--- _id: '1488' 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. 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. article_number: e1002382 author: - first_name: Paul full_name: Riccio, Paul last_name: Riccio - first_name: Cristina full_name: Cebrián, Cristina last_name: Cebrián - first_name: Hui full_name: Zong, Hui last_name: Zong - first_name: Simon full_name: Hippenmeyer, Simon id: 37B36620-F248-11E8-B48F-1D18A9856A87 last_name: Hippenmeyer orcid: 0000-0003-2279-1061 - first_name: Frank full_name: Costantini, Frank last_name: Costantini 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. PLoS Biology. 2016;14(2). doi:10.1371/journal.pbio.1002382 apa: 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. Public Library of Science. https://doi.org/10.1371/journal.pbio.1002382 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.” PLoS Biology. Public Library of Science, 2016. https://doi.org/10.1371/journal.pbio.1002382. 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,” PLoS Biology, vol. 14, no. 2. Public Library of Science, 2016. 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.” PLoS Biology, vol. 14, no. 2, e1002382, Public Library of Science, 2016, doi:10.1371/journal.pbio.1002382. short: P. Riccio, C. Cebrián, H. Zong, S. Hippenmeyer, F. Costantini, PLoS Biology 14 (2016). date_created: 2018-12-11T11:52:19Z date_published: 2016-02-19T00:00:00Z date_updated: 2023-02-23T10:01:08Z day: '19' ddc: - '570' department: - _id: SiHi doi: 10.1371/journal.pbio.1002382 file: - access_level: open_access checksum: 7f8fa1b3a29f94c0a14dd4465278cdbc content_type: application/pdf creator: system date_created: 2018-12-12T10:13:42Z date_updated: 2020-07-14T12:44:57Z file_id: '5027' file_name: IST-2016-517-v1+1_journal.pbio.1002382_1_.PDF file_size: 5904773 relation: main_file file_date_updated: 2020-07-14T12:44:57Z has_accepted_license: '1' intvolume: ' 14' issue: '2' language: - iso: eng month: '02' oa: 1 oa_version: Published Version publication: PLoS Biology publication_status: published publisher: Public Library of Science publist_id: '5699' pubrep_id: '517' quality_controlled: '1' related_material: record: - id: '9703' relation: research_data status: deleted scopus_import: 1 status: public title: Ret and Etv4 promote directed movements of progenitor cells during renal branching morphogenesis tmp: image: /images/cc_by.png legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0) short: CC BY (4.0) type: journal_article user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87 volume: 14 year: '2016' ... --- _id: '1550' 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. 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" author: - first_name: Christian full_name: Mayer, Christian last_name: Mayer - first_name: Xavier full_name: Jaglin, Xavier last_name: Jaglin - first_name: Lucy full_name: Cobbs, Lucy last_name: Cobbs - first_name: Rachel full_name: Bandler, Rachel last_name: Bandler - first_name: Carmen full_name: Streicher, Carmen id: 36BCB99C-F248-11E8-B48F-1D18A9856A87 last_name: Streicher - first_name: Constance full_name: Cepko, Constance last_name: Cepko - first_name: Simon full_name: Hippenmeyer, Simon id: 37B36620-F248-11E8-B48F-1D18A9856A87 last_name: Hippenmeyer orcid: 0000-0003-2279-1061 - first_name: Gord full_name: Fishell, Gord last_name: Fishell citation: ama: Mayer C, Jaglin X, Cobbs L, et al. Clonally related forebrain interneurons disperse broadly across both functional areas and structural boundaries. Neuron. 2015;87(5):989-998. doi:10.1016/j.neuron.2015.07.011 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. Neuron. Elsevier. https://doi.org/10.1016/j.neuron.2015.07.011 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.” Neuron. Elsevier, 2015. https://doi.org/10.1016/j.neuron.2015.07.011. ieee: C. Mayer et al., “Clonally related forebrain interneurons disperse broadly across both functional areas and structural boundaries,” Neuron, vol. 87, no. 5. Elsevier, pp. 989–998, 2015. 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. mla: Mayer, Christian, et al. “Clonally Related Forebrain Interneurons Disperse Broadly across Both Functional Areas and Structural Boundaries.” Neuron, vol. 87, no. 5, Elsevier, 2015, pp. 989–98, doi:10.1016/j.neuron.2015.07.011. short: C. Mayer, X. Jaglin, L. Cobbs, R. Bandler, C. Streicher, C. Cepko, S. Hippenmeyer, G. Fishell, Neuron 87 (2015) 989–998. date_created: 2018-12-11T11:52:40Z date_published: 2015-09-02T00:00:00Z date_updated: 2021-01-12T06:51:32Z day: '02' department: - _id: SiHi doi: 10.1016/j.neuron.2015.07.011 external_id: pmid: - '26299473' intvolume: ' 87' issue: '5' language: - iso: eng main_file_link: - open_access: '1' url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4560602/ month: '09' oa: 1 oa_version: Submitted Version page: 989 - 998 pmid: 1 publication: Neuron publication_status: published publisher: Elsevier publist_id: '5621' quality_controlled: '1' scopus_import: 1 status: public title: Clonally related forebrain interneurons disperse broadly across both functional areas and structural boundaries type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 87 year: '2015' ... --- _id: '1899' abstract: - lang: eng 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. article_processing_charge: No article_type: original author: - first_name: Scott full_name: Williams, Scott last_name: Williams - first_name: Lyndsay full_name: Ratliff, Lyndsay last_name: Ratliff - first_name: Maria P full_name: Postiglione, Maria P id: 2C67902A-F248-11E8-B48F-1D18A9856A87 last_name: Postiglione - first_name: Juergen full_name: Knoblich, Juergen last_name: Knoblich - first_name: Elaine full_name: Fuchs, Elaine last_name: Fuchs citation: 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. Nature Cell Biology. 2014;16(8):758-769. doi:10.1038/ncb3001 apa: Williams, S., Ratliff, L., Postiglione, M. P., Knoblich, J., & Fuchs, E. (2014). Par3-mInsc and Gα i3 cooperate to promote oriented epidermal cell divisions through LGN. Nature Cell Biology. Nature Publishing Group. https://doi.org/10.1038/ncb3001 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.” Nature Cell Biology. Nature Publishing Group, 2014. https://doi.org/10.1038/ncb3001. 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,” Nature Cell Biology, vol. 16, no. 8. Nature Publishing Group, pp. 758–769, 2014. 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.” Nature Cell Biology, vol. 16, no. 8, Nature Publishing Group, 2014, pp. 758–69, doi:10.1038/ncb3001. short: S. Williams, L. Ratliff, M.P. Postiglione, J. Knoblich, E. Fuchs, Nature Cell Biology 16 (2014) 758–769. date_created: 2018-12-11T11:54:36Z date_published: 2014-07-13T00:00:00Z date_updated: 2021-01-12T06:53:55Z day: '13' department: - _id: SiHi doi: 10.1038/ncb3001 external_id: pmid: - '25016959' intvolume: ' 16' issue: '8' language: - iso: eng main_file_link: - open_access: '1' url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4159251/ month: '07' oa: 1 oa_version: Submitted Version page: 758 - 769 pmid: 1 publication: Nature Cell Biology publication_status: published publisher: Nature Publishing Group publist_id: '5196' quality_controlled: '1' scopus_import: 1 status: public title: Par3-mInsc and Gα i3 cooperate to promote oriented epidermal cell divisions through LGN type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 16 year: '2014' ... --- _id: '2022' abstract: - lang: eng 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. author: - first_name: Peng full_name: Gao, Peng last_name: Gao - first_name: Maria P full_name: Postiglione, Maria P id: 2C67902A-F248-11E8-B48F-1D18A9856A87 last_name: Postiglione - first_name: Teresa full_name: Krieger, Teresa last_name: Krieger - first_name: Luisirene full_name: Hernandez, Luisirene last_name: Hernandez - first_name: Chao full_name: Wang, Chao last_name: Wang - first_name: Zhi full_name: Han, Zhi last_name: Han - first_name: Carmen full_name: Streicher, Carmen id: 36BCB99C-F248-11E8-B48F-1D18A9856A87 last_name: Streicher - first_name: Ekaterina full_name: Papusheva, Ekaterina id: 41DB591E-F248-11E8-B48F-1D18A9856A87 last_name: Papusheva - first_name: Ryan full_name: Insolera, Ryan last_name: Insolera - first_name: Kritika full_name: Chugh, Kritika last_name: Chugh - first_name: Oren full_name: Kodish, Oren last_name: Kodish - first_name: Kun full_name: Huang, Kun last_name: Huang - first_name: Benjamin full_name: Simons, Benjamin last_name: Simons - first_name: Liqun full_name: Luo, Liqun last_name: Luo - first_name: Simon full_name: Hippenmeyer, Simon id: 37B36620-F248-11E8-B48F-1D18A9856A87 last_name: Hippenmeyer orcid: 0000-0003-2279-1061 - first_name: Song full_name: Shi, Song last_name: Shi citation: ama: Gao P, Postiglione MP, Krieger T, et al. Deterministic progenitor behavior and unitary production of neurons in the neocortex. Cell. 2014;159(4):775-788. doi:10.1016/j.cell.2014.10.027 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. Cell. Cell Press. https://doi.org/10.1016/j.cell.2014.10.027 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.” Cell. Cell Press, 2014. https://doi.org/10.1016/j.cell.2014.10.027. ieee: P. Gao et al., “Deterministic progenitor behavior and unitary production of neurons in the neocortex,” Cell, vol. 159, no. 4. Cell Press, pp. 775–788, 2014. 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. mla: Gao, Peng, et al. “Deterministic Progenitor Behavior and Unitary Production of Neurons in the Neocortex.” Cell, vol. 159, no. 4, Cell Press, 2014, pp. 775–88, doi:10.1016/j.cell.2014.10.027. 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. date_created: 2018-12-11T11:55:16Z date_published: 2014-11-06T00:00:00Z date_updated: 2021-01-12T06:54:47Z day: '06' ddc: - '570' department: - _id: SiHi - _id: Bio doi: 10.1016/j.cell.2014.10.027 ec_funded: 1 file: - access_level: open_access checksum: 6c5de8329bb2ffa71cba9fda750f14ce content_type: application/pdf creator: system date_created: 2018-12-12T10:08:47Z date_updated: 2020-07-14T12:45:25Z file_id: '4709' file_name: IST-2016-423-v1+1_1-s2.0-S0092867414013154-main.pdf file_size: 4435787 relation: main_file file_date_updated: 2020-07-14T12:45:25Z has_accepted_license: '1' intvolume: ' 159' issue: '4' language: - iso: eng month: '11' oa: 1 oa_version: Published Version page: 775 - 788 project: - _id: 25D61E48-B435-11E9-9278-68D0E5697425 call_identifier: FP7 grant_number: '618444' name: Molecular Mechanisms of Cerebral Cortex Development - _id: 25D7962E-B435-11E9-9278-68D0E5697425 grant_number: RGP0053/2014 name: Quantitative Structure-Function Analysis of Cerebral Cortex Assembly at Clonal Level publication: Cell publication_status: published publisher: Cell Press publist_id: '5050' pubrep_id: '423' quality_controlled: '1' scopus_import: 1 status: public title: Deterministic progenitor behavior and unitary production of neurons in the neocortex tmp: image: /images/cc_by.png legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0) short: CC BY (4.0) type: journal_article user_id: 4435EBFC-F248-11E8-B48F-1D18A9856A87 volume: 159 year: '2014' ... --- _id: '2020' abstract: - lang: eng 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. author: - first_name: Shah full_name: Ali, Shah last_name: Ali - first_name: Simon full_name: Hippenmeyer, Simon id: 37B36620-F248-11E8-B48F-1D18A9856A87 last_name: Hippenmeyer orcid: 0000-0003-2279-1061 - first_name: Lily full_name: Saadat, Lily last_name: Saadat - first_name: Liqun full_name: Luo, Liqun last_name: Luo - first_name: Irving full_name: Weissman, Irving last_name: Weissman - first_name: Reza full_name: Ardehali, Reza last_name: Ardehali citation: 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. PNAS. 2014;111(24):8850-8855. doi:10.1073/pnas.1408233111 apa: 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. National Academy of Sciences. https://doi.org/10.1073/pnas.1408233111 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.” PNAS. National Academy of Sciences, 2014. https://doi.org/10.1073/pnas.1408233111. 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,” PNAS, vol. 111, no. 24. National Academy of Sciences, pp. 8850–8855, 2014. 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.” PNAS, vol. 111, no. 24, National Academy of Sciences, 2014, pp. 8850–55, doi:10.1073/pnas.1408233111. short: S. Ali, S. Hippenmeyer, L. Saadat, L. Luo, I. Weissman, R. Ardehali, PNAS 111 (2014) 8850–8855. date_created: 2018-12-11T11:55:15Z date_published: 2014-06-17T00:00:00Z date_updated: 2021-01-12T06:54:46Z day: '17' department: - _id: SiHi doi: 10.1073/pnas.1408233111 intvolume: ' 111' issue: '24' language: - iso: eng month: '06' oa_version: None page: 8850 - 8855 publication: PNAS publication_status: published publisher: National Academy of Sciences publist_id: '5052' quality_controlled: '1' scopus_import: 1 status: public title: Existing cardiomyocytes generate cardiomyocytes at a low rate after birth in mice type: journal_article user_id: 4435EBFC-F248-11E8-B48F-1D18A9856A87 volume: 111 year: '2014' ... --- _id: '2021' 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. author: - first_name: Joo full_name: William, Joo last_name: William - first_name: Simon full_name: Hippenmeyer, Simon id: 37B36620-F248-11E8-B48F-1D18A9856A87 last_name: Hippenmeyer orcid: 0000-0003-2279-1061 - first_name: Liqun full_name: Luo, Liqun last_name: Luo citation: ama: William J, Hippenmeyer S, Luo L. Dendrite morphogenesis depends on relative levels of NT-3/TrkC signaling. Science. 2014;346(6209):626-629. doi:10.1126/science.1258996 apa: William, J., Hippenmeyer, S., & Luo, L. (2014). Dendrite morphogenesis depends on relative levels of NT-3/TrkC signaling. Science. American Association for the Advancement of Science. https://doi.org/10.1126/science.1258996 chicago: William, Joo, Simon Hippenmeyer, and Liqun Luo. “Dendrite Morphogenesis Depends on Relative Levels of NT-3/TrkC Signaling.” Science. American Association for the Advancement of Science, 2014. https://doi.org/10.1126/science.1258996. ieee: J. William, S. Hippenmeyer, and L. Luo, “Dendrite morphogenesis depends on relative levels of NT-3/TrkC signaling,” Science, vol. 346, no. 6209. American Association for the Advancement of Science, pp. 626–629, 2014. ista: William J, Hippenmeyer S, Luo L. 2014. Dendrite morphogenesis depends on relative levels of NT-3/TrkC signaling. Science. 346(6209), 626–629. mla: William, Joo, et al. “Dendrite Morphogenesis Depends on Relative Levels of NT-3/TrkC Signaling.” Science, vol. 346, no. 6209, American Association for the Advancement of Science, 2014, pp. 626–29, doi:10.1126/science.1258996. short: J. William, S. Hippenmeyer, L. Luo, Science 346 (2014) 626–629. date_created: 2018-12-11T11:55:15Z date_published: 2014-10-31T00:00:00Z date_updated: 2021-01-12T06:54:47Z day: '31' department: - _id: SiHi doi: 10.1126/science.1258996 intvolume: ' 346' issue: '6209' language: - iso: eng main_file_link: - open_access: '1' url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4631524/ month: '10' oa: 1 oa_version: Submitted Version page: 626 - 629 publication: Science publication_status: published publisher: American Association for the Advancement of Science publist_id: '5051' quality_controlled: '1' scopus_import: 1 status: public title: Dendrite morphogenesis depends on relative levels of NT-3/TrkC signaling type: journal_article user_id: 4435EBFC-F248-11E8-B48F-1D18A9856A87 volume: 346 year: '2014' ... --- _id: '2261' abstract: - lang: eng 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. 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" article_number: e34 author: - first_name: Fangfang full_name: Zhu, Fangfang last_name: Zhu - first_name: Matthew full_name: Gamboa, Matthew last_name: Gamboa - first_name: Alfonso full_name: Farruggio, Alfonso last_name: Farruggio - first_name: Simon full_name: Hippenmeyer, Simon id: 37B36620-F248-11E8-B48F-1D18A9856A87 last_name: Hippenmeyer orcid: 0000-0003-2279-1061 - first_name: Bosiljka full_name: Tasic, Bosiljka last_name: Tasic - first_name: Birgitt full_name: Schüle, Birgitt last_name: Schüle - first_name: Yanru full_name: Chen Tsai, Yanru last_name: Chen Tsai - first_name: Michele full_name: Calos, Michele last_name: Calos citation: ama: Zhu F, Gamboa M, Farruggio A, et al. DICE, an efficient system for iterative genomic editing in human pluripotent stem cells. Nucleic Acids Research. 2014;42(5). doi:10.1093/nar/gkt1290 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. Nucleic Acids Research. Oxford University Press. https://doi.org/10.1093/nar/gkt1290 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.” Nucleic Acids Research. Oxford University Press, 2014. https://doi.org/10.1093/nar/gkt1290. ieee: F. Zhu et al., “DICE, an efficient system for iterative genomic editing in human pluripotent stem cells,” Nucleic Acids Research, vol. 42, no. 5. Oxford University Press, 2014. 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.” Nucleic Acids Research, vol. 42, no. 5, e34, Oxford University Press, 2014, doi:10.1093/nar/gkt1290. short: F. Zhu, M. Gamboa, A. Farruggio, S. Hippenmeyer, B. Tasic, B. Schüle, Y. Chen Tsai, M. Calos, Nucleic Acids Research 42 (2014). date_created: 2018-12-11T11:56:38Z date_published: 2014-03-05T00:00:00Z date_updated: 2021-01-12T06:56:22Z day: '05' ddc: - '571' - '610' department: - _id: SiHi doi: 10.1093/nar/gkt1290 file: - access_level: open_access checksum: e9268f5f96a820f04d7ebbf85927c3cb content_type: application/pdf creator: system date_created: 2018-12-12T10:09:15Z date_updated: 2020-07-14T12:45:35Z file_id: '4738' file_name: IST-2018-961-v1+1_2014_Hippenmeyer_DICE.pdf file_size: 11044478 relation: main_file file_date_updated: 2020-07-14T12:45:35Z has_accepted_license: '1' intvolume: ' 42' issue: '5' language: - iso: eng month: '03' oa: 1 oa_version: Preprint publication: Nucleic Acids Research publication_status: published publisher: Oxford University Press publist_id: '4684' pubrep_id: '961' quality_controlled: '1' scopus_import: 1 status: public title: DICE, an efficient system for iterative genomic editing in human pluripotent stem cells tmp: image: /images/cc_by.png legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0) short: CC BY (4.0) type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 42 year: '2014' ... --- _id: '2265' 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. alternative_title: - Advances in Experimental Medicine and Biology author: - first_name: Simon full_name: Hippenmeyer, Simon id: 37B36620-F248-11E8-B48F-1D18A9856A87 last_name: Hippenmeyer orcid: 0000-0003-2279-1061 citation: ama: 'Hippenmeyer S. Molecular pathways controlling the sequential steps of cortical projection neuron migration. In: Nguyen L, ed. Cellular and Molecular Control of Neuronal Migration. Vol 800. Springer; 2014:1-24. doi:10.1007/978-94-007-7687-6_1' apa: Hippenmeyer, S. (2014). Molecular pathways controlling the sequential steps of cortical projection neuron migration. In L. Nguyen (Ed.), Cellular and Molecular Control of Neuronal Migration (Vol. 800, pp. 1–24). Springer. https://doi.org/10.1007/978-94-007-7687-6_1 chicago: Hippenmeyer, Simon. “Molecular Pathways Controlling the Sequential Steps of Cortical Projection Neuron Migration.” In Cellular and Molecular Control of Neuronal Migration, edited by Laurent Nguyen, 800:1–24. Springer, 2014. https://doi.org/10.1007/978-94-007-7687-6_1. ieee: S. Hippenmeyer, “Molecular pathways controlling the sequential steps of cortical projection neuron migration,” in Cellular and Molecular Control of Neuronal Migration, vol. 800, L. Nguyen, Ed. Springer, 2014, pp. 1–24. 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.” Cellular and Molecular Control of Neuronal Migration, edited by Laurent Nguyen, vol. 800, Springer, 2014, pp. 1–24, doi:10.1007/978-94-007-7687-6_1. short: S. Hippenmeyer, in:, L. Nguyen (Ed.), Cellular and Molecular Control of Neuronal Migration, Springer, 2014, pp. 1–24. date_created: 2018-12-11T11:56:39Z date_published: 2014-01-01T00:00:00Z date_updated: 2021-01-12T06:56:23Z day: '01' department: - _id: SiHi doi: 10.1007/978-94-007-7687-6_1 editor: - first_name: Laurent full_name: Nguyen, Laurent last_name: Nguyen intvolume: ' 800' language: - iso: eng month: '01' oa_version: None page: 1 - 24 publication: ' Cellular and Molecular Control of Neuronal Migration' publication_status: published publisher: Springer publist_id: '4679' quality_controlled: '1' scopus_import: 1 status: public title: Molecular pathways controlling the sequential steps of cortical projection neuron migration type: book_chapter user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87 volume: 800 year: '2014' ... --- _id: '2175' 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. article_processing_charge: No author: - first_name: Maria P full_name: Postiglione, Maria P id: 2C67902A-F248-11E8-B48F-1D18A9856A87 last_name: Postiglione - first_name: Simon full_name: Hippenmeyer, Simon id: 37B36620-F248-11E8-B48F-1D18A9856A87 last_name: Hippenmeyer orcid: 0000-0003-2279-1061 citation: ama: 'Postiglione MP, Hippenmeyer S. Monitoring neurogenesis in the cerebral cortex: an update. Future Neurology. 2014;9(3):323-340. doi:10.2217/fnl.14.18' apa: 'Postiglione, M. P., & Hippenmeyer, S. (2014). Monitoring neurogenesis in the cerebral cortex: an update. Future Neurology. Future Science Group. https://doi.org/10.2217/fnl.14.18' chicago: 'Postiglione, Maria P, and Simon Hippenmeyer. “Monitoring Neurogenesis in the Cerebral Cortex: An Update.” Future Neurology. Future Science Group, 2014. https://doi.org/10.2217/fnl.14.18.' ieee: 'M. P. Postiglione and S. Hippenmeyer, “Monitoring neurogenesis in the cerebral cortex: an update,” Future Neurology, vol. 9, no. 3. Future Science Group, pp. 323–340, 2014.' ista: 'Postiglione MP, Hippenmeyer S. 2014. Monitoring neurogenesis in the cerebral cortex: an update. Future Neurology. 9(3), 323–340.' mla: 'Postiglione, Maria P., and Simon Hippenmeyer. “Monitoring Neurogenesis in the Cerebral Cortex: An Update.” Future Neurology, vol. 9, no. 3, Future Science Group, 2014, pp. 323–40, doi:10.2217/fnl.14.18.' short: M.P. Postiglione, S. Hippenmeyer, Future Neurology 9 (2014) 323–340. date_created: 2018-12-11T11:56:09Z date_published: 2014-05-01T00:00:00Z date_updated: 2023-10-17T08:34:27Z day: '01' ddc: - '570' department: - _id: SiHi doi: 10.2217/fnl.14.18 ec_funded: 1 file: - access_level: open_access checksum: ba06659ecadabceec9a37dd8c4586dce content_type: application/pdf creator: system date_created: 2018-12-12T10:10:25Z date_updated: 2020-07-14T12:45:31Z file_id: '4812' file_name: IST-2016-528-v1+1_fnl.14.18.pdf file_size: 3848424 relation: main_file file_date_updated: 2020-07-14T12:45:31Z has_accepted_license: '1' intvolume: ' 9' issue: '3' language: - iso: eng month: '05' oa: 1 oa_version: Published Version page: 323 - 340 project: - _id: 25D61E48-B435-11E9-9278-68D0E5697425 call_identifier: FP7 grant_number: '618444' name: Molecular Mechanisms of Cerebral Cortex Development publication: Future Neurology publication_identifier: eissn: - 1748-6971 issn: - 1479-6708 publication_status: published publisher: Future Science Group publist_id: '4806' pubrep_id: '528' quality_controlled: '1' scopus_import: '1' status: public title: 'Monitoring neurogenesis in the cerebral cortex: an update' tmp: image: /images/cc_by_nc_nd.png legal_code_url: https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode name: Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0) short: CC BY-NC-ND (4.0) type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 9 year: '2014' ... --- _id: '2264' abstract: - lang: eng text: Faithful progression through the cell cycle is crucial to the maintenance and developmental potential of stem cells. Here, we demonstrate that neural stem cells (NSCs) and intermediate neural progenitor cells (NPCs) employ a zinc-finger transcription factor specificity protein 2 (Sp2) as a cell cycle regulator in two temporally and spatially distinct progenitor domains. Differential conditional deletion of Sp2 in early embryonic cerebral cortical progenitors, and perinatal olfactory bulb progenitors disrupted transitions through G1, G2 and M phases, whereas DNA synthesis appeared intact. Cell-autonomous function of Sp2 was identified by deletion of Sp2 using mosaic analysis with double markers, which clearly established that conditional Sp2-null NSCs and NPCs are M phase arrested in vivo. Importantly, conditional deletion of Sp2 led to a decline in the generation of NPCs and neurons in the developing and postnatal brains. Our findings implicate Sp2-dependent mechanisms as novel regulators of cell cycle progression, the absence of which disrupts neurogenesis in the embryonic and postnatal brain. article_processing_charge: No author: - first_name: Huixuan full_name: Liang, Huixuan last_name: Liang - first_name: Guanxi full_name: Xiao, Guanxi last_name: Xiao - first_name: Haifeng full_name: Yin, Haifeng last_name: Yin - first_name: Simon full_name: Hippenmeyer, Simon id: 37B36620-F248-11E8-B48F-1D18A9856A87 last_name: Hippenmeyer orcid: 0000-0003-2279-1061 - first_name: Jonathan full_name: Horowitz, Jonathan last_name: Horowitz - first_name: Troy full_name: Ghashghaei, Troy last_name: Ghashghaei citation: ama: Liang H, Xiao G, Yin H, Hippenmeyer S, Horowitz J, Ghashghaei T. Neural development is dependent on the function of specificity protein 2 in cell cycle progression. Development. 2013;140(3):552-561. doi:10.1242/dev.085621 apa: Liang, H., Xiao, G., Yin, H., Hippenmeyer, S., Horowitz, J., & Ghashghaei, T. (2013). Neural development is dependent on the function of specificity protein 2 in cell cycle progression. Development. Company of Biologists. https://doi.org/10.1242/dev.085621 chicago: Liang, Huixuan, Guanxi Xiao, Haifeng Yin, Simon Hippenmeyer, Jonathan Horowitz, and Troy Ghashghaei. “Neural Development Is Dependent on the Function of Specificity Protein 2 in Cell Cycle Progression.” Development. Company of Biologists, 2013. https://doi.org/10.1242/dev.085621. ieee: H. Liang, G. Xiao, H. Yin, S. Hippenmeyer, J. Horowitz, and T. Ghashghaei, “Neural development is dependent on the function of specificity protein 2 in cell cycle progression,” Development, vol. 140, no. 3. Company of Biologists, pp. 552–561, 2013. ista: Liang H, Xiao G, Yin H, Hippenmeyer S, Horowitz J, Ghashghaei T. 2013. Neural development is dependent on the function of specificity protein 2 in cell cycle progression. Development. 140(3), 552–561. mla: Liang, Huixuan, et al. “Neural Development Is Dependent on the Function of Specificity Protein 2 in Cell Cycle Progression.” Development, vol. 140, no. 3, Company of Biologists, 2013, pp. 552–61, doi:10.1242/dev.085621. short: H. Liang, G. Xiao, H. Yin, S. Hippenmeyer, J. Horowitz, T. Ghashghaei, Development 140 (2013) 552–561. date_created: 2018-12-11T11:56:39Z date_published: 2013-02-01T00:00:00Z date_updated: 2021-01-12T06:56:23Z day: '01' department: - _id: SiHi doi: 10.1242/dev.085621 external_id: pmid: - '23293287' intvolume: ' 140' issue: '3' language: - iso: eng main_file_link: - open_access: '1' url: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3561788/ month: '02' oa: 1 oa_version: Submitted Version page: 552 - 561 pmid: 1 publication: Development publication_status: published publisher: Company of Biologists publist_id: '4681' quality_controlled: '1' scopus_import: 1 status: public title: Neural development is dependent on the function of specificity protein 2 in cell cycle progression type: journal_article user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87 volume: 140 year: '2013' ... --- _id: '2303' abstract: - lang: eng text: MADM (Mosaic Analysis with Double Markers) technology offers a genetic approach in mice to visualize and concomitantly manipulate genetically defined cells at clonal level and single cell resolution. MADM employs Cre recombinase/loxP-dependent interchromosomal mitotic recombination to reconstitute two split marker genes—green GFP and red tdTomato—and can label sparse clones of homozygous mutant cells in one color and wild-type cells in the other color in an otherwise unlabeled background. At present, major MADM applications include lineage tracing, single cell labeling, conditional knockouts in small populations of cells and induction of uniparental chromosome disomy to assess effects of genomic imprinting. MADM can be applied universally in the mouse with the sole limitation being the specificity of the promoter controlling Cre recombinase expression. Here I review recent developments and extensions of the MADM technique and give an overview of the major discoveries and progresses enabled by the implementation of the novel genetic MADM tools. acknowledgement: This work was supported by IST Austria institutional funds. article_type: review author: - first_name: Simon full_name: Hippenmeyer, Simon id: 37B36620-F248-11E8-B48F-1D18A9856A87 last_name: Hippenmeyer orcid: 0000-0003-2279-1061 citation: ama: Hippenmeyer S. Dissection of gene function at clonal level using mosaic analysis with double markers. Frontiers in Biology. 2013;8(6):557-568. doi:10.1007/s11515-013-1279-6 apa: Hippenmeyer, S. (2013). Dissection of gene function at clonal level using mosaic analysis with double markers. Frontiers in Biology. Springer. https://doi.org/10.1007/s11515-013-1279-6 chicago: Hippenmeyer, Simon. “Dissection of Gene Function at Clonal Level Using Mosaic Analysis with Double Markers.” Frontiers in Biology. Springer, 2013. https://doi.org/10.1007/s11515-013-1279-6. ieee: S. Hippenmeyer, “Dissection of gene function at clonal level using mosaic analysis with double markers,” Frontiers in Biology, vol. 8, no. 6. Springer, pp. 557–568, 2013. ista: Hippenmeyer S. 2013. Dissection of gene function at clonal level using mosaic analysis with double markers. Frontiers in Biology. 8(6), 557–568. mla: Hippenmeyer, Simon. “Dissection of Gene Function at Clonal Level Using Mosaic Analysis with Double Markers.” Frontiers in Biology, vol. 8, no. 6, Springer, 2013, pp. 557–68, doi:10.1007/s11515-013-1279-6. short: S. Hippenmeyer, Frontiers in Biology 8 (2013) 557–568. date_created: 2018-12-11T11:56:52Z date_published: 2013-09-03T00:00:00Z date_updated: 2021-01-12T06:56:39Z day: '03' department: - _id: SiHi doi: 10.1007/s11515-013-1279-6 intvolume: ' 8' issue: '6' language: - iso: eng month: '09' oa_version: None page: 557 - 568 publication: Frontiers in Biology publication_status: published publisher: Springer publist_id: '4624' quality_controlled: '1' scopus_import: 1 status: public title: Dissection of gene function at clonal level using mosaic analysis with double markers type: journal_article user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87 volume: 8 year: '2013' ... --- _id: '2838' 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. article_number: e54285 author: - first_name: Gloria full_name: Arquè Fuste, Gloria id: 3CF33908-F248-11E8-B48F-1D18A9856A87 last_name: Arquè Fuste - first_name: Anna full_name: Casanovas, Anna last_name: Casanovas - first_name: Mara full_name: Dierssen, Mara last_name: Dierssen citation: 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. PLoS One. 2013;8(1). doi:10.1371/journal.pone.0054285' apa: '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. Public Library of Science. https://doi.org/10.1371/journal.pone.0054285' 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.” PLoS One. Public Library of Science, 2013. https://doi.org/10.1371/journal.pone.0054285.' 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,” PLoS One, vol. 8, no. 1. Public Library of Science, 2013.' 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.' 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.” PLoS One, vol. 8, no. 1, e54285, Public Library of Science, 2013, doi:10.1371/journal.pone.0054285.' short: G. Arquè Fuste, A. Casanovas, M. Dierssen, PLoS One 8 (2013). date_created: 2018-12-11T11:59:52Z date_published: 2013-01-16T00:00:00Z date_updated: 2021-01-12T07:00:07Z day: '16' ddc: - '570' department: - _id: SiHi doi: 10.1371/journal.pone.0054285 file: - access_level: open_access checksum: 512733b21419574a45f10cabef3d7f81 content_type: application/pdf creator: system date_created: 2018-12-12T10:15:38Z date_updated: 2020-07-14T12:45:50Z file_id: '5160' file_name: IST-2016-407-v1+1_journal.pone.0054285.pdf file_size: 4795977 relation: main_file file_date_updated: 2020-07-14T12:45:50Z has_accepted_license: '1' intvolume: ' 8' issue: '1' language: - iso: eng month: '01' oa: 1 oa_version: Published Version publication: PLoS One publication_status: published publisher: Public Library of Science publist_id: '3960' pubrep_id: '407' quality_controlled: '1' scopus_import: 1 status: public title: 'Dyrk1A is dynamically expressed on subsets of motor neurons and in the neuromuscular junction: Possible role in Down syndrome' tmp: image: /images/cc_by.png legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0) short: CC BY (4.0) type: journal_article user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87 volume: 8 year: '2013' ... --- _id: '2855' abstract: - lang: eng text: Genomic imprinting leads to preferred expression of either the maternal or paternal alleles of a subset of genes. Imprinting is essential for mammalian development, and its deregulation causes many diseases. However, the functional relevance of imprinting at the cellular level is poorly understood for most imprinted genes. We used mosaic analysis with double markers (MADM) in mice to create uniparental disomies (UPDs) and to visualize imprinting effects with single-cell resolution. Although chromosome 12 UPD did not produce detectable phenotypes, chromosome 7 UPD caused highly significant paternal growth dominance in the liver and lung, but not in the brain or heart. A single gene on chromosome 7, encoding the secreted insulin-like growth factor 2 (IGF2), accounts for most of the paternal dominance effect. Mosaic analyses implied additional imprinted loci on chromosome 7 acting cell autonomously to transmit the IGF2 signal. Our study reveals chromosome- and cell-type specificity of genomic imprinting effects. author: - first_name: Simon full_name: Hippenmeyer, Simon id: 37B36620-F248-11E8-B48F-1D18A9856A87 last_name: Hippenmeyer orcid: 0000-0003-2279-1061 - first_name: Randy full_name: Johnson, Randy last_name: Johnson - first_name: Liqun full_name: Luo, Liqun last_name: Luo citation: ama: Hippenmeyer S, Johnson R, Luo L. Mosaic analysis with double markers reveals cell type specific paternal growth dominance. Cell Reports. 2013;3(3):960-967. doi:10.1016/j.celrep.2013.02.002 apa: Hippenmeyer, S., Johnson, R., & Luo, L. (2013). Mosaic analysis with double markers reveals cell type specific paternal growth dominance. Cell Reports. Cell Press. https://doi.org/10.1016/j.celrep.2013.02.002 chicago: Hippenmeyer, Simon, Randy Johnson, and Liqun Luo. “Mosaic Analysis with Double Markers Reveals Cell Type Specific Paternal Growth Dominance.” Cell Reports. Cell Press, 2013. https://doi.org/10.1016/j.celrep.2013.02.002. ieee: S. Hippenmeyer, R. Johnson, and L. Luo, “Mosaic analysis with double markers reveals cell type specific paternal growth dominance,” Cell Reports, vol. 3, no. 3. Cell Press, pp. 960–967, 2013. ista: Hippenmeyer S, Johnson R, Luo L. 2013. Mosaic analysis with double markers reveals cell type specific paternal growth dominance. Cell Reports. 3(3), 960–967. mla: Hippenmeyer, Simon, et al. “Mosaic Analysis with Double Markers Reveals Cell Type Specific Paternal Growth Dominance.” Cell Reports, vol. 3, no. 3, Cell Press, 2013, pp. 960–67, doi:10.1016/j.celrep.2013.02.002. short: S. Hippenmeyer, R. Johnson, L. Luo, Cell Reports 3 (2013) 960–967. date_created: 2018-12-11T11:59:57Z date_published: 2013-03-28T00:00:00Z date_updated: 2021-01-12T07:00:16Z day: '28' ddc: - '570' department: - _id: SiHi doi: 10.1016/j.celrep.2013.02.002 file: - access_level: open_access checksum: 6e977b918e81384cd571ec5a9d812289 content_type: application/pdf creator: system date_created: 2018-12-12T10:17:20Z date_updated: 2020-07-14T12:45:51Z file_id: '5274' file_name: IST-2016-405-v1+1_1-s2.0-S2211124713000612-main.pdf file_size: 1907211 relation: main_file file_date_updated: 2020-07-14T12:45:51Z has_accepted_license: '1' intvolume: ' 3' issue: '3' language: - iso: eng month: '03' oa: 1 oa_version: Published Version page: 960 - 967 publication: Cell Reports publication_status: published publisher: Cell Press publist_id: '3937' pubrep_id: '405' quality_controlled: '1' scopus_import: 1 status: public title: Mosaic analysis with double markers reveals cell type specific paternal growth dominance tmp: image: /images/cc_by_nc_nd.png legal_code_url: https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode name: Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0) short: CC BY-NC-ND (4.0) type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 3 year: '2013' ... --- _id: '2263' abstract: - lang: eng text: Nestin-cre transgenic mice have been widely used to direct recombination to neural stem cells (NSCs) and intermediate neural progenitor cells (NPCs). Here we report that a readily utilized, and the only commercially available, Nestin-cre line is insufficient for directing recombination in early embryonic NSCs and NPCs. Analysis of recombination efficiency in multiple cre-dependent reporters and a genetic mosaic line revealed consistent temporal and spatial patterns of recombination in NSCs and NPCs. For comparison we utilized a knock-in Emx1cre line and found robust recombination in NSCs and NPCs in ventricular and subventricular zones of the cerebral cortices as early as embryonic day 12.5. In addition we found that the rate of Nestin-cre driven recombination only reaches sufficiently high levels in NSCs and NPCs during late embryonic and early postnatal periods. These findings are important when commercially available cre lines are considered for directing recombination to embryonic NSCs and NPCs. author: - first_name: Huixuan full_name: Liang, Huixuan last_name: Liang - first_name: Simon full_name: Hippenmeyer, Simon id: 37B36620-F248-11E8-B48F-1D18A9856A87 last_name: Hippenmeyer orcid: 0000-0003-2279-1061 - first_name: H. full_name: Ghashghaei, H. last_name: Ghashghaei citation: ama: Liang H, Hippenmeyer S, Ghashghaei H. A Nestin-cre transgenic mouse is insufficient for recombination in early embryonic neural progenitors. Biology open. 2012;1(12):1200-1203. doi:10.1242/bio.20122287 apa: Liang, H., Hippenmeyer, S., & Ghashghaei, H. (2012). A Nestin-cre transgenic mouse is insufficient for recombination in early embryonic neural progenitors. Biology Open. The Company of Biologists. https://doi.org/10.1242/bio.20122287 chicago: Liang, Huixuan, Simon Hippenmeyer, and H. Ghashghaei. “A Nestin-Cre Transgenic Mouse Is Insufficient for Recombination in Early Embryonic Neural Progenitors.” Biology Open. The Company of Biologists, 2012. https://doi.org/10.1242/bio.20122287. ieee: H. Liang, S. Hippenmeyer, and H. Ghashghaei, “A Nestin-cre transgenic mouse is insufficient for recombination in early embryonic neural progenitors,” Biology open, vol. 1, no. 12. The Company of Biologists, pp. 1200–1203, 2012. ista: Liang H, Hippenmeyer S, Ghashghaei H. 2012. A Nestin-cre transgenic mouse is insufficient for recombination in early embryonic neural progenitors. Biology open. 1(12), 1200–1203. mla: Liang, Huixuan, et al. “A Nestin-Cre Transgenic Mouse Is Insufficient for Recombination in Early Embryonic Neural Progenitors.” Biology Open, vol. 1, no. 12, The Company of Biologists, 2012, pp. 1200–03, doi:10.1242/bio.20122287. short: H. Liang, S. Hippenmeyer, H. Ghashghaei, Biology Open 1 (2012) 1200–1203. date_created: 2018-12-11T11:56:38Z date_published: 2012-12-15T00:00:00Z date_updated: 2021-01-12T06:56:23Z day: '15' ddc: - '576' department: - _id: SiHi doi: 10.1242/bio.20122287 file: - access_level: open_access checksum: 605a1800b81227848c361fd6ba7d22ba content_type: application/pdf creator: system date_created: 2018-12-12T10:13:09Z date_updated: 2020-07-14T12:45:35Z file_id: '4990' file_name: IST-2015-387-v1+1_1200.full.pdf file_size: 726695 relation: main_file file_date_updated: 2020-07-14T12:45:35Z has_accepted_license: '1' intvolume: ' 1' issue: '12' language: - iso: eng license: https://creativecommons.org/licenses/by-nc-sa/4.0/ month: '12' oa: 1 oa_version: Published Version page: 1200 - 1203 publication: Biology open publication_status: published publisher: The Company of Biologists publist_id: '4682' pubrep_id: '387' quality_controlled: '1' scopus_import: 1 status: public title: A Nestin-cre transgenic mouse is insufficient for recombination in early embryonic neural progenitors tmp: image: /images/cc_by_nc_sa.png legal_code_url: https://creativecommons.org/licenses/by-nc-sa/4.0/legalcode name: Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC BY-NC-SA 4.0) short: CC BY-NC-SA (4.0) type: journal_article user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87 volume: 1 year: '2012' ...