; Hippenmeyer, S. (2014). Monitoring neurogenesis in the cerebral cortex: an update. <i>Future Neurology</i>. Future Science Group. <a href=\"https://doi.org/10.2217/fnl.14.18\">https://doi.org/10.2217/fnl.14.18</a>","mla":"Postiglione, Maria P., and Simon Hippenmeyer. “Monitoring Neurogenesis in the Cerebral Cortex: An Update.” <i>Future Neurology</i>, vol. 9, no. 3, Future Science Group, 2014, pp. 323–40, doi:<a href=\"https://doi.org/10.2217/fnl.14.18\">10.2217/fnl.14.18</a>.","ista":"Postiglione MP, Hippenmeyer S. 2014. Monitoring neurogenesis in the cerebral cortex: an update. Future Neurology. 9(3), 323–340."},"intvolume":"         9","has_accepted_license":"1","publication_status":"published","oa":1,"date_published":"2014-05-01T00:00:00Z","ddc":["570"],"year":"2014","_id":"2175","date_updated":"2023-10-17T08:34:27Z","abstract":[{"lang":"eng","text":"The cerebral cortex, the seat of our cognitive abilities, is composed of an intricate network of billions of excitatory projection and inhibitory interneurons. Postmitotic cortical neurons are generated by a diverse set of neural stem cell progenitors within dedicated zones and defined periods of neurogenesis during embryonic development. Disruptions in neurogenesis can lead to alterations in the neuronal cytoarchitecture, which is thought to represent a major underlying cause for several neurological disorders, including microcephaly, autism and epilepsy. Although a number of signaling pathways regulating neurogenesis have been described, the precise cellular and molecular mechanisms regulating the functional neural stem cell properties in cortical neurogenesis remain unclear. Here, we discuss the most up-to-date strategies to monitor the fundamental mechanistic parameters of neuronal progenitor proliferation, and recent advances deciphering the logic and dynamics of neurogenesis."}],"type":"journal_article","oa_version":"Published Version","month":"05","page":"323 - 340","date_created":"2018-12-11T11:56:09Z","file_date_updated":"2020-07-14T12:45:31Z","volume":9},{"language":[{"iso":"eng"}],"issue":"5","doi":"10.1093/nar/gkt1290","quality_controlled":"1","pubrep_id":"961","publication":"Nucleic Acids Research","scopus_import":1,"tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","image":"/images/cc_by.png","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","short":"CC BY (4.0)"},"user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","publisher":"Oxford University Press","department":[{"_id":"SiHi"}],"title":"DICE, an efficient system for iterative genomic editing in human pluripotent stem cells","article_number":"e34","publist_id":"4684","author":[{"first_name":"Fangfang","last_name":"Zhu","full_name":"Zhu, Fangfang"},{"first_name":"Matthew","last_name":"Gamboa","full_name":"Gamboa, Matthew"},{"full_name":"Farruggio, Alfonso","first_name":"Alfonso","last_name":"Farruggio"},{"orcid":"0000-0003-2279-1061","id":"37B36620-F248-11E8-B48F-1D18A9856A87","full_name":"Hippenmeyer, Simon","first_name":"Simon","last_name":"Hippenmeyer"},{"full_name":"Tasic, Bosiljka","last_name":"Tasic","first_name":"Bosiljka"},{"full_name":"Schüle, Birgitt","last_name":"Schüle","first_name":"Birgitt"},{"full_name":"Chen Tsai, Yanru","last_name":"Chen Tsai","first_name":"Yanru"},{"full_name":"Calos, Michele","last_name":"Calos","first_name":"Michele"}],"file":[{"creator":"system","file_size":11044478,"content_type":"application/pdf","relation":"main_file","file_name":"IST-2018-961-v1+1_2014_Hippenmeyer_DICE.pdf","access_level":"open_access","date_created":"2018-12-12T10:09:15Z","checksum":"e9268f5f96a820f04d7ebbf85927c3cb","file_id":"4738","date_updated":"2020-07-14T12:45:35Z"}],"day":"05","intvolume":"        42","citation":{"apa":"Zhu, F., Gamboa, M., Farruggio, A., Hippenmeyer, S., Tasic, B., Schüle, B., … Calos, M. (2014). DICE, an efficient system for iterative genomic editing in human pluripotent stem cells. <i>Nucleic Acids Research</i>. Oxford University Press. <a href=\"https://doi.org/10.1093/nar/gkt1290\">https://doi.org/10.1093/nar/gkt1290</a>","ista":"Zhu F, Gamboa M, Farruggio A, Hippenmeyer S, Tasic B, Schüle B, Chen Tsai Y, Calos M. 2014. DICE, an efficient system for iterative genomic editing in human pluripotent stem cells. Nucleic Acids Research. 42(5), e34.","mla":"Zhu, Fangfang, et al. “DICE, an Efficient System for Iterative Genomic Editing in Human Pluripotent Stem Cells.” <i>Nucleic Acids Research</i>, vol. 42, no. 5, e34, Oxford University Press, 2014, doi:<a href=\"https://doi.org/10.1093/nar/gkt1290\">10.1093/nar/gkt1290</a>.","ama":"Zhu F, Gamboa M, Farruggio A, et al. DICE, an efficient system for iterative genomic editing in human pluripotent stem cells. <i>Nucleic Acids Research</i>. 2014;42(5). doi:<a href=\"https://doi.org/10.1093/nar/gkt1290\">10.1093/nar/gkt1290</a>","short":"F. Zhu, M. Gamboa, A. Farruggio, S. Hippenmeyer, B. Tasic, B. Schüle, Y. Chen Tsai, M. Calos, Nucleic Acids Research 42 (2014).","chicago":"Zhu, Fangfang, Matthew Gamboa, Alfonso Farruggio, Simon Hippenmeyer, Bosiljka Tasic, Birgitt Schüle, Yanru Chen Tsai, and Michele Calos. “DICE, an Efficient System for Iterative Genomic Editing in Human Pluripotent Stem Cells.” <i>Nucleic Acids Research</i>. Oxford University Press, 2014. <a href=\"https://doi.org/10.1093/nar/gkt1290\">https://doi.org/10.1093/nar/gkt1290</a>.","ieee":"F. Zhu <i>et al.</i>, “DICE, an efficient system for iterative genomic editing in human pluripotent stem cells,” <i>Nucleic Acids Research</i>, vol. 42, no. 5. Oxford University Press, 2014."},"status":"public","date_published":"2014-03-05T00:00:00Z","ddc":["571","610"],"publication_status":"published","oa":1,"has_accepted_license":"1","_id":"2261","acknowledgement":"California Institute for Regenerative Medicine [RT2-01880 and TR2-01756]. Funding for open access charge: California Institute for Regenerative Medicine [RT2-01880 and TR2-01756]\r\nCC BY 3,0","year":"2014","volume":42,"date_created":"2018-12-11T11:56:38Z","file_date_updated":"2020-07-14T12:45:35Z","abstract":[{"text":"To reveal the full potential of human pluripotent stem cells, new methods for rapid, site-specific genomic engineering are needed. Here, we describe a system for precise genetic modification of human embryonic stem cells (ESCs) and induced pluripotent stem cells (iPSCs). We identified a novel human locus, H11, located in a safe, intergenic, transcriptionally active region of chromosome 22, as the recipient site, to provide robust, ubiquitous expression of inserted genes. Recipient cell lines were established by site-specific placement of a ‘landing pad’ cassette carrying attP sites for phiC31 and Bxb1 integrases at the H11 locus by spontaneous or TALEN-assisted homologous recombination. Dual integrase cassette exchange (DICE) mediated by phiC31 and Bxb1 integrases was used to insert genes of interest flanked by phiC31 and Bxb1 attB sites at the H11 locus, replacing the landing pad. This system provided complete control over content, direction and copy number of inserted genes, with a specificity of 100%. A series of genes, including mCherry and various combinations of the neural transcription factors LMX1a, FOXA2 and OTX2, were inserted in recipient cell lines derived from H9 ESC, as well as iPSC lines derived from a Parkinson’s disease patient and a normal sibling control. The DICE system offers rapid, efficient and precise gene insertion in ESC and iPSC and is particularly well suited for repeated modifications of the same locus.","lang":"eng"}],"date_updated":"2021-01-12T06:56:22Z","type":"journal_article","oa_version":"Preprint","month":"03"},{"alternative_title":["Advances in Experimental Medicine and Biology"],"status":"public","editor":[{"full_name":"Nguyen, Laurent","first_name":"Laurent","last_name":"Nguyen"}],"intvolume":"       800","language":[{"iso":"eng"}],"citation":{"chicago":"Hippenmeyer, Simon. “Molecular Pathways Controlling the Sequential Steps of Cortical Projection Neuron Migration.” In <i> Cellular and Molecular Control of Neuronal Migration</i>, edited by Laurent Nguyen, 800:1–24. Springer, 2014. <a href=\"https://doi.org/10.1007/978-94-007-7687-6_1\">https://doi.org/10.1007/978-94-007-7687-6_1</a>.","ieee":"S. Hippenmeyer, “Molecular pathways controlling the sequential steps of cortical projection neuron migration,” in <i> Cellular and Molecular Control of Neuronal Migration</i>, vol. 800, L. Nguyen, Ed. Springer, 2014, pp. 1–24.","short":"S. Hippenmeyer, in:, L. Nguyen (Ed.),  Cellular and Molecular Control of Neuronal Migration, Springer, 2014, pp. 1–24.","ama":"Hippenmeyer S. Molecular pathways controlling the sequential steps of cortical projection neuron migration. In: Nguyen L, ed. <i> Cellular and Molecular Control of Neuronal Migration</i>. Vol 800. Springer; 2014:1-24. doi:<a href=\"https://doi.org/10.1007/978-94-007-7687-6_1\">10.1007/978-94-007-7687-6_1</a>","apa":"Hippenmeyer, S. (2014). Molecular pathways controlling the sequential steps of cortical projection neuron migration. In L. Nguyen (Ed.), <i> Cellular and Molecular Control of Neuronal Migration</i> (Vol. 800, pp. 1–24). Springer. <a href=\"https://doi.org/10.1007/978-94-007-7687-6_1\">https://doi.org/10.1007/978-94-007-7687-6_1</a>","ista":"Hippenmeyer S. 2014.Molecular pathways controlling the sequential steps of cortical projection neuron migration. In:  Cellular and Molecular Control of Neuronal Migration. Advances in Experimental Medicine and Biology, vol. 800, 1–24.","mla":"Hippenmeyer, Simon. “Molecular Pathways Controlling the Sequential Steps of Cortical Projection Neuron Migration.” <i> Cellular and Molecular Control of Neuronal Migration</i>, edited by Laurent Nguyen, vol. 800, Springer, 2014, pp. 1–24, doi:<a href=\"https://doi.org/10.1007/978-94-007-7687-6_1\">10.1007/978-94-007-7687-6_1</a>."},"publication_status":"published","doi":"10.1007/978-94-007-7687-6_1","date_published":"2014-01-01T00:00:00Z","quality_controlled":"1","publisher":"Springer","user_id":"3E5EF7F0-F248-11E8-B48F-1D18A9856A87","department":[{"_id":"SiHi"}],"year":"2014","_id":"2265","publication":" Cellular and Molecular Control of Neuronal Migration","scopus_import":1,"author":[{"first_name":"Simon","last_name":"Hippenmeyer","id":"37B36620-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0003-2279-1061","full_name":"Hippenmeyer, Simon"}],"page":"1 - 24","type":"book_chapter","oa_version":"None","month":"01","abstract":[{"lang":"eng","text":"Coordinated migration of newly-born neurons to their target territories is essential for correct neuronal circuit assembly in the developing brain. Although a cohort of signaling pathways has been implicated in the regulation of cortical projection neuron migration, the precise molecular mechanisms and how a balanced interplay of cell-autonomous and non-autonomous functions of candidate signaling molecules controls the discrete steps in the migration process, are just being revealed. In this chapter, I will focally review recent advances that improved our understanding of the cell-autonomous and possible cell-nonautonomous functions of the evolutionarily conserved LIS1/NDEL1-complex in regulating the sequential steps of cortical projection neuron migration. I will then elaborate on the emerging concept that the Reelin signaling pathway, acts exactly at precise stages in the course of cortical projection neuron migration. Lastly, I will discuss how finely tuned transcriptional programs and downstream effectors govern particular aspects in driving radial migration at discrete stages and how they regulate the precise positioning of cortical projection neurons in the developing cerebral cortex."}],"date_updated":"2021-01-12T06:56:23Z","day":"01","title":"Molecular pathways controlling the sequential steps of cortical projection neuron migration","volume":800,"publist_id":"4679","date_created":"2018-12-11T11:56:39Z"},{"date_updated":"2021-01-12T07:00:07Z","abstract":[{"lang":"eng","text":"Individuals with Down syndrome (DS) present important motor deficits that derive from altered motor development of infants and young children. DYRK1A, a candidate gene for DS abnormalities has been implicated in motor function due to its expression in motor nuclei in the adult brain, and its overexpression in DS mouse models leads to hyperactivity and altered motor learning. However, its precise role in the adult motor system, or its possible involvement in postnatal locomotor development has not yet been clarified. During the postnatal period we observed time-specific expression of Dyrk1A in discrete subsets of brainstem nuclei and spinal cord motor neurons. Interestingly, we describe for the first time the presence of Dyrk1A in the presynaptic terminal of the neuromuscular junctions and its axonal transport from the facial nucleus, suggesting a function for Dyrk1A in these structures. Relevant to DS, Dyrk1A overexpression in transgenic mice (TgDyrk1A) produces motor developmental alterations possibly contributing to DS motor phenotypes and modifies the numbers of motor cholinergic neurons, suggesting that the kinase may have a role in the development of the brainstem and spinal cord motor system."}],"month":"01","type":"journal_article","oa_version":"Published Version","date_created":"2018-12-11T11:59:52Z","file_date_updated":"2020-07-14T12:45:50Z","volume":8,"year":"2013","_id":"2838","has_accepted_license":"1","oa":1,"publication_status":"published","date_published":"2013-01-16T00:00:00Z","ddc":["570"],"status":"public","citation":{"apa":"Arquè Fuste, G., Casanovas, A., &#38; Dierssen, M. (2013). Dyrk1A is dynamically expressed on subsets of motor neurons and in the neuromuscular junction: Possible role in Down syndrome. <i>PLoS One</i>. Public Library of Science. <a href=\"https://doi.org/10.1371/journal.pone.0054285\">https://doi.org/10.1371/journal.pone.0054285</a>","mla":"Arquè Fuste, Gloria, et al. “Dyrk1A Is Dynamically Expressed on Subsets of Motor Neurons and in the Neuromuscular Junction: Possible Role in Down Syndrome.” <i>PLoS One</i>, vol. 8, no. 1, e54285, Public Library of Science, 2013, doi:<a href=\"https://doi.org/10.1371/journal.pone.0054285\">10.1371/journal.pone.0054285</a>.","ista":"Arquè Fuste G, Casanovas A, Dierssen M. 2013. Dyrk1A is dynamically expressed on subsets of motor neurons and in the neuromuscular junction: Possible role in Down syndrome. PLoS One. 8(1), e54285.","ama":"Arquè Fuste G, Casanovas A, Dierssen M. Dyrk1A is dynamically expressed on subsets of motor neurons and in the neuromuscular junction: Possible role in Down syndrome. <i>PLoS One</i>. 2013;8(1). doi:<a href=\"https://doi.org/10.1371/journal.pone.0054285\">10.1371/journal.pone.0054285</a>","short":"G. Arquè Fuste, A. Casanovas, M. Dierssen, PLoS One 8 (2013).","chicago":"Arquè Fuste, Gloria, Anna Casanovas, and Mara Dierssen. “Dyrk1A Is Dynamically Expressed on Subsets of Motor Neurons and in the Neuromuscular Junction: Possible Role in Down Syndrome.” <i>PLoS One</i>. Public Library of Science, 2013. <a href=\"https://doi.org/10.1371/journal.pone.0054285\">https://doi.org/10.1371/journal.pone.0054285</a>.","ieee":"G. Arquè Fuste, A. Casanovas, and M. Dierssen, “Dyrk1A is dynamically expressed on subsets of motor neurons and in the neuromuscular junction: Possible role in Down syndrome,” <i>PLoS One</i>, vol. 8, no. 1. Public Library of Science, 2013."},"intvolume":"         8","day":"16","file":[{"creator":"system","relation":"main_file","content_type":"application/pdf","file_size":4795977,"file_name":"IST-2016-407-v1+1_journal.pone.0054285.pdf","access_level":"open_access","date_created":"2018-12-12T10:15:38Z","checksum":"512733b21419574a45f10cabef3d7f81","date_updated":"2020-07-14T12:45:50Z","file_id":"5160"}],"author":[{"last_name":"Arquè Fuste","first_name":"Gloria","full_name":"Arquè Fuste, Gloria","id":"3CF33908-F248-11E8-B48F-1D18A9856A87"},{"full_name":"Casanovas, Anna","first_name":"Anna","last_name":"Casanovas"},{"full_name":"Dierssen, Mara","last_name":"Dierssen","first_name":"Mara"}],"publist_id":"3960","title":"Dyrk1A is dynamically expressed on subsets of motor neurons and in the neuromuscular junction: Possible role in Down syndrome","article_number":"e54285","department":[{"_id":"SiHi"}],"user_id":"3E5EF7F0-F248-11E8-B48F-1D18A9856A87","publisher":"Public Library of Science","scopus_import":1,"tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","image":"/images/cc_by.png","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","short":"CC BY (4.0)"},"publication":"PLoS One","pubrep_id":"407","quality_controlled":"1","doi":"10.1371/journal.pone.0054285","language":[{"iso":"eng"}],"issue":"1"}]