--- _id: '14794' abstract: - lang: eng text: "Mosaic analysis with double markers (MADM) technology enables the sparse labeling of genetically defined neurons. We present a protocol for time-lapse imaging of cortical projection neuron migration in mice using MADM. We describe steps for the isolation, culturing, and 4D imaging of neuronal dynamics in MADM-labeled brain tissue. While this protocol is compatible with other single-cell labeling methods, the MADM approach provides a genetic platform for the functional assessment of cell-autonomous candidate gene function and the relative contribution of non-cell-autonomous effects.\r\n\r\nFor complete details on the use and execution of this protocol, please refer to Hansen et al. (2022),1 Contreras et al. (2021),2 and Amberg and Hippenmeyer (2021).3" acknowledged_ssus: - _id: Bio - _id: PreCl acknowledgement: We thank Florian Pauler for discussion and his expert technical support. This research was supported by the Scientific Service Units (SSU) at IST Austria through resources provided by the Imaging and Optics Facility (IOF) and Preclinical Facility (PCF). A.H.H. was a recipient of a DOC Fellowship (24812) of the Austrian Academy of Sciences. article_number: '102795' article_processing_charge: Yes article_type: review author: - first_name: Andi H full_name: Hansen, Andi H id: 38853E16-F248-11E8-B48F-1D18A9856A87 last_name: Hansen - first_name: Simon full_name: Hippenmeyer, Simon id: 37B36620-F248-11E8-B48F-1D18A9856A87 last_name: Hippenmeyer orcid: 0000-0003-2279-1061 citation: ama: Hansen AH, Hippenmeyer S. Time-lapse imaging of cortical projection neuron migration in mice using mosaic analysis with double markers. STAR Protocols. 2024;5(1). doi:10.1016/j.xpro.2023.102795 apa: Hansen, A. H., & Hippenmeyer, S. (2024). Time-lapse imaging of cortical projection neuron migration in mice using mosaic analysis with double markers. STAR Protocols. Elsevier. https://doi.org/10.1016/j.xpro.2023.102795 chicago: Hansen, Andi H, and Simon Hippenmeyer. “Time-Lapse Imaging of Cortical Projection Neuron Migration in Mice Using Mosaic Analysis with Double Markers.” STAR Protocols. Elsevier, 2024. https://doi.org/10.1016/j.xpro.2023.102795. ieee: A. H. Hansen and S. Hippenmeyer, “Time-lapse imaging of cortical projection neuron migration in mice using mosaic analysis with double markers,” STAR Protocols, vol. 5, no. 1. Elsevier, 2024. ista: Hansen AH, Hippenmeyer S. 2024. Time-lapse imaging of cortical projection neuron migration in mice using mosaic analysis with double markers. STAR Protocols. 5(1), 102795. mla: Hansen, Andi H., and Simon Hippenmeyer. “Time-Lapse Imaging of Cortical Projection Neuron Migration in Mice Using Mosaic Analysis with Double Markers.” STAR Protocols, vol. 5, no. 1, 102795, Elsevier, 2024, doi:10.1016/j.xpro.2023.102795. short: A.H. Hansen, S. Hippenmeyer, STAR Protocols 5 (2024). date_created: 2024-01-14T23:00:56Z date_published: 2024-01-01T00:00:00Z date_updated: 2024-01-17T10:32:31Z day: '01' department: - _id: SiHi doi: 10.1016/j.xpro.2023.102795 external_id: pmid: - '38165800' intvolume: ' 5' issue: '1' language: - iso: eng main_file_link: - open_access: '1' url: https://doi.org/10.1016/j.xpro.2023.102795 month: '01' oa: 1 oa_version: Published Version pmid: 1 project: - _id: 2625A13E-B435-11E9-9278-68D0E5697425 grant_number: '24812' name: Molecular Mechanisms of Radial Neuronal Migration publication: STAR Protocols publication_identifier: eissn: - 2666-1667 publication_status: epub_ahead publisher: Elsevier quality_controlled: '1' related_material: link: - relation: software url: http://github.com/hippenmeyerlab scopus_import: '1' status: public title: Time-lapse imaging of cortical projection neuron migration in mice using mosaic analysis with double markers type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 5 year: '2024' ... --- _id: '12875' abstract: - lang: eng text: The superior colliculus (SC) in the mammalian midbrain is essential for multisensory integration and is composed of a rich diversity of excitatory and inhibitory neurons and glia. However, the developmental principles directing the generation of SC cell-type diversity are not understood. Here, we pursued systematic cell lineage tracing in silico and in vivo, preserving full spatial information, using genetic mosaic analysis with double markers (MADM)-based clonal analysis with single-cell sequencing (MADM-CloneSeq). The analysis of clonally related cell lineages revealed that radial glial progenitors (RGPs) in SC are exceptionally multipotent. Individual resident RGPs have the capacity to produce all excitatory and inhibitory SC neuron types, even at the stage of terminal division. While individual clonal units show no pre-defined cellular composition, the establishment of appropriate relative proportions of distinct neuronal types occurs in a PTEN-dependent manner. Collectively, our findings provide an inaugural framework at the single-RGP/-cell level of the mammalian SC ontogeny. acknowledged_ssus: - _id: Bio - _id: M-Shop - _id: LifeSc - _id: PreCl acknowledgement: "We thank Liqun Luo for his continued support, for providing essential resources for generating Fzd10-CreER mice which were generated in his laboratory, and for comments on the manuscript; W. Zhong for providing Nestin-Cre transgenic mouse line for this study; A. Heger for mouse colony management; R. Beattie and T. Asenov for designing and producing components of acute slice recovery chamber for MADM-CloneSeq experiments; and K. Leopold, J. Rodarte and N. Amberg for initial experiments, technical support and/or assistance. This study was supported by the Scientific Service Units (SSU) of IST Austria through resources provided by the Imaging & Optics Facility (IOF), Laboratory Support Facility (LSF), Miba Machine Shop, and Pre-clinical Facility (PCF). G.C. received funding from European Commission (IST plus postdoctoral fellowship). This work was supported by ISTA institutional\r\nfunds; the Austrian Science Fund Special Research Programmes (FWF SFB F78 Neuro Stem Modulation) to S.H. " article_processing_charge: Yes (via OA deal) article_type: original author: - first_name: Giselle T full_name: Cheung, Giselle T id: 471195F6-F248-11E8-B48F-1D18A9856A87 last_name: Cheung orcid: 0000-0001-8457-2572 - first_name: Florian full_name: Pauler, Florian id: 48EA0138-F248-11E8-B48F-1D18A9856A87 last_name: Pauler orcid: 0000-0002-7462-0048 - first_name: Peter full_name: Koppensteiner, Peter id: 3B8B25A8-F248-11E8-B48F-1D18A9856A87 last_name: Koppensteiner orcid: 0000-0002-3509-1948 - first_name: Thomas full_name: Krausgruber, Thomas last_name: Krausgruber - first_name: Carmen full_name: Streicher, Carmen id: 36BCB99C-F248-11E8-B48F-1D18A9856A87 last_name: Streicher - first_name: Martin full_name: Schrammel, Martin id: f13e7cae-e8bd-11ed-841a-96dedf69f46d last_name: Schrammel - first_name: Natalie Y full_name: Özgen, Natalie Y id: e68ece33-f6e0-11ea-865d-ae1031dcc090 last_name: Özgen - first_name: Alexis full_name: Ivec, Alexis id: 1d144691-e8be-11ed-9b33-bdd3077fad4c last_name: Ivec - first_name: Christoph full_name: Bock, Christoph last_name: Bock - first_name: Ryuichi full_name: Shigemoto, Ryuichi id: 499F3ABC-F248-11E8-B48F-1D18A9856A87 last_name: Shigemoto orcid: 0000-0001-8761-9444 - first_name: Simon full_name: Hippenmeyer, Simon id: 37B36620-F248-11E8-B48F-1D18A9856A87 last_name: Hippenmeyer orcid: 0000-0003-2279-1061 citation: ama: Cheung GT, Pauler F, Koppensteiner P, et al. Multipotent progenitors instruct ontogeny of the superior colliculus. Neuron. 2024;112(2):230-246.e11. doi:10.1016/j.neuron.2023.11.009 apa: Cheung, G. T., Pauler, F., Koppensteiner, P., Krausgruber, T., Streicher, C., Schrammel, M., … Hippenmeyer, S. (2024). Multipotent progenitors instruct ontogeny of the superior colliculus. Neuron. Elsevier. https://doi.org/10.1016/j.neuron.2023.11.009 chicago: Cheung, Giselle T, Florian Pauler, Peter Koppensteiner, Thomas Krausgruber, Carmen Streicher, Martin Schrammel, Natalie Y Özgen, et al. “Multipotent Progenitors Instruct Ontogeny of the Superior Colliculus.” Neuron. Elsevier, 2024. https://doi.org/10.1016/j.neuron.2023.11.009. ieee: G. T. Cheung et al., “Multipotent progenitors instruct ontogeny of the superior colliculus,” Neuron, vol. 112, no. 2. Elsevier, p. 230–246.e11, 2024. ista: Cheung GT, Pauler F, Koppensteiner P, Krausgruber T, Streicher C, Schrammel M, Özgen NY, Ivec A, Bock C, Shigemoto R, Hippenmeyer S. 2024. Multipotent progenitors instruct ontogeny of the superior colliculus. Neuron. 112(2), 230–246.e11. mla: Cheung, Giselle T., et al. “Multipotent Progenitors Instruct Ontogeny of the Superior Colliculus.” Neuron, vol. 112, no. 2, Elsevier, 2024, p. 230–246.e11, doi:10.1016/j.neuron.2023.11.009. short: G.T. Cheung, F. Pauler, P. Koppensteiner, T. Krausgruber, C. Streicher, M. Schrammel, N.Y. Özgen, A. Ivec, C. Bock, R. Shigemoto, S. Hippenmeyer, Neuron 112 (2024) 230–246.e11. date_created: 2023-04-27T09:41:48Z date_published: 2024-01-17T00:00:00Z date_updated: 2024-03-05T09:43:02Z day: '17' ddc: - '570' department: - _id: SiHi - _id: RySh doi: 10.1016/j.neuron.2023.11.009 external_id: pmid: - '38096816' file: - access_level: open_access checksum: 32b3788f7085cf44a84108d8faaff3ce content_type: application/pdf creator: dernst date_created: 2024-02-06T13:56:15Z date_updated: 2024-02-06T13:56:15Z file_id: '14944' file_name: 2024_Neuron_Cheung.pdf file_size: 5942467 relation: main_file success: 1 file_date_updated: 2024-02-06T13:56:15Z has_accepted_license: '1' intvolume: ' 112' issue: '2' language: - iso: eng month: '01' oa: 1 oa_version: Published Version page: 230-246.e11 pmid: 1 project: - _id: 059F6AB4-7A3F-11EA-A408-12923DDC885E grant_number: F07805 name: Molecular Mechanisms of Neural Stem Cell Lineage Progression publication: Neuron publication_identifier: issn: - 0896-6273 publication_status: published publisher: Elsevier quality_controlled: '1' related_material: link: - description: News on ISTA Website relation: press_release url: https://ista.ac.at/en/news/the-pedigree-of-brain-cells/ scopus_import: '1' status: public title: Multipotent progenitors instruct ontogeny of the superior colliculus 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: 112 year: '2024' ... --- _id: '12542' abstract: - lang: eng text: In this issue of Neuron, Espinosa-Medina et al.1 present the TEMPO (Temporal Encoding and Manipulation in a Predefined Order) system, which enables the marking and genetic manipulation of sequentially generated cell lineages in vertebrate species in vivo. article_processing_charge: No article_type: letter_note author: - first_name: Ana full_name: Villalba Requena, Ana id: 68cb85a0-39f7-11eb-9559-9aaab4f6a247 last_name: Villalba Requena orcid: 0000-0002-5615-5277 - first_name: Simon full_name: Hippenmeyer, Simon id: 37B36620-F248-11E8-B48F-1D18A9856A87 last_name: Hippenmeyer orcid: 0000-0003-2279-1061 citation: ama: Villalba Requena A, Hippenmeyer S. Going back in time with TEMPO. Neuron. 2023;111(3):291-293. doi:10.1016/j.neuron.2023.01.006 apa: Villalba Requena, A., & Hippenmeyer, S. (2023). Going back in time with TEMPO. Neuron. Elsevier. https://doi.org/10.1016/j.neuron.2023.01.006 chicago: Villalba Requena, Ana, and Simon Hippenmeyer. “Going Back in Time with TEMPO.” Neuron. Elsevier, 2023. https://doi.org/10.1016/j.neuron.2023.01.006. ieee: A. Villalba Requena and S. Hippenmeyer, “Going back in time with TEMPO,” Neuron, vol. 111, no. 3. Elsevier, pp. 291–293, 2023. ista: Villalba Requena A, Hippenmeyer S. 2023. Going back in time with TEMPO. Neuron. 111(3), 291–293. mla: Villalba Requena, Ana, and Simon Hippenmeyer. “Going Back in Time with TEMPO.” Neuron, vol. 111, no. 3, Elsevier, 2023, pp. 291–93, doi:10.1016/j.neuron.2023.01.006. short: A. Villalba Requena, S. Hippenmeyer, Neuron 111 (2023) 291–293. date_created: 2023-02-12T23:00:58Z date_published: 2023-02-01T00:00:00Z date_updated: 2023-08-01T13:10:27Z day: '01' department: - _id: SiHi doi: 10.1016/j.neuron.2023.01.006 external_id: isi: - '000994473300001' intvolume: ' 111' isi: 1 issue: '3' language: - iso: eng month: '02' oa_version: None page: 291-293 publication: Neuron publication_identifier: eissn: - 1097-4199 publication_status: published publisher: Elsevier quality_controlled: '1' scopus_import: '1' status: public title: Going back in time with TEMPO type: journal_article user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8 volume: 111 year: '2023' ... --- _id: '12679' abstract: - lang: eng text: How to generate a brain of correct size and with appropriate cell-type diversity during development is a major question in Neuroscience. In the developing neocortex, radial glial progenitor (RGP) cells are the main neural stem cells that produce cortical excitatory projection neurons, glial cells, and establish the prospective postnatal stem cell niche in the lateral ventricles. RGPs follow a tightly orchestrated developmental program that when disrupted can result in severe cortical malformations such as microcephaly and megalencephaly. The precise cellular and molecular mechanisms instructing faithful RGP lineage progression are however not well understood. This review will summarize recent conceptual advances that contribute to our understanding of the general principles of RGP lineage progression. acknowledgement: "I wish to thank all current and past members of the Hippenmeyer laboratory at ISTA for exciting discussions on the subject of this review. I apologize to colleagues whose work I could not cite and/or discuss in the frame of the available space. Work in the Hippenmeyer laboratory on the\r\ndiscussed topic is supported by ISTA institutional funds, FWF SFB F78 to S.H., and the European Research Council (ERC) under the European Union’s Horizon 2020 Research and Innovation Programme (grant agree-ment no. 725780 LinPro) to SH." article_number: '102695' article_processing_charge: Yes (via OA deal) 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. Principles of neural stem cell lineage progression: Insights from developing cerebral cortex. Current Opinion in Neurobiology. 2023;79(4). doi:10.1016/j.conb.2023.102695' apa: 'Hippenmeyer, S. (2023). Principles of neural stem cell lineage progression: Insights from developing cerebral cortex. Current Opinion in Neurobiology. Elsevier. https://doi.org/10.1016/j.conb.2023.102695' chicago: 'Hippenmeyer, Simon. “Principles of Neural Stem Cell Lineage Progression: Insights from Developing Cerebral Cortex.” Current Opinion in Neurobiology. Elsevier, 2023. https://doi.org/10.1016/j.conb.2023.102695.' ieee: 'S. Hippenmeyer, “Principles of neural stem cell lineage progression: Insights from developing cerebral cortex,” Current Opinion in Neurobiology, vol. 79, no. 4. Elsevier, 2023.' ista: 'Hippenmeyer S. 2023. Principles of neural stem cell lineage progression: Insights from developing cerebral cortex. Current Opinion in Neurobiology. 79(4), 102695.' mla: 'Hippenmeyer, Simon. “Principles of Neural Stem Cell Lineage Progression: Insights from Developing Cerebral Cortex.” Current Opinion in Neurobiology, vol. 79, no. 4, 102695, Elsevier, 2023, doi:10.1016/j.conb.2023.102695.' short: S. Hippenmeyer, Current Opinion in Neurobiology 79 (2023). date_created: 2023-02-26T12:24:21Z date_published: 2023-04-01T00:00:00Z date_updated: 2023-08-16T12:30:25Z day: '01' ddc: - '570' department: - _id: SiHi doi: 10.1016/j.conb.2023.102695 ec_funded: 1 external_id: isi: - '000953497700001' pmid: - '36842274' file: - access_level: open_access checksum: 4d11c4ca87e6cbc4d2ac46d3225ea615 content_type: application/pdf creator: dernst date_created: 2023-08-16T12:29:06Z date_updated: 2023-08-16T12:29:06Z file_id: '14071' file_name: 2023_CurrentOpinionNeurobio_Hippenmeyer.pdf file_size: 1787894 relation: main_file success: 1 file_date_updated: 2023-08-16T12:29:06Z has_accepted_license: '1' intvolume: ' 79' isi: 1 issue: '4' keyword: - General Neuroscience language: - iso: eng month: '04' oa: 1 oa_version: Published Version pmid: 1 project: - _id: 059F6AB4-7A3F-11EA-A408-12923DDC885E grant_number: F07805 name: Molecular Mechanisms of Neural Stem Cell Lineage Progression - _id: 260018B0-B435-11E9-9278-68D0E5697425 call_identifier: H2020 grant_number: '725780' name: Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development publication: Current Opinion in Neurobiology publication_identifier: issn: - 0959-4388 publication_status: published publisher: Elsevier quality_controlled: '1' scopus_import: '1' status: public title: 'Principles of neural stem cell lineage progression: Insights from developing cerebral cortex' 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: 79 year: '2023' ... --- _id: '12562' abstract: - lang: eng text: Presynaptic inputs determine the pattern of activation of postsynaptic neurons in a neural circuit. Molecular and genetic pathways that regulate the selective formation of subsets of presynaptic inputs are largely unknown, despite significant understanding of the general process of synaptogenesis. In this study, we have begun to identify such factors using the spinal monosynaptic stretch reflex circuit as a model system. In this neuronal circuit, Ia proprioceptive afferents establish monosynaptic connections with spinal motor neurons that project to the same muscle (termed homonymous connections) or muscles with related or synergistic function. However, monosynaptic connections are not formed with motor neurons innervating muscles with antagonistic functions. The ETS transcription factor ER81 (also known as ETV1) is expressed by all proprioceptive afferents, but only a small set of motor neuron pools in the lumbar spinal cord of the mouse. Here we use conditional mouse genetic techniques to eliminate Er81 expression selectively from motor neurons. We find that ablation of Er81 in motor neurons reduces synaptic inputs from proprioceptive afferents conveying information from homonymous and synergistic muscles, with no change observed in the connectivity pattern from antagonistic proprioceptive afferents. In summary, these findings suggest a role for ER81 in defined motor neuron pools to control the assembly of specific presynaptic inputs and thereby influence the profile of activation of these motor neurons. acknowledgement: The authors gratefully thank Dr. Silvia Arber, University of Basel and Friedrich Miescher Institute for Biomedical Research, for support and in whose lab the data were collected. For advice on statistical analysis, we thank Michael Bottomley from the Statistical Consulting Center, College of Science and Mathematics, Wright State University. article_processing_charge: No article_type: original author: - first_name: David R. full_name: Ladle, David R. last_name: Ladle - first_name: Simon full_name: Hippenmeyer, Simon id: 37B36620-F248-11E8-B48F-1D18A9856A87 last_name: Hippenmeyer orcid: 0000-0003-2279-1061 citation: ama: Ladle DR, Hippenmeyer S. Loss of ETV1/ER81 in motor neurons leads to reduced monosynaptic inputs from proprioceptive sensory neurons. Journal of Neurophysiology. 2023;129(3):501-512. doi:10.1152/jn.00172.2022 apa: Ladle, D. R., & Hippenmeyer, S. (2023). Loss of ETV1/ER81 in motor neurons leads to reduced monosynaptic inputs from proprioceptive sensory neurons. Journal of Neurophysiology. American Physiological Society. https://doi.org/10.1152/jn.00172.2022 chicago: Ladle, David R., and Simon Hippenmeyer. “Loss of ETV1/ER81 in Motor Neurons Leads to Reduced Monosynaptic Inputs from Proprioceptive Sensory Neurons.” Journal of Neurophysiology. American Physiological Society, 2023. https://doi.org/10.1152/jn.00172.2022. ieee: D. R. Ladle and S. Hippenmeyer, “Loss of ETV1/ER81 in motor neurons leads to reduced monosynaptic inputs from proprioceptive sensory neurons,” Journal of Neurophysiology, vol. 129, no. 3. American Physiological Society, pp. 501–512, 2023. ista: Ladle DR, Hippenmeyer S. 2023. Loss of ETV1/ER81 in motor neurons leads to reduced monosynaptic inputs from proprioceptive sensory neurons. Journal of Neurophysiology. 129(3), 501–512. mla: Ladle, David R., and Simon Hippenmeyer. “Loss of ETV1/ER81 in Motor Neurons Leads to Reduced Monosynaptic Inputs from Proprioceptive Sensory Neurons.” Journal of Neurophysiology, vol. 129, no. 3, American Physiological Society, 2023, pp. 501–12, doi:10.1152/jn.00172.2022. short: D.R. Ladle, S. Hippenmeyer, Journal of Neurophysiology 129 (2023) 501–512. date_created: 2023-02-15T14:46:14Z date_published: 2023-03-01T00:00:00Z date_updated: 2023-09-05T12:13:34Z day: '01' department: - _id: SiHi doi: 10.1152/jn.00172.2022 external_id: isi: - '000957721600001' pmid: - '36695533' intvolume: ' 129' isi: 1 issue: '3' keyword: - Physiology - General Neuroscience language: - iso: eng month: '03' oa_version: None page: 501-512 pmid: 1 publication: Journal of Neurophysiology publication_identifier: eissn: - 1522-1598 issn: - 0022-3077 publication_status: published publisher: American Physiological Society quality_controlled: '1' status: public title: Loss of ETV1/ER81 in motor neurons leads to reduced monosynaptic inputs from proprioceptive sensory neurons type: journal_article user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1 volume: 129 year: '2023' ... --- _id: '14647' abstract: - lang: eng text: In the developing vertebrate central nervous system, neurons and glia typically arise sequentially from common progenitors. Here, we report that the transcription factor Forkhead Box G1 (Foxg1) regulates gliogenesis in the mouse neocortex via distinct cell-autonomous roles in progenitors and in postmitotic neurons that regulate different aspects of the gliogenic FGF signalling pathway. We demonstrate that loss of Foxg1 in cortical progenitors at neurogenic stages causes premature astrogliogenesis. We identify a novel FOXG1 target, the pro-gliogenic FGF pathway component Fgfr3, which is suppressed by FOXG1 cell-autonomously to maintain neurogenesis. Furthermore, FOXG1 can also suppress premature astrogliogenesis triggered by the augmentation of FGF signalling. We identify a second novel function of FOXG1 in regulating the expression of gliogenic ligand FGF18 in new born neocortical upper-layer neurons. Loss of FOXG1 in postmitotic neurons increases Fgf18 expression and enhances gliogenesis in the progenitors. These results fit well with the model that new born neurons secrete cues that trigger progenitors to produce the next wave of cell types, astrocytes. If FGF signalling is attenuated in Foxg1 null progenitors, they progress to oligodendrocyte production. Therefore, loss of FOXG1 transitions the progenitor to a gliogenic state, producing either astrocytes or oligodendrocytes depending on FGF signalling levels. Our results uncover how FOXG1 integrates extrinsic signalling via the FGF pathway to regulate the sequential generation of neurons, astrocytes, and oligodendrocytes in the cerebral cortex. acknowledgement: "We thank Dr. Shital Suryavanshi and the animal house staff of the Tata Institute of\r\nFundamental Research (TIFR) for their excellent support; Gord Fishell and Goichi Miyoshi for\r\nthe Foxg1 floxed mouse line; Hiroshi Kawasaki for the plasmids pCAG-FGF8 and pCAGsFGFR3c. We thank Prof. S.K. Lee for the Foxg1lox/lox genotyping primers and protocol. We thank Dr. Deepak Modi and Dr. Vainav Patel for allowing us to use the NIRRCH FACS Facility and the staff of the NIRRCH and TIFR FACS facilities for their assistance.\r\nWe thank Denis Jabaudon for his critical comments on the manuscript and members of the\r\nJabaudon lab for helpful discussions. This work was funded by the Department of Atomic\r\nEnergy (DAE), Govt. of India (Project Identification no. RTI4003, DAE OM no.\r\n1303/2/2019/R&D-II/DAE/2079)." article_processing_charge: No author: - first_name: Mahima full_name: Bose, Mahima last_name: Bose - first_name: Varun full_name: Suresh, Varun last_name: Suresh - first_name: Urvi full_name: Mishra, Urvi last_name: Mishra - first_name: Ishita full_name: Talwar, Ishita last_name: Talwar - first_name: Anuradha full_name: Yadav, Anuradha last_name: Yadav - first_name: Shiona full_name: Biswas, Shiona last_name: Biswas - first_name: Simon full_name: Hippenmeyer, Simon id: 37B36620-F248-11E8-B48F-1D18A9856A87 last_name: Hippenmeyer orcid: 0000-0003-2279-1061 - first_name: Shubha full_name: Tole, Shubha last_name: Tole citation: ama: Bose M, Suresh V, Mishra U, et al. Dual role of FOXG1 in regulating gliogenesis in the developing neocortex via the FGF signalling pathway. bioRxiv. doi:10.1101/2023.11.30.569337 apa: Bose, M., Suresh, V., Mishra, U., Talwar, I., Yadav, A., Biswas, S., … Tole, S. (n.d.). Dual role of FOXG1 in regulating gliogenesis in the developing neocortex via the FGF signalling pathway. bioRxiv. Cold Spring Harbor Laboratory. https://doi.org/10.1101/2023.11.30.569337 chicago: Bose, Mahima, Varun Suresh, Urvi Mishra, Ishita Talwar, Anuradha Yadav, Shiona Biswas, Simon Hippenmeyer, and Shubha Tole. “Dual Role of FOXG1 in Regulating Gliogenesis in the Developing Neocortex via the FGF Signalling Pathway.” BioRxiv. Cold Spring Harbor Laboratory, n.d. https://doi.org/10.1101/2023.11.30.569337. ieee: M. Bose et al., “Dual role of FOXG1 in regulating gliogenesis in the developing neocortex via the FGF signalling pathway,” bioRxiv. Cold Spring Harbor Laboratory. ista: Bose M, Suresh V, Mishra U, Talwar I, Yadav A, Biswas S, Hippenmeyer S, Tole S. Dual role of FOXG1 in regulating gliogenesis in the developing neocortex via the FGF signalling pathway. bioRxiv, 10.1101/2023.11.30.569337. mla: Bose, Mahima, et al. “Dual Role of FOXG1 in Regulating Gliogenesis in the Developing Neocortex via the FGF Signalling Pathway.” BioRxiv, Cold Spring Harbor Laboratory, doi:10.1101/2023.11.30.569337. short: M. Bose, V. Suresh, U. Mishra, I. Talwar, A. Yadav, S. Biswas, S. Hippenmeyer, S. Tole, BioRxiv (n.d.). date_created: 2023-12-06T13:07:01Z date_published: 2023-12-01T00:00:00Z date_updated: 2023-12-11T07:37:17Z day: '01' department: - _id: SiHi doi: 10.1101/2023.11.30.569337 language: - iso: eng main_file_link: - open_access: '1' url: https://doi.org/10.1101/2023.11.30.569337 month: '12' oa: 1 oa_version: Preprint publication: bioRxiv publication_status: submitted publisher: Cold Spring Harbor Laboratory status: public title: Dual role of FOXG1 in regulating gliogenesis in the developing neocortex via the FGF signalling pathway type: preprint user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 year: '2023' ... --- _id: '14683' abstract: - lang: eng text: "Mosaic analysis with double markers (MADM) technology enables the generation of genetic mosaic tissue in mice and high-resolution phenotyping at the individual cell level. Here, we present a protocol for isolating MADM-labeled cells with high yield for downstream molecular analyses using fluorescence-activated cell sorting (FACS). We describe steps for generating MADM-labeled mice, perfusion, single-cell suspension, and debris removal. We then detail procedures for cell sorting by FACS and downstream analysis. This protocol is suitable for embryonic to adult mice.\r\nFor complete details on the use and execution of this protocol, please refer to Contreras et al. (2021).1" acknowledged_ssus: - _id: Bio - _id: PreCl acknowledgement: This research was supported by the Scientific Service Units (SSU) at IST Austria through resources provided by the Imaging & Optics Facility (IOF) and Preclinical Facilities (PCF). N.A. received support from FWF Firnberg-Programme (T 1031). G.C. received support from the European Union’s Horizon 2020 research and innovation programme under the Marie Skłodowska-Curie grant agreement no. 754411 as an ISTplus postdoctoral fellow. This work was also supported by IST Austria institutional funds, FWF SFB F78 to S.H., and the European Research Council (ERC) under the European Union’s Horizon 2020 research and innovation programme (grant agreement no. 725780 LinPro) to S.H. article_number: '102771' article_processing_charge: No article_type: review author: - first_name: Nicole full_name: Amberg, Nicole id: 4CD6AAC6-F248-11E8-B48F-1D18A9856A87 last_name: Amberg orcid: 0000-0002-3183-8207 - first_name: Giselle T full_name: Cheung, Giselle T id: 471195F6-F248-11E8-B48F-1D18A9856A87 last_name: Cheung orcid: 0000-0001-8457-2572 - first_name: Simon full_name: Hippenmeyer, Simon id: 37B36620-F248-11E8-B48F-1D18A9856A87 last_name: Hippenmeyer orcid: 0000-0003-2279-1061 citation: ama: Amberg N, Cheung GT, Hippenmeyer S. Protocol for sorting cells from mouse brains labeled with mosaic analysis with double markers by flow cytometry. STAR Protocols. 2023;5(1). doi:10.1016/j.xpro.2023.102771 apa: Amberg, N., Cheung, G. T., & Hippenmeyer, S. (2023). Protocol for sorting cells from mouse brains labeled with mosaic analysis with double markers by flow cytometry. STAR Protocols. Elsevier. https://doi.org/10.1016/j.xpro.2023.102771 chicago: Amberg, Nicole, Giselle T Cheung, and Simon Hippenmeyer. “Protocol for Sorting Cells from Mouse Brains Labeled with Mosaic Analysis with Double Markers by Flow Cytometry.” STAR Protocols. Elsevier, 2023. https://doi.org/10.1016/j.xpro.2023.102771. ieee: N. Amberg, G. T. Cheung, and S. Hippenmeyer, “Protocol for sorting cells from mouse brains labeled with mosaic analysis with double markers by flow cytometry,” STAR Protocols, vol. 5, no. 1. Elsevier, 2023. ista: Amberg N, Cheung GT, Hippenmeyer S. 2023. Protocol for sorting cells from mouse brains labeled with mosaic analysis with double markers by flow cytometry. STAR Protocols. 5(1), 102771. mla: Amberg, Nicole, et al. “Protocol for Sorting Cells from Mouse Brains Labeled with Mosaic Analysis with Double Markers by Flow Cytometry.” STAR Protocols, vol. 5, no. 1, 102771, Elsevier, 2023, doi:10.1016/j.xpro.2023.102771. short: N. Amberg, G.T. Cheung, S. Hippenmeyer, STAR Protocols 5 (2023). date_created: 2023-12-13T11:48:05Z date_published: 2023-12-08T00:00:00Z date_updated: 2023-12-18T08:06:14Z day: '08' ddc: - '570' department: - _id: SiHi doi: 10.1016/j.xpro.2023.102771 ec_funded: 1 external_id: pmid: - '38070137' intvolume: ' 5' issue: '1' keyword: - General Immunology and Microbiology - General Biochemistry - Genetics and Molecular Biology - General Neuroscience language: - iso: eng main_file_link: - open_access: '1' url: https://doi.org/10.1016/j.xpro.2023.102771 month: '12' oa: 1 oa_version: Submitted Version pmid: 1 project: - _id: 268F8446-B435-11E9-9278-68D0E5697425 call_identifier: FWF grant_number: T0101031 name: Role of Eed in neural stem cell lineage progression - _id: 260C2330-B435-11E9-9278-68D0E5697425 call_identifier: H2020 grant_number: '754411' name: ISTplus - Postdoctoral Fellowships - _id: 059F6AB4-7A3F-11EA-A408-12923DDC885E grant_number: F07805 name: Molecular Mechanisms of Neural Stem Cell Lineage Progression - _id: 260018B0-B435-11E9-9278-68D0E5697425 call_identifier: H2020 grant_number: '725780' name: Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development publication: STAR Protocols publication_identifier: issn: - 2666-1667 publication_status: epub_ahead publisher: Elsevier quality_controlled: '1' scopus_import: '1' status: public title: Protocol for sorting cells from mouse brains labeled with mosaic analysis with double markers by flow cytometry 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: 5 year: '2023' ... --- _id: '14757' abstract: - lang: eng text: The cerebral cortex is comprised of a vast cell-type diversity sequentially generated by cortical progenitor cells. Faithful progenitor lineage progression requires the tight orchestration of distinct molecular and cellular mechanisms regulating proper progenitor proliferation behavior and differentiation. Correct execution of developmental programs involves a complex interplay of cell intrinsic and tissue-wide mechanisms. Many studies over the past decades have been able to determine a plethora of genes critically involved in cortical development. However, only a few made use of genetic paradigms with sparse and global gene deletion to probe cell-autonomous vs. tissue-wide contribution. In this chapter, we will elaborate on the importance of dissecting the cell-autonomous and tissue-wide mechanisms to gain a precise understanding of gene function during radial glial progenitor lineage progression. article_processing_charge: No author: - first_name: Ana full_name: Villalba Requena, Ana id: 68cb85a0-39f7-11eb-9559-9aaab4f6a247 last_name: Villalba Requena orcid: 0000-0002-5615-5277 - first_name: Nicole full_name: Amberg, Nicole id: 4CD6AAC6-F248-11E8-B48F-1D18A9856A87 last_name: Amberg orcid: 0000-0002-3183-8207 - first_name: Simon full_name: Hippenmeyer, Simon id: 37B36620-F248-11E8-B48F-1D18A9856A87 last_name: Hippenmeyer orcid: 0000-0003-2279-1061 citation: ama: 'Villalba Requena A, Amberg N, Hippenmeyer S. Interplay of Cell‐autonomous Gene Function and Tissue‐wide Mechanisms Regulating Radial Glial Progenitor Lineage Progression. In: Huttner W, ed. Neocortical Neurogenesis in Development and Evolution. Wiley; 2023:169-191. doi:10.1002/9781119860914.ch10' apa: Villalba Requena, A., Amberg, N., & Hippenmeyer, S. (2023). Interplay of Cell‐autonomous Gene Function and Tissue‐wide Mechanisms Regulating Radial Glial Progenitor Lineage Progression. In W. Huttner (Ed.), Neocortical Neurogenesis in Development and Evolution (pp. 169–191). Wiley. https://doi.org/10.1002/9781119860914.ch10 chicago: Villalba Requena, Ana, Nicole Amberg, and Simon Hippenmeyer. “Interplay of Cell‐autonomous Gene Function and Tissue‐wide Mechanisms Regulating Radial Glial Progenitor Lineage Progression.” In Neocortical Neurogenesis in Development and Evolution, edited by Wieland Huttner, 169–91. Wiley, 2023. https://doi.org/10.1002/9781119860914.ch10. ieee: A. Villalba Requena, N. Amberg, and S. Hippenmeyer, “Interplay of Cell‐autonomous Gene Function and Tissue‐wide Mechanisms Regulating Radial Glial Progenitor Lineage Progression,” in Neocortical Neurogenesis in Development and Evolution, W. Huttner, Ed. Wiley, 2023, pp. 169–191. ista: 'Villalba Requena A, Amberg N, Hippenmeyer S. 2023.Interplay of Cell‐autonomous Gene Function and Tissue‐wide Mechanisms Regulating Radial Glial Progenitor Lineage Progression. In: Neocortical Neurogenesis in Development and Evolution. , 169–191.' mla: Villalba Requena, Ana, et al. “Interplay of Cell‐autonomous Gene Function and Tissue‐wide Mechanisms Regulating Radial Glial Progenitor Lineage Progression.” Neocortical Neurogenesis in Development and Evolution, edited by Wieland Huttner, Wiley, 2023, pp. 169–91, doi:10.1002/9781119860914.ch10. short: A. Villalba Requena, N. Amberg, S. Hippenmeyer, in:, W. Huttner (Ed.), Neocortical Neurogenesis in Development and Evolution, Wiley, 2023, pp. 169–191. date_created: 2024-01-08T13:16:36Z date_published: 2023-08-08T00:00:00Z date_updated: 2024-01-09T09:46:57Z day: '08' department: - _id: SiHi doi: 10.1002/9781119860914.ch10 editor: - first_name: Wieland full_name: Huttner, Wieland last_name: Huttner language: - iso: eng month: '08' oa_version: None page: 169-191 publication: Neocortical Neurogenesis in Development and Evolution publication_identifier: eisbn: - '9781119860914' publication_status: published publisher: Wiley quality_controlled: '1' scopus_import: '1' status: public title: Interplay of Cell‐autonomous Gene Function and Tissue‐wide Mechanisms Regulating Radial Glial Progenitor Lineage Progression type: book_chapter user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 year: '2023' ... --- _id: '14783' abstract: - lang: eng text: Connexin 43, an astroglial gap junction protein, is enriched in perisynaptic astroglial processes and plays major roles in synaptic transmission. We have previously found that astroglial Cx43 controls synaptic glutamate levels and allows for activity-dependent glutamine release to sustain physiological synaptic transmissions and cognitiogns. However, whether Cx43 is important for the release of synaptic vesicles, which is a critical component of synaptic efficacy, remains unanswered. Here, using transgenic mice with a glial conditional knockout of Cx43 (Cx43−/−), we investigate whether and how astrocytes regulate the release of synaptic vesicles from hippocampal synapses. We report that CA1 pyramidal neurons and their synapses develop normally in the absence of astroglial Cx43. However, a significant impairment in synaptic vesicle distribution and release dynamics were observed. In particular, the FM1-43 assays performed using two-photon live imaging and combined with multi-electrode array stimulation in acute hippocampal slices, revealed a slower rate of synaptic vesicle release in Cx43−/− mice. Furthermore, paired-pulse recordings showed that synaptic vesicle release probability was also reduced and is dependent on glutamine supply via Cx43 hemichannel (HC). Taken together, we have uncovered a role for Cx43 in regulating presynaptic functions by controlling the rate and probability of synaptic vesicle release. Our findings further highlight the significance of astroglial Cx43 in synaptic transmission and efficacy. acknowledgement: 'This research was funded by grants from the European Research Council (Consolidator grant #683154) and European Union’s Horizon 2020 research and innovation program (Marie Sklodowska-Curie Innovative Training Networks, grant #722053, EU-GliaPhD) to N.R., as well as from FP7-PEOPLE Marie Curie Intra-European Fellowship for career development (grant #622289) to G.C. We thank Elena Dossi, Grégory Ghézali, and Jérémie Teillon for support with setting up the MEA system for the two-photon microscope. We would also like to thank Tayfun Palaz for their technical assistance with the EM preparations.' article_number: '1133' article_processing_charge: Yes article_type: original author: - first_name: Giselle T full_name: Cheung, Giselle T id: 471195F6-F248-11E8-B48F-1D18A9856A87 last_name: Cheung orcid: 0000-0001-8457-2572 - first_name: Oana full_name: Chever, Oana last_name: Chever - first_name: Astrid full_name: Rollenhagen, Astrid last_name: Rollenhagen - first_name: Nicole full_name: Quenech’du, Nicole last_name: Quenech’du - first_name: Pascal full_name: Ezan, Pascal last_name: Ezan - first_name: Joachim H. R. full_name: Lübke, Joachim H. R. last_name: Lübke - first_name: Nathalie full_name: Rouach, Nathalie last_name: Rouach citation: ama: Cheung GT, Chever O, Rollenhagen A, et al. Astroglial connexin 43 regulates synaptic vesicle release at hippocampal synapses. Cells. 2023;12(8). doi:10.3390/cells12081133 apa: Cheung, G. T., Chever, O., Rollenhagen, A., Quenech’du, N., Ezan, P., Lübke, J. H. R., & Rouach, N. (2023). Astroglial connexin 43 regulates synaptic vesicle release at hippocampal synapses. Cells. MDPI. https://doi.org/10.3390/cells12081133 chicago: Cheung, Giselle T, Oana Chever, Astrid Rollenhagen, Nicole Quenech’du, Pascal Ezan, Joachim H. R. Lübke, and Nathalie Rouach. “Astroglial Connexin 43 Regulates Synaptic Vesicle Release at Hippocampal Synapses.” Cells. MDPI, 2023. https://doi.org/10.3390/cells12081133. ieee: G. T. Cheung et al., “Astroglial connexin 43 regulates synaptic vesicle release at hippocampal synapses,” Cells, vol. 12, no. 8. MDPI, 2023. ista: Cheung GT, Chever O, Rollenhagen A, Quenech’du N, Ezan P, Lübke JHR, Rouach N. 2023. Astroglial connexin 43 regulates synaptic vesicle release at hippocampal synapses. Cells. 12(8), 1133. mla: Cheung, Giselle T., et al. “Astroglial Connexin 43 Regulates Synaptic Vesicle Release at Hippocampal Synapses.” Cells, vol. 12, no. 8, 1133, MDPI, 2023, doi:10.3390/cells12081133. short: G.T. Cheung, O. Chever, A. Rollenhagen, N. Quenech’du, P. Ezan, J.H.R. Lübke, N. Rouach, Cells 12 (2023). date_created: 2024-01-10T09:46:35Z date_published: 2023-04-11T00:00:00Z date_updated: 2024-01-16T09:29:35Z day: '11' ddc: - '570' department: - _id: SiHi doi: 10.3390/cells12081133 external_id: isi: - '000977445700001' pmid: - '37190042' file: - access_level: open_access checksum: 6798cd75d8857976fbc58a43fd173d68 content_type: application/pdf creator: dernst date_created: 2024-01-16T09:26:52Z date_updated: 2024-01-16T09:26:52Z file_id: '14808' file_name: 2023_Cells_Cheung.pdf file_size: 7931643 relation: main_file success: 1 file_date_updated: 2024-01-16T09:26:52Z has_accepted_license: '1' intvolume: ' 12' isi: 1 issue: '8' keyword: - General Medicine language: - iso: eng month: '04' oa: 1 oa_version: Published Version pmid: 1 publication: Cells publication_identifier: issn: - 2073-4409 publication_status: published publisher: MDPI quality_controlled: '1' status: public title: Astroglial connexin 43 regulates synaptic vesicle release at hippocampal synapses 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: 12 year: '2023' ... --- _id: '12802' abstract: - lang: eng text: Little is known about the critical metabolic changes that neural cells have to undergo during development and how temporary shifts in this program can influence brain circuitries and behavior. Inspired by the discovery that mutations in SLC7A5, a transporter of metabolically essential large neutral amino acids (LNAAs), lead to autism, we employed metabolomic profiling to study the metabolic states of the cerebral cortex across different developmental stages. We found that the forebrain undergoes significant metabolic remodeling throughout development, with certain groups of metabolites showing stage-specific changes, but what are the consequences of perturbing this metabolic program? By manipulating Slc7a5 expression in neural cells, we found that the metabolism of LNAAs and lipids are interconnected in the cortex. Deletion of Slc7a5 in neurons affects the postnatal metabolic state, leading to a shift in lipid metabolism. Additionally, it causes stage- and cell-type-specific alterations in neuronal activity patterns, resulting in a long-term circuit dysfunction. acknowledged_ssus: - _id: PreCl - _id: EM-Fac - _id: Bio - _id: LifeSc acknowledgement: We thank A. Freeman and V. Voronin for technical assistance, S. Deixler, A. Stichelberger, M. Schunn, and the Preclinical Facility for managing our animal colony. We thank L. Andersen and J. Sonntag, who were involved in generating the MADM lines. We thank the ISTA LSF Mass Spectrometry Core Facility for assistance with the proteomic analysis, as well as the ISTA electron microscopy and Imaging and Optics facility for technical support. Metabolomics LC-MS/MS analysis was performed by the Metabolomics Facility at Vienna BioCenter Core Facilities (VBCF). We acknowledge the support of the EMBL Metabolomics Core Facility (MCF) for lipidomics and intracellular metabolomics mass spectrometry data acquisition and analysis. RNA sequencing was performed by the Next Generation Sequencing Facility at VBCF. Schematics were generated using Biorender.com. This work was supported by the Austrian Science Fund (FWF, DK W1232-B24) and by the European Union’s Horizon 2020 research and innovation program (ERC) grant 725780 (LinPro) to S.H. and 715508 (REVERSEAUTISM) to G.N. article_processing_charge: Yes (via OA deal) article_type: original author: - first_name: Lisa full_name: Knaus, Lisa id: 3B2ABCF4-F248-11E8-B48F-1D18A9856A87 last_name: Knaus - first_name: Bernadette full_name: Basilico, Bernadette id: 36035796-5ACA-11E9-A75E-7AF2E5697425 last_name: Basilico orcid: 0000-0003-1843-3173 - first_name: Daniel full_name: Malzl, Daniel last_name: Malzl - first_name: Maria full_name: Gerykova Bujalkova, Maria last_name: Gerykova Bujalkova - first_name: Mateja full_name: Smogavec, Mateja last_name: Smogavec - first_name: Lena A. full_name: Schwarz, Lena A. last_name: Schwarz - first_name: Sarah full_name: Gorkiewicz, Sarah id: f141a35d-15a9-11ec-9fb2-fef6becc7b6f last_name: Gorkiewicz - first_name: Nicole full_name: Amberg, Nicole id: 4CD6AAC6-F248-11E8-B48F-1D18A9856A87 last_name: Amberg orcid: 0000-0002-3183-8207 - first_name: Florian full_name: Pauler, Florian id: 48EA0138-F248-11E8-B48F-1D18A9856A87 last_name: Pauler orcid: 0000-0002-7462-0048 - first_name: Christian full_name: Knittl-Frank, Christian last_name: Knittl-Frank - first_name: Marianna full_name: Tassinari, Marianna id: 7af593f1-d44a-11ed-bf94-a3646a6bb35e last_name: Tassinari - first_name: Nuno full_name: Maulide, Nuno last_name: Maulide - first_name: Thomas full_name: Rülicke, Thomas last_name: Rülicke - first_name: Jörg full_name: Menche, Jörg last_name: Menche - first_name: Simon full_name: Hippenmeyer, Simon id: 37B36620-F248-11E8-B48F-1D18A9856A87 last_name: Hippenmeyer orcid: 0000-0003-2279-1061 - first_name: Gaia full_name: Novarino, Gaia id: 3E57A680-F248-11E8-B48F-1D18A9856A87 last_name: Novarino orcid: 0000-0002-7673-7178 citation: ama: Knaus L, Basilico B, Malzl D, et al. Large neutral amino acid levels tune perinatal neuronal excitability and survival. Cell. 2023;186(9):1950-1967.e25. doi:10.1016/j.cell.2023.02.037 apa: Knaus, L., Basilico, B., Malzl, D., Gerykova Bujalkova, M., Smogavec, M., Schwarz, L. A., … Novarino, G. (2023). Large neutral amino acid levels tune perinatal neuronal excitability and survival. Cell. Elsevier. https://doi.org/10.1016/j.cell.2023.02.037 chicago: Knaus, Lisa, Bernadette Basilico, Daniel Malzl, Maria Gerykova Bujalkova, Mateja Smogavec, Lena A. Schwarz, Sarah Gorkiewicz, et al. “Large Neutral Amino Acid Levels Tune Perinatal Neuronal Excitability and Survival.” Cell. Elsevier, 2023. https://doi.org/10.1016/j.cell.2023.02.037. ieee: L. Knaus et al., “Large neutral amino acid levels tune perinatal neuronal excitability and survival,” Cell, vol. 186, no. 9. Elsevier, p. 1950–1967.e25, 2023. ista: Knaus L, Basilico B, Malzl D, Gerykova Bujalkova M, Smogavec M, Schwarz LA, Gorkiewicz S, Amberg N, Pauler F, Knittl-Frank C, Tassinari M, Maulide N, Rülicke T, Menche J, Hippenmeyer S, Novarino G. 2023. Large neutral amino acid levels tune perinatal neuronal excitability and survival. Cell. 186(9), 1950–1967.e25. mla: Knaus, Lisa, et al. “Large Neutral Amino Acid Levels Tune Perinatal Neuronal Excitability and Survival.” Cell, vol. 186, no. 9, Elsevier, 2023, p. 1950–1967.e25, doi:10.1016/j.cell.2023.02.037. short: L. Knaus, B. Basilico, D. Malzl, M. Gerykova Bujalkova, M. Smogavec, L.A. Schwarz, S. Gorkiewicz, N. Amberg, F. Pauler, C. Knittl-Frank, M. Tassinari, N. Maulide, T. Rülicke, J. Menche, S. Hippenmeyer, G. Novarino, Cell 186 (2023) 1950–1967.e25. date_created: 2023-04-05T08:15:40Z date_published: 2023-04-27T00:00:00Z date_updated: 2024-02-07T08:03:32Z day: '27' ddc: - '570' department: - _id: SiHi - _id: GaNo doi: 10.1016/j.cell.2023.02.037 ec_funded: 1 external_id: isi: - '000991468700001' file: - access_level: open_access checksum: 47e94fbe19e86505b429cb7a5b503ce6 content_type: application/pdf creator: dernst date_created: 2023-05-02T09:26:21Z date_updated: 2023-05-02T09:26:21Z file_id: '12889' file_name: 2023_Cell_Knaus.pdf file_size: 15712841 relation: main_file success: 1 file_date_updated: 2023-05-02T09:26:21Z has_accepted_license: '1' intvolume: ' 186' isi: 1 issue: '9' keyword: - General Biochemistry - Genetics and Molecular Biology language: - iso: eng month: '04' oa: 1 oa_version: Published Version page: 1950-1967.e25 project: - _id: 2548AE96-B435-11E9-9278-68D0E5697425 call_identifier: FWF grant_number: W1232-B24 name: Molecular Drug Targets - _id: 260018B0-B435-11E9-9278-68D0E5697425 call_identifier: H2020 grant_number: '725780' name: Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development - _id: 25444568-B435-11E9-9278-68D0E5697425 call_identifier: H2020 grant_number: '715508' name: Probing the Reversibility of Autism Spectrum Disorders by Employing in vivo and in vitro Models publication: Cell publication_identifier: issn: - 0092-8674 publication_status: published publisher: Elsevier quality_controlled: '1' related_material: link: - description: News on ISTA Website relation: press_release url: https://ista.ac.at/en/news/feed-them-or-lose-them/ record: - id: '13107' relation: dissertation_contains status: public scopus_import: '1' status: public title: Large neutral amino acid levels tune perinatal neuronal excitability and survival 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: 4359f0d1-fa6c-11eb-b949-802e58b17ae8 volume: 186 year: '2023' ... --- _id: '11336' abstract: - lang: eng text: The generation of a correctly-sized cerebral cortex with all-embracing neuronal and glial cell-type diversity critically depends on faithful radial glial progenitor (RGP) cell proliferation/differentiation programs. Temporal RGP lineage progression is regulated by Polycomb Repressive Complex 2 (PRC2) and loss of PRC2 activity results in severe neurogenesis defects and microcephaly. How PRC2-dependent gene expression instructs RGP lineage progression is unknown. Here we utilize Mosaic Analysis with Double Markers (MADM)-based single cell technology and demonstrate that PRC2 is not cell-autonomously required in neurogenic RGPs but rather acts at the global tissue-wide level. Conversely, cortical astrocyte production and maturation is cell-autonomously controlled by PRC2-dependent transcriptional regulation. We thus reveal highly distinct and sequential PRC2 functions in RGP lineage progression that are dependent on complex interplays between intrinsic and tissue-wide properties. In a broader context our results imply a critical role for the genetic and cellular niche environment in neural stem cell behavior. acknowledged_ssus: - _id: PreCl - _id: Bio - _id: LifeSc acknowledgement: We thank A. Heger (IST Austria Preclinical Facility), A. Sommer and C. Czepe (VBCF GmbH, NGS Unit) and S. Gharagozlou for technical support. This research was supported by the Scientific Service Units (SSU) of IST Austria through resources provided by the Imaging & Optics Facility (IOF), Lab Support Facility (LSF), and Preclinical Facility (PCF). N.A. received funding from the FWF Firnberg-Programm (T 1031). The work was supported by IST institutional funds and by the European Research Council (ERC) under the European Union’s Horizon 2020 research and innovation program (grant agreement 725780 LinPro) to S.H. article_number: abq1263 article_processing_charge: No article_type: original author: - first_name: Nicole full_name: Amberg, Nicole id: 4CD6AAC6-F248-11E8-B48F-1D18A9856A87 last_name: Amberg orcid: 0000-0002-3183-8207 - first_name: Florian full_name: Pauler, Florian id: 48EA0138-F248-11E8-B48F-1D18A9856A87 last_name: Pauler - first_name: Carmen full_name: Streicher, Carmen id: 36BCB99C-F248-11E8-B48F-1D18A9856A87 last_name: Streicher - first_name: Simon full_name: Hippenmeyer, Simon id: 37B36620-F248-11E8-B48F-1D18A9856A87 last_name: Hippenmeyer orcid: 0000-0003-2279-1061 citation: ama: Amberg N, Pauler F, Streicher C, Hippenmeyer S. Tissue-wide genetic and cellular landscape shapes the execution of sequential PRC2 functions in neural stem cell lineage progression. Science Advances. 2022;8(44). doi:10.1126/sciadv.abq1263 apa: Amberg, N., Pauler, F., Streicher, C., & Hippenmeyer, S. (2022). Tissue-wide genetic and cellular landscape shapes the execution of sequential PRC2 functions in neural stem cell lineage progression. Science Advances. American Association for the Advancement of Science. https://doi.org/10.1126/sciadv.abq1263 chicago: Amberg, Nicole, Florian Pauler, Carmen Streicher, and Simon Hippenmeyer. “Tissue-Wide Genetic and Cellular Landscape Shapes the Execution of Sequential PRC2 Functions in Neural Stem Cell Lineage Progression.” Science Advances. American Association for the Advancement of Science, 2022. https://doi.org/10.1126/sciadv.abq1263. ieee: N. Amberg, F. Pauler, C. Streicher, and S. Hippenmeyer, “Tissue-wide genetic and cellular landscape shapes the execution of sequential PRC2 functions in neural stem cell lineage progression,” Science Advances, vol. 8, no. 44. American Association for the Advancement of Science, 2022. ista: Amberg N, Pauler F, Streicher C, Hippenmeyer S. 2022. Tissue-wide genetic and cellular landscape shapes the execution of sequential PRC2 functions in neural stem cell lineage progression. Science Advances. 8(44), abq1263. mla: Amberg, Nicole, et al. “Tissue-Wide Genetic and Cellular Landscape Shapes the Execution of Sequential PRC2 Functions in Neural Stem Cell Lineage Progression.” Science Advances, vol. 8, no. 44, abq1263, American Association for the Advancement of Science, 2022, doi:10.1126/sciadv.abq1263. short: N. Amberg, F. Pauler, C. Streicher, S. Hippenmeyer, Science Advances 8 (2022). date_created: 2022-04-26T15:04:50Z date_published: 2022-11-01T00:00:00Z date_updated: 2023-05-31T12:24:10Z day: '01' ddc: - '570' department: - _id: SiHi doi: 10.1126/sciadv.abq1263 ec_funded: 1 file: - access_level: open_access checksum: 0117023e188542082ca6693cf39e7f03 content_type: application/pdf creator: patrickd date_created: 2023-03-21T14:18:10Z date_updated: 2023-03-21T14:18:10Z file_id: '12742' file_name: sciadv.abq1263.pdf file_size: 2973998 relation: main_file success: 1 file_date_updated: 2023-03-21T14:18:10Z has_accepted_license: '1' intvolume: ' 8' issue: '44' language: - iso: eng month: '11' oa: 1 oa_version: Published Version project: - _id: 260018B0-B435-11E9-9278-68D0E5697425 call_identifier: H2020 grant_number: '725780' name: Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development - _id: 268F8446-B435-11E9-9278-68D0E5697425 call_identifier: FWF grant_number: T0101031 name: Role of Eed in neural stem cell lineage progression publication: Science Advances publication_identifier: issn: - 2375-2548 publication_status: published publisher: American Association for the Advancement of Science quality_controlled: '1' related_material: link: - description: News on ISTA website relation: press_release url: https://ista.ac.at/en/news/whole-tissue-shapes-brain-development/ scopus_import: '1' status: public title: Tissue-wide genetic and cellular landscape shapes the execution of sequential PRC2 functions in neural stem cell lineage progression 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: 8 year: '2022' ... --- _id: '9794' abstract: - lang: eng text: 'Lymph nodes (LNs) comprise two main structural elements: fibroblastic reticular cells that form dedicated niches for immune cell interaction and capsular fibroblasts that build a shell around the organ. Immunological challenge causes LNs to increase more than tenfold in size within a few days. Here, we characterized the biomechanics of LN swelling on the cellular and organ scale. We identified lymphocyte trapping by influx and proliferation as drivers of an outward pressure force, causing fibroblastic reticular cells of the T-zone (TRCs) and their associated conduits to stretch. After an initial phase of relaxation, TRCs sensed the resulting strain through cell matrix adhesions, which coordinated local growth and remodeling of the stromal network. While the expanded TRC network readopted its typical configuration, a massive fibrotic reaction of the organ capsule set in and countered further organ expansion. Thus, different fibroblast populations mechanically control LN swelling in a multitier fashion.' acknowledged_ssus: - _id: Bio - _id: EM-Fac - _id: PreCl - _id: LifeSc acknowledgement: This research was supported by the Scientific Service Units of IST Austria through resources provided by the Imaging and Optics, Electron Microscopy, Preclinical and Life Science Facilities. We thank C. Moussion for providing anti-PNAd antibody and D. Critchley for Talin1-floxed mice, and E. Papusheva for providing a custom 3D channel alignment script. This work was supported by a European Research Council grant ERC-CoG-72437 to M.S. M.H. was supported by Czech Sciencundation GACR 20-24603Y and Charles University PRIMUS/20/MED/013. article_processing_charge: No article_type: original author: - first_name: Frank P full_name: Assen, Frank P id: 3A8E7F24-F248-11E8-B48F-1D18A9856A87 last_name: Assen orcid: 0000-0003-3470-6119 - first_name: Jun full_name: Abe, Jun last_name: Abe - first_name: Miroslav full_name: Hons, Miroslav id: 4167FE56-F248-11E8-B48F-1D18A9856A87 last_name: Hons orcid: 0000-0002-6625-3348 - first_name: Robert full_name: Hauschild, Robert id: 4E01D6B4-F248-11E8-B48F-1D18A9856A87 last_name: Hauschild orcid: 0000-0001-9843-3522 - first_name: Shayan full_name: Shamipour, Shayan id: 40B34FE2-F248-11E8-B48F-1D18A9856A87 last_name: Shamipour - first_name: Walter full_name: Kaufmann, Walter id: 3F99E422-F248-11E8-B48F-1D18A9856A87 last_name: Kaufmann orcid: 0000-0001-9735-5315 - first_name: Tommaso full_name: Costanzo, Tommaso id: D93824F4-D9BA-11E9-BB12-F207E6697425 last_name: Costanzo orcid: 0000-0001-9732-3815 - first_name: Gabriel full_name: Krens, Gabriel id: 2B819732-F248-11E8-B48F-1D18A9856A87 last_name: Krens orcid: 0000-0003-4761-5996 - first_name: Markus full_name: Brown, Markus id: 3DAB9AFC-F248-11E8-B48F-1D18A9856A87 last_name: Brown - first_name: Burkhard full_name: Ludewig, Burkhard last_name: Ludewig - first_name: Simon full_name: Hippenmeyer, Simon id: 37B36620-F248-11E8-B48F-1D18A9856A87 last_name: Hippenmeyer orcid: 0000-0003-2279-1061 - first_name: Carl-Philipp J full_name: Heisenberg, Carl-Philipp J id: 39427864-F248-11E8-B48F-1D18A9856A87 last_name: Heisenberg orcid: 0000-0002-0912-4566 - first_name: Wolfgang full_name: Weninger, Wolfgang last_name: Weninger - first_name: Edouard B full_name: Hannezo, Edouard B id: 3A9DB764-F248-11E8-B48F-1D18A9856A87 last_name: Hannezo orcid: 0000-0001-6005-1561 - first_name: Sanjiv A. full_name: Luther, Sanjiv A. last_name: Luther - first_name: Jens V. full_name: Stein, Jens V. last_name: Stein - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-4561-241X citation: ama: Assen FP, Abe J, Hons M, et al. Multitier mechanics control stromal adaptations in swelling lymph nodes. Nature Immunology. 2022;23:1246-1255. doi:10.1038/s41590-022-01257-4 apa: Assen, F. P., Abe, J., Hons, M., Hauschild, R., Shamipour, S., Kaufmann, W., … Sixt, M. K. (2022). Multitier mechanics control stromal adaptations in swelling lymph nodes. Nature Immunology. Springer Nature. https://doi.org/10.1038/s41590-022-01257-4 chicago: Assen, Frank P, Jun Abe, Miroslav Hons, Robert Hauschild, Shayan Shamipour, Walter Kaufmann, Tommaso Costanzo, et al. “Multitier Mechanics Control Stromal Adaptations in Swelling Lymph Nodes.” Nature Immunology. Springer Nature, 2022. https://doi.org/10.1038/s41590-022-01257-4. ieee: F. P. Assen et al., “Multitier mechanics control stromal adaptations in swelling lymph nodes,” Nature Immunology, vol. 23. Springer Nature, pp. 1246–1255, 2022. ista: Assen FP, Abe J, Hons M, Hauschild R, Shamipour S, Kaufmann W, Costanzo T, Krens G, Brown M, Ludewig B, Hippenmeyer S, Heisenberg C-PJ, Weninger W, Hannezo EB, Luther SA, Stein JV, Sixt MK. 2022. Multitier mechanics control stromal adaptations in swelling lymph nodes. Nature Immunology. 23, 1246–1255. mla: Assen, Frank P., et al. “Multitier Mechanics Control Stromal Adaptations in Swelling Lymph Nodes.” Nature Immunology, vol. 23, Springer Nature, 2022, pp. 1246–55, doi:10.1038/s41590-022-01257-4. short: F.P. Assen, J. Abe, M. Hons, R. Hauschild, S. Shamipour, W. Kaufmann, T. Costanzo, G. Krens, M. Brown, B. Ludewig, S. Hippenmeyer, C.-P.J. Heisenberg, W. Weninger, E.B. Hannezo, S.A. Luther, J.V. Stein, M.K. Sixt, Nature Immunology 23 (2022) 1246–1255. date_created: 2021-08-06T09:09:11Z date_published: 2022-07-11T00:00:00Z date_updated: 2023-08-02T06:53:07Z day: '11' ddc: - '570' department: - _id: SiHi - _id: CaHe - _id: EdHa - _id: EM-Fac - _id: Bio - _id: MiSi doi: 10.1038/s41590-022-01257-4 ec_funded: 1 external_id: isi: - '000822975900002' file: - access_level: open_access checksum: 628e7b49809f22c75b428842efe70c68 content_type: application/pdf creator: dernst date_created: 2022-07-25T07:11:32Z date_updated: 2022-07-25T07:11:32Z file_id: '11642' file_name: 2022_NatureImmunology_Assen.pdf file_size: 11475325 relation: main_file success: 1 file_date_updated: 2022-07-25T07:11:32Z has_accepted_license: '1' intvolume: ' 23' isi: 1 language: - iso: eng month: '07' oa: 1 oa_version: Published Version page: 1246-1255 project: - _id: 25FE9508-B435-11E9-9278-68D0E5697425 call_identifier: H2020 grant_number: '724373' name: Cellular navigation along spatial gradients publication: Nature Immunology publication_identifier: eissn: - 1529-2916 issn: - 1529-2908 publication_status: published publisher: Springer Nature quality_controlled: '1' scopus_import: '1' status: public title: Multitier mechanics control stromal adaptations in swelling lymph nodes 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: 4359f0d1-fa6c-11eb-b949-802e58b17ae8 volume: 23 year: '2022' ... --- _id: '10764' abstract: - lang: eng text: Presynaptic glutamate replenishment is fundamental to brain function. In high activity regimes, such as epileptic episodes, this process is thought to rely on the glutamate-glutamine cycle between neurons and astrocytes. However the presence of an astroglial glutamine supply, as well as its functional relevance in vivo in the healthy brain remain controversial, partly due to a lack of tools that can directly examine glutamine transfer. Here, we generated a fluorescent probe that tracks glutamine in live cells, which provides direct visual evidence of an activity-dependent glutamine supply from astroglial networks to presynaptic structures under physiological conditions. This mobilization is mediated by connexin43, an astroglial protein with both gap-junction and hemichannel functions, and is essential for synaptic transmission and object recognition memory. Our findings uncover an indispensable recruitment of astroglial glutamine in physiological synaptic activity and memory via an unconventional pathway, thus providing an astrocyte basis for cognitive processes. acknowledgement: 'We thank D. Mazaud and. J. Cazères for technical assistance. This work was supported by grants from the European Research Council (Consolidator grant #683154) and European Union’s Horizon 2020 research and innovation program (Marie Sklodowska-Curie Innovative Training Networks, grant #722053, EU-GliaPhD) to N.R. and from FP7-PEOPLE Marie Curie Intra-European Fellowship for career development (grant #622289) to G.C.' article_number: '753' article_processing_charge: No article_type: original author: - first_name: Giselle T full_name: Cheung, Giselle T id: 471195F6-F248-11E8-B48F-1D18A9856A87 last_name: Cheung - first_name: Danijela full_name: Bataveljic, Danijela last_name: Bataveljic - first_name: Josien full_name: Visser, Josien last_name: Visser - first_name: Naresh full_name: Kumar, Naresh last_name: Kumar - first_name: Julien full_name: Moulard, Julien last_name: Moulard - first_name: Glenn full_name: Dallérac, Glenn last_name: Dallérac - first_name: Daria full_name: Mozheiko, Daria last_name: Mozheiko - first_name: Astrid full_name: Rollenhagen, Astrid last_name: Rollenhagen - first_name: Pascal full_name: Ezan, Pascal last_name: Ezan - first_name: Cédric full_name: Mongin, Cédric last_name: Mongin - first_name: Oana full_name: Chever, Oana last_name: Chever - first_name: Alexis Pierre full_name: Bemelmans, Alexis Pierre last_name: Bemelmans - first_name: Joachim full_name: Lübke, Joachim last_name: Lübke - first_name: Isabelle full_name: Leray, Isabelle last_name: Leray - first_name: Nathalie full_name: Rouach, Nathalie last_name: Rouach citation: ama: Cheung GT, Bataveljic D, Visser J, et al. Physiological synaptic activity and recognition memory require astroglial glutamine. Nature Communications. 2022;13. doi:10.1038/s41467-022-28331-7 apa: Cheung, G. T., Bataveljic, D., Visser, J., Kumar, N., Moulard, J., Dallérac, G., … Rouach, N. (2022). Physiological synaptic activity and recognition memory require astroglial glutamine. Nature Communications. Springer Nature. https://doi.org/10.1038/s41467-022-28331-7 chicago: Cheung, Giselle T, Danijela Bataveljic, Josien Visser, Naresh Kumar, Julien Moulard, Glenn Dallérac, Daria Mozheiko, et al. “Physiological Synaptic Activity and Recognition Memory Require Astroglial Glutamine.” Nature Communications. Springer Nature, 2022. https://doi.org/10.1038/s41467-022-28331-7. ieee: G. T. Cheung et al., “Physiological synaptic activity and recognition memory require astroglial glutamine,” Nature Communications, vol. 13. Springer Nature, 2022. ista: Cheung GT, Bataveljic D, Visser J, Kumar N, Moulard J, Dallérac G, Mozheiko D, Rollenhagen A, Ezan P, Mongin C, Chever O, Bemelmans AP, Lübke J, Leray I, Rouach N. 2022. Physiological synaptic activity and recognition memory require astroglial glutamine. Nature Communications. 13, 753. mla: Cheung, Giselle T., et al. “Physiological Synaptic Activity and Recognition Memory Require Astroglial Glutamine.” Nature Communications, vol. 13, 753, Springer Nature, 2022, doi:10.1038/s41467-022-28331-7. short: G.T. Cheung, D. Bataveljic, J. Visser, N. Kumar, J. Moulard, G. Dallérac, D. Mozheiko, A. Rollenhagen, P. Ezan, C. Mongin, O. Chever, A.P. Bemelmans, J. Lübke, I. Leray, N. Rouach, Nature Communications 13 (2022). date_created: 2022-02-20T23:01:30Z date_published: 2022-02-08T00:00:00Z date_updated: 2023-08-02T14:25:01Z day: '08' ddc: - '570' department: - _id: SiHi doi: 10.1038/s41467-022-28331-7 external_id: isi: - '000757297200017' pmid: - '35136061' file: - access_level: open_access checksum: 51d580aff2327dd957946208a9749e1a content_type: application/pdf creator: dernst date_created: 2022-02-21T07:51:33Z date_updated: 2022-02-21T07:51:33Z file_id: '10777' file_name: 2022_NatureCommunications_Cheung.pdf file_size: 7910519 relation: main_file success: 1 file_date_updated: 2022-02-21T07:51:33Z has_accepted_license: '1' intvolume: ' 13' isi: 1 language: - iso: eng month: '02' oa: 1 oa_version: Published Version pmid: 1 publication: Nature Communications publication_identifier: eissn: - '20411723' publication_status: published publisher: Springer Nature quality_controlled: '1' scopus_import: '1' status: public title: Physiological synaptic activity and recognition memory require astroglial glutamine 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: 4359f0d1-fa6c-11eb-b949-802e58b17ae8 volume: 13 year: '2022' ... --- _id: '11460' abstract: - lang: eng text: "Background: Proper cerebral cortical development depends on the tightly orchestrated migration of newly born neurons from the inner ventricular and subventricular zones to the outer cortical plate. Any disturbance in this process during prenatal stages may lead to neuronal migration disorders (NMDs), which can vary in extent from focal to global. Furthermore, NMDs show a substantial comorbidity with other neurodevelopmental disorders, notably autism spectrum disorders (ASDs). Our previous work demonstrated focal neuronal migration defects in mice carrying loss-of-function alleles of the recognized autism risk gene WDFY3. However, the cellular origins of these defects in Wdfy3 mutant mice remain elusive and uncovering it will provide critical insight into WDFY3-dependent disease pathology.\r\nMethods: Here, in an effort to untangle the origins of NMDs in Wdfy3lacZ mice, we employed mosaic analysis with double markers (MADM). MADM technology enabled us to genetically distinctly track and phenotypically analyze mutant and wild-type cells concomitantly in vivo using immunofluorescent techniques.\r\nResults: We revealed a cell autonomous requirement of WDFY3 for accurate laminar positioning of cortical projection neurons and elimination of mispositioned cells during early postnatal life. In addition, we identified significant deviations in dendritic arborization, as well as synaptic density and morphology between wild type, heterozygous, and homozygous Wdfy3 mutant neurons in Wdfy3-MADM reporter mice at postnatal stages.\r\nLimitations: While Wdfy3 mutant mice have provided valuable insight into prenatal aspects of ASD pathology that remain inaccessible to investigation in humans, like most animal models, they do not a perfectly replicate all aspects of human ASD biology. The lack of human data makes it indeterminate whether morphological deviations described here apply to ASD patients or some of the other neurodevelopmental conditions associated with WDFY3 mutation.\r\nConclusions: Our genetic approach revealed several cell autonomous requirements of WDFY3 in neuronal development that could underlie the pathogenic mechanisms of WDFY3-related neurodevelopmental conditions. The results are also consistent with findings in other ASD animal models and patients and suggest an important role for WDFY3 in regulating neuronal function and interconnectivity in postnatal life." acknowledgement: "This study was funded by NIMH R21MH115347 to KSZ. KSZ is further supported by Shriners Hospitals for Children.\r\nWe would like to thank Angelo Harlan de Crescenzo for early contributions to this project." article_number: '27' article_processing_charge: No article_type: original author: - first_name: Zachary A. full_name: Schaaf, Zachary A. last_name: Schaaf - first_name: Lyvin full_name: Tat, Lyvin last_name: Tat - first_name: Noemi full_name: Cannizzaro, Noemi last_name: Cannizzaro - first_name: Ralph full_name: Green, Ralph last_name: Green - first_name: Thomas full_name: Rülicke, Thomas last_name: Rülicke - first_name: Simon full_name: Hippenmeyer, Simon id: 37B36620-F248-11E8-B48F-1D18A9856A87 last_name: Hippenmeyer orcid: 0000-0003-2279-1061 - first_name: Konstantinos S. full_name: Zarbalis, Konstantinos S. last_name: Zarbalis citation: ama: Schaaf ZA, Tat L, Cannizzaro N, et al. WDFY3 mutation alters laminar position and morphology of cortical neurons. Molecular Autism. 2022;13. doi:10.1186/s13229-022-00508-3 apa: Schaaf, Z. A., Tat, L., Cannizzaro, N., Green, R., Rülicke, T., Hippenmeyer, S., & Zarbalis, K. S. (2022). WDFY3 mutation alters laminar position and morphology of cortical neurons. Molecular Autism. Springer Nature. https://doi.org/10.1186/s13229-022-00508-3 chicago: Schaaf, Zachary A., Lyvin Tat, Noemi Cannizzaro, Ralph Green, Thomas Rülicke, Simon Hippenmeyer, and Konstantinos S. Zarbalis. “WDFY3 Mutation Alters Laminar Position and Morphology of Cortical Neurons.” Molecular Autism. Springer Nature, 2022. https://doi.org/10.1186/s13229-022-00508-3. ieee: Z. A. Schaaf et al., “WDFY3 mutation alters laminar position and morphology of cortical neurons,” Molecular Autism, vol. 13. Springer Nature, 2022. ista: Schaaf ZA, Tat L, Cannizzaro N, Green R, Rülicke T, Hippenmeyer S, Zarbalis KS. 2022. WDFY3 mutation alters laminar position and morphology of cortical neurons. Molecular Autism. 13, 27. mla: Schaaf, Zachary A., et al. “WDFY3 Mutation Alters Laminar Position and Morphology of Cortical Neurons.” Molecular Autism, vol. 13, 27, Springer Nature, 2022, doi:10.1186/s13229-022-00508-3. short: Z.A. Schaaf, L. Tat, N. Cannizzaro, R. Green, T. Rülicke, S. Hippenmeyer, K.S. Zarbalis, Molecular Autism 13 (2022). date_created: 2022-06-23T14:28:55Z date_published: 2022-06-22T00:00:00Z date_updated: 2023-08-03T07:21:32Z day: '22' ddc: - '570' department: - _id: SiHi doi: 10.1186/s13229-022-00508-3 external_id: isi: - '000814641400001' file: - access_level: open_access checksum: 525d2618e855139089bbfc3e3d49d1b2 content_type: application/pdf creator: dernst date_created: 2022-06-24T08:22:59Z date_updated: 2022-06-24T08:22:59Z file_id: '11461' file_name: 2022_MolecularAutism_Schaaf.pdf file_size: 7552298 relation: main_file success: 1 file_date_updated: 2022-06-24T08:22:59Z has_accepted_license: '1' intvolume: ' 13' isi: 1 keyword: - Psychiatry and Mental health - Developmental Biology - Developmental Neuroscience - Molecular Biology language: - iso: eng month: '06' oa: 1 oa_version: Published Version publication: Molecular Autism publication_identifier: issn: - 2040-2392 publication_status: published publisher: Springer Nature quality_controlled: '1' related_material: link: - relation: erratum url: https://doi.org/10.1186/s13229-023-00539-4 status: public title: WDFY3 mutation alters laminar position and morphology of cortical neurons 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: 4359f0d1-fa6c-11eb-b949-802e58b17ae8 volume: 13 year: '2022' ... --- _id: '11449' abstract: - lang: eng text: Mutations are acquired frequently, such that each cell's genome inscribes its history of cell divisions. Common genomic alterations involve loss of heterozygosity (LOH). LOH accumulates throughout the genome, offering large encoding capacity for inferring cell lineage. Using only single-cell RNA sequencing (scRNA-seq) of mouse brain cells, we found that LOH events spanning multiple genes are revealed as tracts of monoallelically expressed, constitutionally heterozygous single-nucleotide variants (SNVs). We simultaneously inferred cell lineage and marked developmental time points based on X chromosome inactivation and the total number of LOH events while identifying cell types from gene expression patterns. Our results are consistent with progenitor cells giving rise to multiple cortical cell types through stereotyped expansion and distinct waves of neurogenesis. This type of retrospective analysis could be incorporated into scRNA-seq pipelines and, compared with experimental approaches for determining lineage in model organisms, is applicable where genetic engineering is prohibited, such as humans. acknowledgement: D.J.A. thanks Wayne K. Potts, Alan R. Rogers, Kristen Hawkes, Ryk Ward, and Jon Seger for inspiring a young undergraduate to apply evolutionary theory to intraorganism development. Supported by the Paul G. Allen Frontiers Group (University of Washington); NIH R00HG010152 (Dartmouth); and NÖ Forschung und Bildung n[f+b] life science call grant (C13-002) and the European Research Council (ERC) under the European Union’s Horizon 2020 research and innovation program 725780 LinPro to S.H. article_processing_charge: No article_type: original author: - first_name: Donovan J. full_name: Anderson, Donovan J. last_name: Anderson - first_name: Florian full_name: Pauler, Florian id: 48EA0138-F248-11E8-B48F-1D18A9856A87 last_name: Pauler - first_name: Aaron full_name: Mckenna, Aaron last_name: Mckenna - first_name: Jay full_name: Shendure, Jay last_name: Shendure - first_name: Simon full_name: Hippenmeyer, Simon id: 37B36620-F248-11E8-B48F-1D18A9856A87 last_name: Hippenmeyer orcid: 0000-0003-2279-1061 - first_name: Marshall S. full_name: Horwitz, Marshall S. last_name: Horwitz citation: ama: Anderson DJ, Pauler F, Mckenna A, Shendure J, Hippenmeyer S, Horwitz MS. Simultaneous brain cell type and lineage determined by scRNA-seq reveals stereotyped cortical development. Cell Systems. 2022;13(6):438-453.e5. doi:10.1016/j.cels.2022.03.006 apa: Anderson, D. J., Pauler, F., Mckenna, A., Shendure, J., Hippenmeyer, S., & Horwitz, M. S. (2022). Simultaneous brain cell type and lineage determined by scRNA-seq reveals stereotyped cortical development. Cell Systems. Elsevier. https://doi.org/10.1016/j.cels.2022.03.006 chicago: Anderson, Donovan J., Florian Pauler, Aaron Mckenna, Jay Shendure, Simon Hippenmeyer, and Marshall S. Horwitz. “Simultaneous Brain Cell Type and Lineage Determined by ScRNA-Seq Reveals Stereotyped Cortical Development.” Cell Systems. Elsevier, 2022. https://doi.org/10.1016/j.cels.2022.03.006. ieee: D. J. Anderson, F. Pauler, A. Mckenna, J. Shendure, S. Hippenmeyer, and M. S. Horwitz, “Simultaneous brain cell type and lineage determined by scRNA-seq reveals stereotyped cortical development,” Cell Systems, vol. 13, no. 6. Elsevier, p. 438–453.e5, 2022. ista: Anderson DJ, Pauler F, Mckenna A, Shendure J, Hippenmeyer S, Horwitz MS. 2022. Simultaneous brain cell type and lineage determined by scRNA-seq reveals stereotyped cortical development. Cell Systems. 13(6), 438–453.e5. mla: Anderson, Donovan J., et al. “Simultaneous Brain Cell Type and Lineage Determined by ScRNA-Seq Reveals Stereotyped Cortical Development.” Cell Systems, vol. 13, no. 6, Elsevier, 2022, p. 438–453.e5, doi:10.1016/j.cels.2022.03.006. short: D.J. Anderson, F. Pauler, A. Mckenna, J. Shendure, S. Hippenmeyer, M.S. Horwitz, Cell Systems 13 (2022) 438–453.e5. date_created: 2022-06-19T22:01:57Z date_published: 2022-06-15T00:00:00Z date_updated: 2023-08-03T07:19:43Z day: '15' department: - _id: SiHi doi: 10.1016/j.cels.2022.03.006 ec_funded: 1 external_id: isi: - '000814124400002' pmid: - '35452605' intvolume: ' 13' isi: 1 issue: '6' language: - iso: eng main_file_link: - open_access: '1' url: https://doi.org/10.1016/j.cels.2022.03.006 month: '06' oa: 1 oa_version: Published Version page: 438-453.e5 pmid: 1 project: - _id: 260018B0-B435-11E9-9278-68D0E5697425 call_identifier: H2020 grant_number: '725780' name: Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development - _id: 25D92700-B435-11E9-9278-68D0E5697425 grant_number: LS13-002 name: Mapping Cell-Type Specificity of the Genomic Imprintome in the Brain publication: Cell Systems publication_identifier: eissn: - 2405-4720 issn: - 2405-4712 publication_status: published publisher: Elsevier quality_controlled: '1' scopus_import: '1' status: public title: Simultaneous brain cell type and lineage determined by scRNA-seq reveals stereotyped cortical development type: journal_article user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8 volume: 13 year: '2022' ... --- _id: '12283' abstract: - lang: eng text: Neurons extend axons to form the complex circuitry of the mature brain. This depends on the coordinated response and continuous remodelling of the microtubule and F-actin networks in the axonal growth cone. Growth cone architecture remains poorly understood at nanoscales. We therefore investigated mouse hippocampal neuron growth cones using cryo-electron tomography to directly visualise their three-dimensional subcellular architecture with molecular detail. Our data showed that the hexagonal arrays of actin bundles that form filopodia penetrate and terminate deep within the growth cone interior. We directly observed the modulation of these and other growth cone actin bundles by alteration of individual F-actin helical structures. Microtubules with blunt, slightly flared or gently curved ends predominated in the growth cone, frequently contained lumenal particles and exhibited lattice defects. Investigation of the effect of absence of doublecortin, a neurodevelopmental cytoskeleton regulator, on growth cone cytoskeleton showed no major anomalies in overall growth cone organisation or in F-actin subpopulations. However, our data suggested that microtubules sustained more structural defects, highlighting the importance of microtubule integrity during growth cone migration. acknowledgement: "J.A. was supported by a grant from the Medical Research Council (MRC), UK (MR/R000352/1) to C.A.M. Cryo-EM data were collected on equipment funded by the Wellcome Trust, UK (079605/Z/06/Z) and the Biotechnology and Biological Sciences Research Council (BBSRC) UK (BB/L014211/1). F.F.’s salary and institute were supported by Inserm (Institut National de la Santé et de la Recherche Médicale), CNRS (Centre National de la Recherche Scientifique) and Sorbonne Université. F.F.’s group was particularly supported by Agence Nationale de la\r\nRecherche (ANR-16-CE16-0011-03) and Seventh Framework Programme (EUHEALTH-\r\n2013, DESIRE, N° 60253; also funding M.S.’s salary) and the European Cooperation in Science and Technology (COST Action CA16118). Open Access funding provided by Birkbeck College: Birkbeck University of London. Deposited in PMC for immediate release." article_number: '259234' article_processing_charge: No article_type: original author: - first_name: Joseph full_name: Atherton, Joseph last_name: Atherton - first_name: Melissa A full_name: Stouffer, Melissa A id: 4C9372C4-F248-11E8-B48F-1D18A9856A87 last_name: Stouffer - first_name: Fiona full_name: Francis, Fiona last_name: Francis - first_name: Carolyn A. full_name: Moores, Carolyn A. last_name: Moores citation: ama: Atherton J, Stouffer MA, Francis F, Moores CA. Visualising the cytoskeletal machinery in neuronal growth cones using cryo-electron tomography. Journal of Cell Science. 2022;135(7). doi:10.1242/jcs.259234 apa: Atherton, J., Stouffer, M. A., Francis, F., & Moores, C. A. (2022). Visualising the cytoskeletal machinery in neuronal growth cones using cryo-electron tomography. Journal of Cell Science. The Company of Biologists. https://doi.org/10.1242/jcs.259234 chicago: Atherton, Joseph, Melissa A Stouffer, Fiona Francis, and Carolyn A. Moores. “Visualising the Cytoskeletal Machinery in Neuronal Growth Cones Using Cryo-Electron Tomography.” Journal of Cell Science. The Company of Biologists, 2022. https://doi.org/10.1242/jcs.259234. ieee: J. Atherton, M. A. Stouffer, F. Francis, and C. A. Moores, “Visualising the cytoskeletal machinery in neuronal growth cones using cryo-electron tomography,” Journal of Cell Science, vol. 135, no. 7. The Company of Biologists, 2022. ista: Atherton J, Stouffer MA, Francis F, Moores CA. 2022. Visualising the cytoskeletal machinery in neuronal growth cones using cryo-electron tomography. Journal of Cell Science. 135(7), 259234. mla: Atherton, Joseph, et al. “Visualising the Cytoskeletal Machinery in Neuronal Growth Cones Using Cryo-Electron Tomography.” Journal of Cell Science, vol. 135, no. 7, 259234, The Company of Biologists, 2022, doi:10.1242/jcs.259234. short: J. Atherton, M.A. Stouffer, F. Francis, C.A. Moores, Journal of Cell Science 135 (2022). date_created: 2023-01-16T10:03:24Z date_published: 2022-04-01T00:00:00Z date_updated: 2023-08-04T10:28:34Z day: '01' ddc: - '570' department: - _id: SiHi doi: 10.1242/jcs.259234 external_id: isi: - '000783840400010' pmid: - '35383828' file: - access_level: open_access checksum: 4346ed32cb7c89a8ca051c7da68a9a1c content_type: application/pdf creator: dernst date_created: 2023-01-30T11:41:01Z date_updated: 2023-01-30T11:41:01Z file_id: '12461' file_name: 2022_JourCellBiology_Atherton.pdf file_size: 13868733 relation: main_file success: 1 file_date_updated: 2023-01-30T11:41:01Z has_accepted_license: '1' intvolume: ' 135' isi: 1 issue: '7' keyword: - Cell Biology language: - iso: eng month: '04' oa: 1 oa_version: Published Version pmid: 1 publication: Journal of Cell Science publication_identifier: eissn: - 1477-9137 issn: - 0021-9533 publication_status: published publisher: The Company of Biologists quality_controlled: '1' scopus_import: '1' status: public title: Visualising the cytoskeletal machinery in neuronal growth cones using cryo-electron tomography 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: 4359f0d1-fa6c-11eb-b949-802e58b17ae8 volume: 135 year: '2022' ... --- _id: '12282' abstract: - lang: eng text: From a simple thought to a multicellular movement acknowledgement: The authors want to thank Professors Carrie Bernecky, Tom Henzinger, Martin Loose and Gaia Novarino for accepting to be interviewed, thus giving significant contribution to the discussion that lead to this article. article_number: '260017' article_processing_charge: No article_type: letter_note author: - first_name: Nicole full_name: Amberg, Nicole id: 4CD6AAC6-F248-11E8-B48F-1D18A9856A87 last_name: Amberg orcid: 0000-0002-3183-8207 - first_name: Melissa A full_name: Stouffer, Melissa A id: 4C9372C4-F248-11E8-B48F-1D18A9856A87 last_name: Stouffer - first_name: Irene full_name: Vercellino, Irene id: 3ED6AF16-F248-11E8-B48F-1D18A9856A87 last_name: Vercellino orcid: 0000-0001-5618-3449 citation: ama: Amberg N, Stouffer MA, Vercellino I. Operation STEM fatale – how an equity, diversity and inclusion initiative has brought us to reflect on the current challenges in cell biology and science as a whole. Journal of Cell Science. 2022;135(8). doi:10.1242/jcs.260017 apa: Amberg, N., Stouffer, M. A., & Vercellino, I. (2022). Operation STEM fatale – how an equity, diversity and inclusion initiative has brought us to reflect on the current challenges in cell biology and science as a whole. Journal of Cell Science. The Company of Biologists. https://doi.org/10.1242/jcs.260017 chicago: Amberg, Nicole, Melissa A Stouffer, and Irene Vercellino. “Operation STEM Fatale – How an Equity, Diversity and Inclusion Initiative Has Brought Us to Reflect on the Current Challenges in Cell Biology and Science as a Whole.” Journal of Cell Science. The Company of Biologists, 2022. https://doi.org/10.1242/jcs.260017. ieee: N. Amberg, M. A. Stouffer, and I. Vercellino, “Operation STEM fatale – how an equity, diversity and inclusion initiative has brought us to reflect on the current challenges in cell biology and science as a whole,” Journal of Cell Science, vol. 135, no. 8. The Company of Biologists, 2022. ista: Amberg N, Stouffer MA, Vercellino I. 2022. Operation STEM fatale – how an equity, diversity and inclusion initiative has brought us to reflect on the current challenges in cell biology and science as a whole. Journal of Cell Science. 135(8), 260017. mla: Amberg, Nicole, et al. “Operation STEM Fatale – How an Equity, Diversity and Inclusion Initiative Has Brought Us to Reflect on the Current Challenges in Cell Biology and Science as a Whole.” Journal of Cell Science, vol. 135, no. 8, 260017, The Company of Biologists, 2022, doi:10.1242/jcs.260017. short: N. Amberg, M.A. Stouffer, I. Vercellino, Journal of Cell Science 135 (2022). date_created: 2023-01-16T10:03:14Z date_published: 2022-04-19T00:00:00Z date_updated: 2023-08-04T10:28:04Z day: '19' department: - _id: SiHi - _id: LeSa doi: 10.1242/jcs.260017 external_id: isi: - '000798123600015' pmid: - '35438168' intvolume: ' 135' isi: 1 issue: '8' language: - iso: eng month: '04' oa_version: None pmid: 1 publication: Journal of Cell Science publication_identifier: eissn: - 1477-9137 issn: - 0021-9533 publication_status: published publisher: The Company of Biologists quality_controlled: '1' scopus_import: '1' status: public title: Operation STEM fatale – how an equity, diversity and inclusion initiative has brought us to reflect on the current challenges in cell biology and science as a whole type: journal_article user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8 volume: 135 year: '2022' ... --- _id: '10792' abstract: - lang: eng text: "Background\r\nProper cerebral cortical development depends on the tightly orchestrated migration of newly born neurons from the inner ventricular and subventricular zones to the outer cortical plate. Any disturbance in this process during prenatal stages may lead to neuronal migration disorders (NMDs), which can vary in extent from focal to global. Furthermore, NMDs show a substantial comorbidity with other neurodevelopmental disorders, notably autism spectrum disorders (ASDs). Our previous work demonstrated focal neuronal migration defects in mice carrying loss-of-function alleles of the recognized autism risk gene WDFY3. However, the cellular origins of these defects in Wdfy3 mutant mice remain elusive and uncovering it will provide critical insight into WDFY3-dependent disease pathology .\r\nMethods\r\nHere, in an effort to untangle the origins of NMDs in Wdfy3lacZ mice, we employed mosaic analysis with double markers (MADM). MADM technology enabled us to genetically distinctly track and phenotypically analyze mutant and wild type cells concomitantly in vivo using immunofluorescent techniques.\r\nResults\r\nWe revealed a cell autonomous requirement of WDFY3 for accurate laminar positioning of cortical projection neurons and elimination of mispositioned cells during early postnatal life. In addition, we identified significant deviations in dendritic arborization, as well as synaptic density and morphology between wild type, heterozygous, and homozygous Wdfy3 mutant neurons in Wdfy3-MADM reporter mice at postnatal stages. Limitations While Wdfy3 mutant mice have provided valuable insight into prenatal aspects of ASD pathology that remain inaccessible to investigation in humans, like most animal models, they do not a perfectly replicate all aspects of human ASD biology. The lack of human data makes it indeterminate whether morphological deviations described here apply to ASD patients.\r\nConclusions\r\n\uFEFFOur genetic approach revealed several cell autonomous requirements of Wdfy3 in neuronal development that could underly the pathogenic mechanisms of WDFY3-related ASD conditions. The results are also consistent with findings in other ASD animal models and patients and suggest an important role for Wdfy3 in regulating neuronal function and interconnectivity in postnatal life." article_processing_charge: No author: - first_name: Zachary full_name: Schaaf, Zachary last_name: Schaaf - first_name: Lyvin full_name: Tat, Lyvin last_name: Tat - first_name: Noemi full_name: Cannizzaro, Noemi last_name: Cannizzaro - first_name: Ralph full_name: Green, Ralph last_name: Green - first_name: Thomas full_name: Rülicke, Thomas last_name: Rülicke - first_name: Simon full_name: Hippenmeyer, Simon id: 37B36620-F248-11E8-B48F-1D18A9856A87 last_name: Hippenmeyer orcid: 0000-0003-2279-1061 - first_name: K full_name: Zarbalis, K last_name: Zarbalis citation: ama: Schaaf Z, Tat L, Cannizzaro N, et al. WDFY3 cell autonomously controls neuronal migration. doi:10.21203/rs.3.rs-1316167/v1 apa: Schaaf, Z., Tat, L., Cannizzaro, N., Green, R., Rülicke, T., Hippenmeyer, S., & Zarbalis, K. (n.d.). WDFY3 cell autonomously controls neuronal migration. Research Square. https://doi.org/10.21203/rs.3.rs-1316167/v1 chicago: Schaaf, Zachary, Lyvin Tat, Noemi Cannizzaro, Ralph Green, Thomas Rülicke, Simon Hippenmeyer, and K Zarbalis. “WDFY3 Cell Autonomously Controls Neuronal Migration.” Research Square, n.d. https://doi.org/10.21203/rs.3.rs-1316167/v1. ieee: Z. Schaaf et al., “WDFY3 cell autonomously controls neuronal migration.” Research Square. ista: Schaaf Z, Tat L, Cannizzaro N, Green R, Rülicke T, Hippenmeyer S, Zarbalis K. WDFY3 cell autonomously controls neuronal migration. 10.21203/rs.3.rs-1316167/v1. mla: Schaaf, Zachary, et al. WDFY3 Cell Autonomously Controls Neuronal Migration. Research Square, doi:10.21203/rs.3.rs-1316167/v1. short: Z. Schaaf, L. Tat, N. Cannizzaro, R. Green, T. Rülicke, S. Hippenmeyer, K. Zarbalis, (n.d.). date_created: 2022-02-25T07:53:26Z date_published: 2022-02-16T00:00:00Z date_updated: 2023-10-17T13:06:52Z day: '16' department: - _id: SiHi doi: 10.21203/rs.3.rs-1316167/v1 external_id: pmid: - PPR454733 language: - iso: eng main_file_link: - open_access: '1' url: https://doi.org/10.21203/rs.3.rs-1316167/v1 month: '02' oa: 1 oa_version: Preprint page: '30' pmid: 1 publication_identifier: eissn: - 2693-5015 publication_status: submitted publisher: Research Square status: public title: WDFY3 cell autonomously controls neuronal migration 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: preprint user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 year: '2022' ... --- _id: '10791' abstract: - lang: eng text: The mammalian neocortex is composed of diverse neuronal and glial cell classes that broadly arrange in six distinct laminae. Cortical layers emerge during development and defects in the developmental programs that orchestrate cortical lamination are associated with neurodevelopmental diseases. The developmental principle of cortical layer formation depends on concerted radial projection neuron migration, from their birthplace to their final target position. Radial migration occurs in defined sequential steps, regulated by a large array of signaling pathways. However, based on genetic loss-of-function experiments, most studies have thus far focused on the role of cell-autonomous gene function. Yet, cortical neuron migration in situ is a complex process and migrating neurons traverse along diverse cellular compartments and environments. The role of tissue-wide properties and genetic state in radial neuron migration is however not clear. Here we utilized mosaic analysis with double markers (MADM) technology to either sparsely or globally delete gene function, followed by quantitative single-cell phenotyping. The MADM-based gene ablation paradigms in combination with computational modeling demonstrated that global tissue-wide effects predominate cell-autonomous gene function albeit in a gene-specific manner. Our results thus suggest that the genetic landscape in a tissue critically affects the overall migration phenotype of individual cortical projection neurons. In a broader context, our findings imply that global tissue-wide effects represent an essential component of the underlying etiology associated with focal malformations of cortical development in particular, and neurological diseases in general. acknowledged_ssus: - _id: LifeSc - _id: PreCl - _id: Bio acknowledgement: "A.H.H. was a recipient of a DOC Fellowship (24812) of the Austrian Academy of Sciences. This work also received support from IST Austria institutional funds; the People Programme (Marie Curie Actions) of the European Union’s Seventh Framework Programme (FP7/2007–2013) under REA grant agreement No 618444 to S.H.\r\nAPC funding was obtained by IST Austria institutional funds.\r\nWe thank A. Sommer and C. Czepe (VBCF GmbH, NGS Unit), L. Andersen, J. Sonntag and J. Renno for technical support and/or initial experiments; M. Sixt, J. Nimpf and all members of the Hippenmeyer lab for discussion. This research was supported by the Scientific Service Units of IST Austria through resources provided by the Imaging and Optics Facility, Lab Support Facility and Preclinical Facility." article_number: kvac009 article_processing_charge: No article_type: original author: - first_name: Andi H full_name: Hansen, Andi H id: 38853E16-F248-11E8-B48F-1D18A9856A87 last_name: Hansen - first_name: Florian full_name: Pauler, Florian id: 48EA0138-F248-11E8-B48F-1D18A9856A87 last_name: Pauler orcid: 0000-0002-7462-0048 - first_name: Michael full_name: Riedl, Michael id: 3BE60946-F248-11E8-B48F-1D18A9856A87 last_name: Riedl orcid: 0000-0003-4844-6311 - first_name: Carmen full_name: Streicher, Carmen id: 36BCB99C-F248-11E8-B48F-1D18A9856A87 last_name: Streicher - first_name: Anna-Magdalena full_name: Heger, Anna-Magdalena id: 4B76FFD2-F248-11E8-B48F-1D18A9856A87 last_name: Heger - first_name: Susanne full_name: Laukoter, Susanne id: 2D6B7A9A-F248-11E8-B48F-1D18A9856A87 last_name: Laukoter orcid: 0000-0002-7903-3010 - first_name: Christoph M full_name: Sommer, Christoph M id: 4DF26D8C-F248-11E8-B48F-1D18A9856A87 last_name: Sommer orcid: 0000-0003-1216-9105 - first_name: Armel full_name: Nicolas, Armel id: 2A103192-F248-11E8-B48F-1D18A9856A87 last_name: Nicolas - first_name: Björn full_name: Hof, Björn id: 3A374330-F248-11E8-B48F-1D18A9856A87 last_name: Hof orcid: 0000-0003-2057-2754 - first_name: Li Huei full_name: Tsai, Li Huei last_name: Tsai - first_name: Thomas full_name: Rülicke, Thomas last_name: Rülicke - first_name: Simon full_name: Hippenmeyer, Simon id: 37B36620-F248-11E8-B48F-1D18A9856A87 last_name: Hippenmeyer orcid: 0000-0003-2279-1061 citation: ama: Hansen AH, Pauler F, Riedl M, et al. Tissue-wide effects override cell-intrinsic gene function in radial neuron migration. Oxford Open Neuroscience. 2022;1(1). doi:10.1093/oons/kvac009 apa: Hansen, A. H., Pauler, F., Riedl, M., Streicher, C., Heger, A.-M., Laukoter, S., … Hippenmeyer, S. (2022). Tissue-wide effects override cell-intrinsic gene function in radial neuron migration. Oxford Open Neuroscience. Oxford Academic. https://doi.org/10.1093/oons/kvac009 chicago: Hansen, Andi H, Florian Pauler, Michael Riedl, Carmen Streicher, Anna-Magdalena Heger, Susanne Laukoter, Christoph M Sommer, et al. “Tissue-Wide Effects Override Cell-Intrinsic Gene Function in Radial Neuron Migration.” Oxford Open Neuroscience. Oxford Academic, 2022. https://doi.org/10.1093/oons/kvac009. ieee: A. H. Hansen et al., “Tissue-wide effects override cell-intrinsic gene function in radial neuron migration,” Oxford Open Neuroscience, vol. 1, no. 1. Oxford Academic, 2022. ista: Hansen AH, Pauler F, Riedl M, Streicher C, Heger A-M, Laukoter S, Sommer CM, Nicolas A, Hof B, Tsai LH, Rülicke T, Hippenmeyer S. 2022. Tissue-wide effects override cell-intrinsic gene function in radial neuron migration. Oxford Open Neuroscience. 1(1), kvac009. mla: Hansen, Andi H., et al. “Tissue-Wide Effects Override Cell-Intrinsic Gene Function in Radial Neuron Migration.” Oxford Open Neuroscience, vol. 1, no. 1, kvac009, Oxford Academic, 2022, doi:10.1093/oons/kvac009. short: A.H. Hansen, F. Pauler, M. Riedl, C. Streicher, A.-M. Heger, S. Laukoter, C.M. Sommer, A. Nicolas, B. Hof, L.H. Tsai, T. Rülicke, S. Hippenmeyer, Oxford Open Neuroscience 1 (2022). date_created: 2022-02-25T07:52:11Z date_published: 2022-07-07T00:00:00Z date_updated: 2023-11-30T10:55:12Z day: '07' ddc: - '570' department: - _id: SiHi - _id: BjHo - _id: LifeSc - _id: EM-Fac doi: 10.1093/oons/kvac009 ec_funded: 1 file: - access_level: open_access checksum: 822e76e056c07099d1fb27d1ece5941b content_type: application/pdf creator: dernst date_created: 2023-08-16T08:00:30Z date_updated: 2023-08-16T08:00:30Z file_id: '14061' file_name: 2023_OxfordOpenNeuroscience_Hansen.pdf file_size: 4846551 relation: main_file success: 1 file_date_updated: 2023-08-16T08:00:30Z has_accepted_license: '1' intvolume: ' 1' issue: '1' language: - iso: eng month: '07' oa: 1 oa_version: Published Version project: - _id: 25D61E48-B435-11E9-9278-68D0E5697425 call_identifier: FP7 grant_number: '618444' name: Molecular Mechanisms of Cerebral Cortex Development - _id: 2625A13E-B435-11E9-9278-68D0E5697425 grant_number: '24812' name: Molecular Mechanisms of Radial Neuronal Migration publication: Oxford Open Neuroscience publication_identifier: eissn: - 2753-149X publication_status: published publisher: Oxford Academic quality_controlled: '1' related_material: record: - id: '12726' relation: dissertation_contains status: public - id: '14530' relation: dissertation_contains status: public status: public title: Tissue-wide effects override cell-intrinsic gene function in radial neuron migration 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: 1 year: '2022' ... --- _id: '9082' abstract: - lang: eng text: Acquired mutations are sufficiently frequent such that the genome of a single cell offers a record of its history of cell divisions. Among more common somatic genomic alterations are loss of heterozygosity (LOH). Large LOH events are potentially detectable in single cell RNA sequencing (scRNA-seq) datasets as tracts of monoallelic expression for constitutionally heterozygous single nucleotide variants (SNVs) located among contiguous genes. We identified runs of monoallelic expression, consistent with LOH, uniquely distributed throughout the genome in single cell brain cortex transcriptomes of F1 hybrids involving different inbred mouse strains. We then phylogenetically reconstructed single cell lineages and simultaneously identified cell types by corresponding gene expression patterns. Our results are consistent with progenitor cells giving rise to multiple cortical cell types through stereotyped expansion and distinct waves of neurogenesis. Compared to engineered recording systems, LOH events accumulate throughout the genome and across the lifetime of an organism, affording tremendous capacity for encoding lineage information and increasing resolution for later cell divisions. This approach can conceivably be computationally incorporated into scRNA-seq analysis and may be useful for organisms where genetic engineering is prohibitive, such as humans. acknowledgement: "We thank Bill Bolosky, Microsoft Research, for earlier work showing proof of concept in TCGA\r\nbulk RNA-seq data. Supported by the Paul G. Allen Frontiers Group (University of Washington);\r\nNIH R00HG010152 (Dartmouth); and NÖ Forschung und Bildung n[f+b] life science call grant\r\n(C13-002) to SH, and the European Research Council (ERC) under the European Union’s\r\nHorizon 2020 research and innovation program 725780 LinPro to SH." article_processing_charge: No author: - first_name: Donovan J. full_name: Anderson, Donovan J. last_name: Anderson - first_name: Florian full_name: Pauler, Florian id: 48EA0138-F248-11E8-B48F-1D18A9856A87 last_name: Pauler - first_name: Aaron full_name: McKenna, Aaron last_name: McKenna - first_name: Jay full_name: Shendure, Jay last_name: Shendure - first_name: Simon full_name: Hippenmeyer, Simon id: 37B36620-F248-11E8-B48F-1D18A9856A87 last_name: Hippenmeyer orcid: 0000-0003-2279-1061 - first_name: Marshall S. full_name: Horwitz, Marshall S. last_name: Horwitz citation: ama: Anderson DJ, Pauler F, McKenna A, Shendure J, Hippenmeyer S, Horwitz MS. Simultaneous identification of brain cell type and lineage via single cell RNA sequencing. bioRxiv. doi:10.1101/2020.12.31.425016 apa: Anderson, D. J., Pauler, F., McKenna, A., Shendure, J., Hippenmeyer, S., & Horwitz, M. S. (n.d.). Simultaneous identification of brain cell type and lineage via single cell RNA sequencing. bioRxiv. Cold Spring Harbor Laboratory. https://doi.org/10.1101/2020.12.31.425016 chicago: Anderson, Donovan J., Florian Pauler, Aaron McKenna, Jay Shendure, Simon Hippenmeyer, and Marshall S. Horwitz. “Simultaneous Identification of Brain Cell Type and Lineage via Single Cell RNA Sequencing.” BioRxiv. Cold Spring Harbor Laboratory, n.d. https://doi.org/10.1101/2020.12.31.425016. ieee: D. J. Anderson, F. Pauler, A. McKenna, J. Shendure, S. Hippenmeyer, and M. S. Horwitz, “Simultaneous identification of brain cell type and lineage via single cell RNA sequencing,” bioRxiv. Cold Spring Harbor Laboratory. ista: Anderson DJ, Pauler F, McKenna A, Shendure J, Hippenmeyer S, Horwitz MS. Simultaneous identification of brain cell type and lineage via single cell RNA sequencing. bioRxiv, 10.1101/2020.12.31.425016. mla: Anderson, Donovan J., et al. “Simultaneous Identification of Brain Cell Type and Lineage via Single Cell RNA Sequencing.” BioRxiv, Cold Spring Harbor Laboratory, doi:10.1101/2020.12.31.425016. short: D.J. Anderson, F. Pauler, A. McKenna, J. Shendure, S. Hippenmeyer, M.S. Horwitz, BioRxiv (n.d.). date_created: 2021-02-04T07:23:23Z date_published: 2021-01-01T00:00:00Z date_updated: 2021-02-04T07:29:53Z day: '01' department: - _id: SiHi doi: 10.1101/2020.12.31.425016 ec_funded: 1 language: - iso: eng main_file_link: - open_access: '1' url: https://doi.org/10.1101/2020.12.31.425016 month: '01' oa: 1 oa_version: Preprint project: - _id: 260018B0-B435-11E9-9278-68D0E5697425 call_identifier: H2020 grant_number: '725780' name: Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development publication: bioRxiv publication_status: submitted publisher: Cold Spring Harbor Laboratory status: public title: Simultaneous identification of brain cell type and lineage via single cell RNA sequencing type: preprint user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 year: '2021' ... --- _id: '6995' abstract: - lang: eng text: Human brain organoids represent a powerful tool for the study of human neurological diseases particularly those that impact brain growth and structure. However, many neurological diseases lack obvious anatomical abnormalities, yet significantly impact neural network functions, raising the question of whether organoids possess sufficient neural network architecture and complexity to model these conditions. Here, we explore the network level functions of brain organoids using calcium sensor imaging and extracellular recording approaches that together reveal the existence of complex oscillatory network behaviors reminiscent of intact brain preparations. We further demonstrate strikingly abnormal epileptiform network activity in organoids derived from a Rett Syndrome patient despite only modest anatomical differences from isogenically matched controls, and rescue with an unconventional neuromodulatory drug Pifithrin-α. Together, these findings provide an essential foundation for the utilization of human brain organoids to study intact and disordered human brain network formation and illustrate their utility in therapeutic discovery. acknowledgement: We thank S. Butler, T. Carmichael and members of the laboratory of B.G.N. for helpful discussions and comments on the manuscript; N. Vishlaghi and F. Turcios-Hernandez for technical assistance, and J. Lee, S.-K. Lee, H. Shinagawa and K. Yoshikawa for valuable reagents. We also thank the UCLA Eli and Edythe Broad Stem Cell Research Center (BSCRC) and Intellectual and Developmental Disabilities Research Center microscopy cores for access to imaging facilities. This work was supported by grants from the California Institute for Regenerative Medicine (CIRM) (DISC1-08819 to B.G.N.), the National Institute of Health (R01NS089817, R01DA051897 and P50HD103557 to B.G.N.; K08NS119747 to R.A.S.; K99HD096105 to M.W.; R01MH123922, R01MH121521 and P50HD103557 to M.J.G.; R01GM099134 to K.P.; R01NS103788 to W.E.L.; R01NS088571 to J.M.P.; R01NS030549 and R01AG050474 to I.M.), and research awards from the UCLA Jonsson Comprehensive Cancer Center and BSCRC Ablon Scholars Program (to B.G.N.), the BSCRC Innovation Program (to B.G.N., K.P. and W.E.L.), the UCLA BSCRC Steffy Brain Aging Research Fund (to B.G.N. and W.E.L.) and the UCLA Clinical and Translational Science Institute (to B.G.N.), Paul Allen Family Foundation Frontiers Group (to K.P. and W.E.L.), the March of Dimes Foundation (to W.E.L.) and the Simons Foundation Autism Research Initiative Bridge to Independence Program (to R.A.S. and M.J.G.). R.A.S. was also supported by the UCLA/NINDS Translational Neuroscience Training Grant (R25NS065723), a Research and Training Fellowship from the American Epilepsy Society, a Taking Flight Award from CURE Epilepsy and a Clinician Scientist training award from the UCLA BSCRC. J.E.B. was supported by the UCLA BSCRC Rose Hills Foundation Graduate Scholarship Training Program. M.W. was supported by postdoctoral training awards provided by the UCLA BSCRC and the Uehara Memorial Foundation. O.A.M. and A.K. were supported in part by the UCLA-California State University Northridge CIRM-Bridges training program (EDUC2-08411). We also acknowledge the support of the IDDRC Cells, Circuits and Systems Analysis, Microscopy and Genetics and Genomics Cores of the Semel Institute of Neuroscience at UCLA, which are supported by the NICHD (U54HD087101 and P50HD10355701). We lastly acknowledge support from a Quantitative and Computational Biosciences Collaboratory Postdoctoral Fellowship to S.M. and the Quantitative and Computational Biosciences Collaboratory community, directed by M. Pellegrini. alternative_title: - Nature Neuroscience article_processing_charge: Yes author: - first_name: Ranmal A. full_name: Samarasinghe, Ranmal A. last_name: Samarasinghe - first_name: Osvaldo full_name: Miranda, Osvaldo id: 862A3C56-A8BF-11E9-B4FA-D9E3E5697425 last_name: Miranda orcid: 0000-0001-6618-6889 - first_name: Jessie E. full_name: Buth, Jessie E. last_name: Buth - first_name: Simon full_name: Mitchell, Simon last_name: Mitchell - first_name: Isabella full_name: Ferando, Isabella last_name: Ferando - first_name: Momoko full_name: Watanabe, Momoko last_name: Watanabe - first_name: Arinnae full_name: Kurdian, Arinnae last_name: Kurdian - first_name: Peyman full_name: Golshani, Peyman last_name: Golshani - first_name: Kathrin full_name: Plath, Kathrin last_name: Plath - first_name: William E. full_name: Lowry, William E. last_name: Lowry - first_name: Jack M. full_name: Parent, Jack M. last_name: Parent - first_name: Istvan full_name: Mody, Istvan last_name: Mody - first_name: Bennett G. full_name: Novitch, Bennett G. last_name: Novitch citation: ama: Samarasinghe RA, Miranda O, Buth JE, et al. Identification of Neural Oscillations and Epileptiform Changes in Human Brain Organoids. Vol 24. Springer Nature; 2021. doi:10.1038/s41593-021-00906-5 apa: Samarasinghe, R. A., Miranda, O., Buth, J. E., Mitchell, S., Ferando, I., Watanabe, M., … Novitch, B. G. (2021). Identification of neural oscillations and epileptiform changes in human brain organoids (Vol. 24). Springer Nature. https://doi.org/10.1038/s41593-021-00906-5 chicago: Samarasinghe, Ranmal A., Osvaldo Miranda, Jessie E. Buth, Simon Mitchell, Isabella Ferando, Momoko Watanabe, Arinnae Kurdian, et al. Identification of Neural Oscillations and Epileptiform Changes in Human Brain Organoids. Vol. 24. Springer Nature, 2021. https://doi.org/10.1038/s41593-021-00906-5. ieee: R. A. Samarasinghe et al., Identification of neural oscillations and epileptiform changes in human brain organoids, vol. 24. Springer Nature, 2021. ista: Samarasinghe RA, Miranda O, Buth JE, Mitchell S, Ferando I, Watanabe M, Kurdian A, Golshani P, Plath K, Lowry WE, Parent JM, Mody I, Novitch BG. 2021. Identification of neural oscillations and epileptiform changes in human brain organoids, Springer Nature, 32p. mla: Samarasinghe, Ranmal A., et al. Identification of Neural Oscillations and Epileptiform Changes in Human Brain Organoids. Vol. 24, Springer Nature, 2021, doi:10.1038/s41593-021-00906-5. short: R.A. Samarasinghe, O. Miranda, J.E. Buth, S. Mitchell, I. Ferando, M. Watanabe, A. Kurdian, P. Golshani, K. Plath, W.E. Lowry, J.M. Parent, I. Mody, B.G. Novitch, Identification of Neural Oscillations and Epileptiform Changes in Human Brain Organoids, Springer Nature, 2021. date_created: 2019-11-10T11:23:58Z date_published: 2021-08-23T00:00:00Z date_updated: 2023-08-04T10:49:44Z day: '23' department: - _id: GradSch - _id: SiHi doi: 10.1038/s41593-021-00906-5 external_id: isi: - '000687516300001' pmid: - '34426698 ' intvolume: ' 24' isi: 1 language: - iso: eng main_file_link: - open_access: '1' url: https://doi.org/10.1038/s41593-021-00906-5 month: '08' oa: 1 oa_version: Published Version page: '32' pmid: 1 publication_identifier: eissn: - 1546-1726 issn: - 1097-6256 publication_status: published publisher: Springer Nature status: public title: Identification of neural oscillations and epileptiform changes in human brain organoids type: technical_report user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8 volume: 24 year: '2021' ... --- _id: '8546' abstract: - lang: eng text: Brain neurons arise from relatively few progenitors generating an enormous diversity of neuronal types. Nonetheless, a cardinal feature of mammalian brain neurogenesis is thought to be that excitatory and inhibitory neurons derive from separate, spatially segregated progenitors. Whether bi-potential progenitors with an intrinsic capacity to generate both lineages exist and how such a fate decision may be regulated are unknown. Using cerebellar development as a model, we discover that individual progenitors can give rise to both inhibitory and excitatory lineages. Gradations of Notch activity determine the fates of the progenitors and their daughters. Daughters with the highest levels of Notch activity retain the progenitor fate, while intermediate levels of Notch activity generate inhibitory neurons, and daughters with very low levels of Notch signaling adopt the excitatory fate. Therefore, Notch-mediated binary cell fate choice is a mechanism for regulating the ratio of excitatory to inhibitory neurons from common progenitors. acknowledgement: This work was supported by the program “Investissements d’avenir” ANR-10-IAIHU-06 , ICM , a Sorbonne Université Emergence grant, an Allen Distinguished Investigator Award , and the Roger De Spoelberch Foundation Prize (to B.A.H.); Armenise-Harvard Foundation , AIRC , and CARITRO (to L.T.); and the European Research Council under the European Union’s Horizon 2020 research and innovation programme grant agreement no. 725780 LinPro (to S.H.). T.Z. and T.L. were supported by doctoral fellowships from the China Scholarship Council and A.H.H. by a doctoral DOC fellowship of the Austrian Academy of Sciences ( 24812 ). All animal work was conducted at the PHENO-ICMice facility. The Core is supported by 2 “Investissements d’avenir” (ANR-10- IAIHU-06 and ANR-11-INBS-0011-NeurATRIS) and the “Fondation pour la Recherche Médicale.” Light microscopy work was carried out at ICM’s imaging core facility, ICM.Quant, and analysis of scRNA-seq data was carried out at ICM’s bioinformatics core facility, iCONICS. We thank Paulina Ejsmont, Natalia Danda, and Nathalie De Geest for technical support. We are grateful to Dr. Shahragim TAJBAKHSH for providing R26Rstop-NICD-nGFP transgenic mice, Dr. Bart De Strooper for Psn1-deficient mice, Dr. Jean-Christophe Marine for Gt(ROSA)26SortdTom reporter mice, and Dr. Martinez Barbera for Sox2CreERT2 mice. We also give thanks to Dr. Mikio Hoshino for providing Atoh1 and Ptf1a antibodies. B.A.H. is an Einstein Visiting Fellow of the Berlin Institute of Health . article_number: '109208' article_processing_charge: No article_type: original author: - first_name: Tingting full_name: Zhang, Tingting last_name: Zhang - first_name: Tengyuan full_name: Liu, Tengyuan last_name: Liu - first_name: Natalia full_name: Mora, Natalia last_name: Mora - first_name: Justine full_name: Guegan, Justine last_name: Guegan - first_name: Mathilde full_name: Bertrand, Mathilde last_name: Bertrand - first_name: Ximena full_name: Contreras, Ximena id: 475990FE-F248-11E8-B48F-1D18A9856A87 last_name: Contreras - first_name: Andi H full_name: Hansen, Andi H id: 38853E16-F248-11E8-B48F-1D18A9856A87 last_name: Hansen - first_name: Carmen full_name: Streicher, Carmen id: 36BCB99C-F248-11E8-B48F-1D18A9856A87 last_name: Streicher - first_name: Marica full_name: Anderle, Marica last_name: Anderle - first_name: Natasha full_name: Danda, Natasha last_name: Danda - first_name: Luca full_name: Tiberi, Luca last_name: Tiberi - first_name: Simon full_name: Hippenmeyer, Simon id: 37B36620-F248-11E8-B48F-1D18A9856A87 last_name: Hippenmeyer orcid: 0000-0003-2279-1061 - first_name: Bassem A. full_name: Hassan, Bassem A. last_name: Hassan citation: ama: Zhang T, Liu T, Mora N, et al. Generation of excitatory and inhibitory neurons from common progenitors via Notch signaling in the cerebellum. Cell Reports. 2021;35(10). doi:10.1016/j.celrep.2021.109208 apa: Zhang, T., Liu, T., Mora, N., Guegan, J., Bertrand, M., Contreras, X., … Hassan, B. A. (2021). Generation of excitatory and inhibitory neurons from common progenitors via Notch signaling in the cerebellum. Cell Reports. Elsevier. https://doi.org/10.1016/j.celrep.2021.109208 chicago: Zhang, Tingting, Tengyuan Liu, Natalia Mora, Justine Guegan, Mathilde Bertrand, Ximena Contreras, Andi H Hansen, et al. “Generation of Excitatory and Inhibitory Neurons from Common Progenitors via Notch Signaling in the Cerebellum.” Cell Reports. Elsevier, 2021. https://doi.org/10.1016/j.celrep.2021.109208. ieee: T. Zhang et al., “Generation of excitatory and inhibitory neurons from common progenitors via Notch signaling in the cerebellum,” Cell Reports, vol. 35, no. 10. Elsevier, 2021. ista: Zhang T, Liu T, Mora N, Guegan J, Bertrand M, Contreras X, Hansen AH, Streicher C, Anderle M, Danda N, Tiberi L, Hippenmeyer S, Hassan BA. 2021. Generation of excitatory and inhibitory neurons from common progenitors via Notch signaling in the cerebellum. Cell Reports. 35(10), 109208. mla: Zhang, Tingting, et al. “Generation of Excitatory and Inhibitory Neurons from Common Progenitors via Notch Signaling in the Cerebellum.” Cell Reports, vol. 35, no. 10, 109208, Elsevier, 2021, doi:10.1016/j.celrep.2021.109208. short: T. Zhang, T. Liu, N. Mora, J. Guegan, M. Bertrand, X. Contreras, A.H. Hansen, C. Streicher, M. Anderle, N. Danda, L. Tiberi, S. Hippenmeyer, B.A. Hassan, Cell Reports 35 (2021). date_created: 2020-09-21T12:00:48Z date_published: 2021-06-08T00:00:00Z date_updated: 2023-08-04T11:00:48Z day: '08' ddc: - '570' department: - _id: SiHi doi: 10.1016/j.celrep.2021.109208 ec_funded: 1 external_id: isi: - '000659894300001' pmid: - '34107249 ' file: - access_level: open_access checksum: 7def3d42ebc8f5675efb6f38819e3e2e content_type: application/pdf creator: cziletti date_created: 2021-06-15T14:01:35Z date_updated: 2021-06-15T14:01:35Z file_id: '9554' file_name: 2021_CellReports_Zhang.pdf file_size: 8900385 relation: main_file success: 1 file_date_updated: 2021-06-15T14:01:35Z has_accepted_license: '1' intvolume: ' 35' isi: 1 issue: '10' language: - iso: eng license: https://creativecommons.org/licenses/by-nc-nd/4.0/ month: '06' oa: 1 oa_version: Published Version pmid: 1 project: - _id: 260018B0-B435-11E9-9278-68D0E5697425 call_identifier: H2020 grant_number: '725780' name: Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development - _id: 2625A13E-B435-11E9-9278-68D0E5697425 grant_number: '24812' name: Molecular Mechanisms of Radial Neuronal Migration publication: Cell Reports publication_identifier: eissn: - ' 22111247' publication_status: published publisher: Elsevier quality_controlled: '1' related_material: link: - relation: earlier_version url: https://doi.org/10.1101/2020.03.18.997205 scopus_import: '1' status: public title: Generation of excitatory and inhibitory neurons from common progenitors via Notch signaling in the cerebellum 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: 4359f0d1-fa6c-11eb-b949-802e58b17ae8 volume: 35 year: '2021' ... --- _id: '9188' abstract: - lang: eng text: Genomic imprinting is an epigenetic mechanism that results in parental allele-specific expression of ~1% of all genes in mouse and human. Imprinted genes are key developmental regulators and play pivotal roles in many biological processes such as nutrient transfer from the mother to offspring and neuronal development. Imprinted genes are also involved in human disease, including neurodevelopmental disorders, and often occur in clusters that are regulated by a common imprint control region (ICR). In extra-embryonic tissues ICRs can act over large distances, with the largest surrounding Igf2r spanning over 10 million base-pairs. Besides classical imprinted expression that shows near exclusive maternal or paternal expression, widespread biased imprinted expression has been identified mainly in brain. In this review we discuss recent developments mapping cell type specific imprinted expression in extra-embryonic tissues and neocortex in the mouse. We highlight the advantages of using an inducible uniparental chromosome disomy (UPD) system to generate cells carrying either two maternal or two paternal copies of a specific chromosome to analyze the functional consequences of genomic imprinting. Mosaic Analysis with Double Markers (MADM) allows fluorescent labeling and concomitant induction of UPD sparsely in specific cell types, and thus to over-express or suppress all imprinted genes on that chromosome. To illustrate the utility of this technique, we explain how MADM-induced UPD revealed new insights about the function of the well-studied Cdkn1c imprinted gene, and how MADM-induced UPDs led to identification of highly cell type specific phenotypes related to perturbed imprinted expression in the mouse neocortex. Finally, we give an outlook on how MADM could be used to probe cell type specific imprinted expression in other tissues in mouse, particularly in extra-embryonic tissues. acknowledgement: We thank Melissa Stouffer for critically reading the manuscript. This work was supported by IST Austria institutional funds; NÖ Forschung und Bildung n[f + b] life science call grant (C13-002) to S.H. and the European Research Council (ERC) under the European Union's Horizon 2020 research and innovation program (grant agreement 725780 LinPro) to S.H. article_number: '104986' article_processing_charge: Yes (via OA deal) article_type: original author: - first_name: Florian full_name: Pauler, Florian id: 48EA0138-F248-11E8-B48F-1D18A9856A87 last_name: Pauler - first_name: Quanah full_name: Hudson, Quanah last_name: Hudson - first_name: Susanne full_name: Laukoter, Susanne id: 2D6B7A9A-F248-11E8-B48F-1D18A9856A87 last_name: Laukoter - first_name: Simon full_name: Hippenmeyer, Simon id: 37B36620-F248-11E8-B48F-1D18A9856A87 last_name: Hippenmeyer orcid: 0000-0003-2279-1061 citation: ama: Pauler F, Hudson Q, Laukoter S, Hippenmeyer S. Inducible uniparental chromosome disomy to probe genomic imprinting at single-cell level in brain and beyond. Neurochemistry International. 2021;145(5). doi:10.1016/j.neuint.2021.104986 apa: Pauler, F., Hudson, Q., Laukoter, S., & Hippenmeyer, S. (2021). Inducible uniparental chromosome disomy to probe genomic imprinting at single-cell level in brain and beyond. Neurochemistry International. Elsevier. https://doi.org/10.1016/j.neuint.2021.104986 chicago: Pauler, Florian, Quanah Hudson, Susanne Laukoter, and Simon Hippenmeyer. “Inducible Uniparental Chromosome Disomy to Probe Genomic Imprinting at Single-Cell Level in Brain and Beyond.” Neurochemistry International. Elsevier, 2021. https://doi.org/10.1016/j.neuint.2021.104986. ieee: F. Pauler, Q. Hudson, S. Laukoter, and S. Hippenmeyer, “Inducible uniparental chromosome disomy to probe genomic imprinting at single-cell level in brain and beyond,” Neurochemistry International, vol. 145, no. 5. Elsevier, 2021. ista: Pauler F, Hudson Q, Laukoter S, Hippenmeyer S. 2021. Inducible uniparental chromosome disomy to probe genomic imprinting at single-cell level in brain and beyond. Neurochemistry International. 145(5), 104986. mla: Pauler, Florian, et al. “Inducible Uniparental Chromosome Disomy to Probe Genomic Imprinting at Single-Cell Level in Brain and Beyond.” Neurochemistry International, vol. 145, no. 5, 104986, Elsevier, 2021, doi:10.1016/j.neuint.2021.104986. short: F. Pauler, Q. Hudson, S. Laukoter, S. Hippenmeyer, Neurochemistry International 145 (2021). date_created: 2021-02-23T12:31:43Z date_published: 2021-05-01T00:00:00Z date_updated: 2023-08-07T13:48:26Z day: '01' ddc: - '570' department: - _id: SiHi doi: 10.1016/j.neuint.2021.104986 ec_funded: 1 external_id: isi: - '000635575000005' pmid: - '33600873' file: - access_level: open_access checksum: c6d7a40089cd29e289f9b22e75768304 content_type: application/pdf creator: kschuh date_created: 2021-08-11T12:30:38Z date_updated: 2021-08-11T12:30:38Z file_id: '9883' file_name: 2021_NCI_Pauler.pdf file_size: 7083499 relation: main_file success: 1 file_date_updated: 2021-08-11T12:30:38Z has_accepted_license: '1' intvolume: ' 145' isi: 1 issue: '5' keyword: - Cell Biology - Cellular and Molecular Neuroscience language: - iso: eng month: '05' oa: 1 oa_version: Published Version pmid: 1 project: - _id: 260018B0-B435-11E9-9278-68D0E5697425 call_identifier: H2020 grant_number: '725780' name: Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development - _id: 25D92700-B435-11E9-9278-68D0E5697425 grant_number: LS13-002 name: Mapping Cell-Type Specificity of the Genomic Imprintome in the Brain publication: Neurochemistry International publication_identifier: issn: - 0197-0186 publication_status: published publisher: Elsevier quality_controlled: '1' scopus_import: '1' status: public title: Inducible uniparental chromosome disomy to probe genomic imprinting at single-cell level in brain and beyond 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: 4359f0d1-fa6c-11eb-b949-802e58b17ae8 volume: 145 year: '2021' ... --- _id: '9601' abstract: - lang: eng text: 'In mammalian genomes, differentially methylated regions (DMRs) and histone marks including trimethylation of histone 3 lysine 27 (H3K27me3) at imprinted genes are asymmetrically inherited to control parentally-biased gene expression. However, neither parent-of-origin-specific transcription nor imprints have been comprehensively mapped at the blastocyst stage of preimplantation development. Here, we address this by integrating transcriptomic and epigenomic approaches in mouse preimplantation embryos. We find that seventy-one genes exhibit previously unreported parent-of-origin-specific expression in blastocysts (nBiX: novel blastocyst-imprinted expressed). Uniparental expression of nBiX genes disappears soon after implantation. Micro-whole-genome bisulfite sequencing (µWGBS) of individual uniparental blastocysts detects 859 DMRs. We further find that 16% of nBiX genes are associated with a DMR, whereas most are associated with parentally-biased H3K27me3, suggesting a role for Polycomb-mediated imprinting in blastocysts. nBiX genes are clustered: five clusters contained at least one published imprinted gene, and five clusters exclusively contained nBiX genes. These data suggest that early development undergoes a complex program of stage-specific imprinting involving different tiers of regulation.' acknowledgement: The authors thank Robert Feil and Anton Wutz for helpful discussions and comments, Samuel Collombet and Peter Fraser for sharing embryo TAD coordinates, and Andy Riddel at the Cambridge Stem Cell Institute and Thomas Sauer at the Max Perutz Laboratories FACS facility for flow-sorting. We thank the team of the Biomedical Sequencing Facility at the CeMM and the Vienna Biocenter Core Facilities (VBCF) for support with next-generation sequencing. We are grateful to animal care teams at the University of Bath and MRC Harwell. A.C.F.P. acknowledges support from the UK Medical Research Council (MR/N000080/1 and MR/N020294/1) and Biotechnology and Biological Sciences Research Council (BB/P009506/1). L.S. is part of the FWF doctoral programme SMICH and supported by an Austrian Academy of Sciences DOC Fellowship. M.L. is funded by a Vienna Research Group for Young Investigators grant (VRG14-006) by the Vienna Science and Technology Fund (WWTF) and by the Austrian Science Fund FWF (I3786 and P31334). article_number: '3804' article_processing_charge: No article_type: original author: - first_name: Laura full_name: Santini, Laura last_name: Santini - first_name: Florian full_name: Halbritter, Florian last_name: Halbritter - first_name: Fabian full_name: Titz-Teixeira, Fabian last_name: Titz-Teixeira - first_name: Toru full_name: Suzuki, Toru last_name: Suzuki - first_name: Maki full_name: Asami, Maki last_name: Asami - first_name: Xiaoyan full_name: Ma, Xiaoyan last_name: Ma - first_name: Julia full_name: Ramesmayer, Julia last_name: Ramesmayer - first_name: Andreas full_name: Lackner, Andreas last_name: Lackner - first_name: Nick full_name: Warr, Nick last_name: Warr - first_name: Florian full_name: Pauler, Florian id: 48EA0138-F248-11E8-B48F-1D18A9856A87 last_name: Pauler orcid: 0000-0002-7462-0048 - first_name: Simon full_name: Hippenmeyer, Simon id: 37B36620-F248-11E8-B48F-1D18A9856A87 last_name: Hippenmeyer orcid: 0000-0003-2279-1061 - first_name: Ernest full_name: Laue, Ernest last_name: Laue - first_name: Matthias full_name: Farlik, Matthias last_name: Farlik - first_name: Christoph full_name: Bock, Christoph last_name: Bock - first_name: Andreas full_name: Beyer, Andreas last_name: Beyer - first_name: Anthony C.F. full_name: Perry, Anthony C.F. last_name: Perry - first_name: Martin full_name: Leeb, Martin last_name: Leeb citation: ama: Santini L, Halbritter F, Titz-Teixeira F, et al. Genomic imprinting in mouse blastocysts is predominantly associated with H3K27me3. Nature Communications. 2021;12(1). doi:10.1038/s41467-021-23510-4 apa: Santini, L., Halbritter, F., Titz-Teixeira, F., Suzuki, T., Asami, M., Ma, X., … Leeb, M. (2021). Genomic imprinting in mouse blastocysts is predominantly associated with H3K27me3. Nature Communications. Springer Nature. https://doi.org/10.1038/s41467-021-23510-4 chicago: Santini, Laura, Florian Halbritter, Fabian Titz-Teixeira, Toru Suzuki, Maki Asami, Xiaoyan Ma, Julia Ramesmayer, et al. “Genomic Imprinting in Mouse Blastocysts Is Predominantly Associated with H3K27me3.” Nature Communications. Springer Nature, 2021. https://doi.org/10.1038/s41467-021-23510-4. ieee: L. Santini et al., “Genomic imprinting in mouse blastocysts is predominantly associated with H3K27me3,” Nature Communications, vol. 12, no. 1. Springer Nature, 2021. ista: Santini L, Halbritter F, Titz-Teixeira F, Suzuki T, Asami M, Ma X, Ramesmayer J, Lackner A, Warr N, Pauler F, Hippenmeyer S, Laue E, Farlik M, Bock C, Beyer A, Perry ACF, Leeb M. 2021. Genomic imprinting in mouse blastocysts is predominantly associated with H3K27me3. Nature Communications. 12(1), 3804. mla: Santini, Laura, et al. “Genomic Imprinting in Mouse Blastocysts Is Predominantly Associated with H3K27me3.” Nature Communications, vol. 12, no. 1, 3804, Springer Nature, 2021, doi:10.1038/s41467-021-23510-4. short: L. Santini, F. Halbritter, F. Titz-Teixeira, T. Suzuki, M. Asami, X. Ma, J. Ramesmayer, A. Lackner, N. Warr, F. Pauler, S. Hippenmeyer, E. Laue, M. Farlik, C. Bock, A. Beyer, A.C.F. Perry, M. Leeb, Nature Communications 12 (2021). date_created: 2021-06-27T22:01:46Z date_published: 2021-07-12T00:00:00Z date_updated: 2023-08-10T13:53:23Z day: '12' ddc: - '570' department: - _id: SiHi doi: 10.1038/s41467-021-23510-4 external_id: isi: - '000667248600005' file: - access_level: open_access checksum: 75dd89d09945185b2d14b2434a0bcb50 content_type: application/pdf creator: asandaue date_created: 2021-06-28T08:04:22Z date_updated: 2021-06-28T08:04:22Z file_id: '9608' file_name: 2021_NatureCommunications_Santini.pdf file_size: 2156554 relation: main_file success: 1 file_date_updated: 2021-06-28T08:04:22Z has_accepted_license: '1' intvolume: ' 12' isi: 1 issue: '1' language: - iso: eng month: '07' oa: 1 oa_version: Published Version publication: Nature Communications publication_identifier: eissn: - '20411723' publication_status: published publisher: Springer Nature quality_controlled: '1' scopus_import: '1' status: public title: Genomic imprinting in mouse blastocysts is predominantly associated with H3K27me3 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: 4359f0d1-fa6c-11eb-b949-802e58b17ae8 volume: 12 year: '2021' ... --- _id: '9603' abstract: - lang: eng text: Mosaic analysis with double markers (MADM) offers one approach to visualize and concomitantly manipulate genetically defined cells in mice with single-cell resolution. MADM applications include the analysis of lineage, single-cell morphology and physiology, genomic imprinting phenotypes, and dissection of cell-autonomous gene functions in vivo in health and disease. Yet, MADM can only be applied to <25% of all mouse genes on select chromosomes to date. To overcome this limitation, we generate transgenic mice with knocked-in MADM cassettes near the centromeres of all 19 autosomes and validate their use across organs. With this resource, >96% of the entire mouse genome can now be subjected to single-cell genetic mosaic analysis. Beyond a proof of principle, we apply our MADM library to systematically trace sister chromatid segregation in distinct mitotic cell lineages. We find striking chromosome-specific biases in segregation patterns, reflecting a putative mechanism for the asymmetric segregation of genetic determinants in somatic stem cell division. acknowledged_ssus: - _id: Bio - _id: LifeSc - _id: PreCl acknowledgement: We thank the Bioimaging, Life Science, and Pre-Clinical Facilities at IST Austria; M.P. Postiglione, C. Simbriger, K. Valoskova, C. Schwayer, T. Hussain, M. Pieber, and V. Wimmer for initial experiments, technical support, and/or assistance; R. Shigemoto for sharing iv (Dnah11 mutant) mice; and M. Sixt and all members of the Hippenmeyer lab for discussion. This work was supported by National Institutes of Health grants ( R01-NS050580 to L.L. and F32MH096361 to L.A.S.). L.L. is an investigator of HHMI. N.A. received support from FWF Firnberg-Programm ( T 1031 ). A.H.H. is a recipient of a DOC Fellowship (24812) of the Austrian Academy of Sciences . This work also received support from IST Austria institutional funds , FWF SFB F78 to S.H., the People Programme (Marie Curie Actions) of the European Union’s Seventh Framework Programme ( FP7/2007-2013 ) under REA grant agreement no 618444 to S.H., and the European Research Council (ERC) under the European Union’s Horizon 2020 Research and Innovation Programme (grant agreement no. 725780 LinPro ) to S.H. article_number: '109274' article_processing_charge: No article_type: original author: - first_name: Ximena full_name: Contreras, Ximena id: 475990FE-F248-11E8-B48F-1D18A9856A87 last_name: Contreras - first_name: Nicole full_name: Amberg, Nicole id: 4CD6AAC6-F248-11E8-B48F-1D18A9856A87 last_name: Amberg orcid: 0000-0002-3183-8207 - first_name: Amarbayasgalan full_name: Davaatseren, Amarbayasgalan id: 70ADC922-B424-11E9-99E3-BA18E6697425 last_name: Davaatseren - first_name: Andi H full_name: Hansen, Andi H id: 38853E16-F248-11E8-B48F-1D18A9856A87 last_name: Hansen - first_name: Johanna full_name: Sonntag, Johanna id: 32FE7D7C-F248-11E8-B48F-1D18A9856A87 last_name: Sonntag - first_name: Lill full_name: Andersen, Lill last_name: Andersen - first_name: Tina full_name: Bernthaler, Tina last_name: Bernthaler - first_name: Carmen full_name: Streicher, Carmen id: 36BCB99C-F248-11E8-B48F-1D18A9856A87 last_name: Streicher - first_name: Anna-Magdalena full_name: Heger, Anna-Magdalena id: 4B76FFD2-F248-11E8-B48F-1D18A9856A87 last_name: Heger - first_name: Randy L. full_name: Johnson, Randy L. last_name: Johnson - first_name: Lindsay A. full_name: Schwarz, Lindsay A. last_name: Schwarz - first_name: Liqun full_name: Luo, Liqun last_name: Luo - first_name: Thomas full_name: Rülicke, Thomas last_name: Rülicke - first_name: Simon full_name: Hippenmeyer, Simon id: 37B36620-F248-11E8-B48F-1D18A9856A87 last_name: Hippenmeyer orcid: 0000-0003-2279-1061 citation: ama: Contreras X, Amberg N, Davaatseren A, et al. A genome-wide library of MADM mice for single-cell genetic mosaic analysis. Cell Reports. 2021;35(12). doi:10.1016/j.celrep.2021.109274 apa: Contreras, X., Amberg, N., Davaatseren, A., Hansen, A. H., Sonntag, J., Andersen, L., … Hippenmeyer, S. (2021). A genome-wide library of MADM mice for single-cell genetic mosaic analysis. Cell Reports. Cell Press. https://doi.org/10.1016/j.celrep.2021.109274 chicago: Contreras, Ximena, Nicole Amberg, Amarbayasgalan Davaatseren, Andi H Hansen, Johanna Sonntag, Lill Andersen, Tina Bernthaler, et al. “A Genome-Wide Library of MADM Mice for Single-Cell Genetic Mosaic Analysis.” Cell Reports. Cell Press, 2021. https://doi.org/10.1016/j.celrep.2021.109274. ieee: X. Contreras et al., “A genome-wide library of MADM mice for single-cell genetic mosaic analysis,” Cell Reports, vol. 35, no. 12. Cell Press, 2021. ista: Contreras X, Amberg N, Davaatseren A, Hansen AH, Sonntag J, Andersen L, Bernthaler T, Streicher C, Heger A-M, Johnson RL, Schwarz LA, Luo L, Rülicke T, Hippenmeyer S. 2021. A genome-wide library of MADM mice for single-cell genetic mosaic analysis. Cell Reports. 35(12), 109274. mla: Contreras, Ximena, et al. “A Genome-Wide Library of MADM Mice for Single-Cell Genetic Mosaic Analysis.” Cell Reports, vol. 35, no. 12, 109274, Cell Press, 2021, doi:10.1016/j.celrep.2021.109274. short: X. Contreras, N. Amberg, A. Davaatseren, A.H. Hansen, J. Sonntag, L. Andersen, T. Bernthaler, C. Streicher, A.-M. Heger, R.L. Johnson, L.A. Schwarz, L. Luo, T. Rülicke, S. Hippenmeyer, Cell Reports 35 (2021). date_created: 2021-06-27T22:01:48Z date_published: 2021-06-22T00:00:00Z date_updated: 2023-08-10T13:55:00Z day: '22' ddc: - '570' department: - _id: SiHi - _id: LoSw - _id: PreCl doi: 10.1016/j.celrep.2021.109274 ec_funded: 1 external_id: isi: - '000664463600016' file: - access_level: open_access checksum: d49520fdcbbb5c2f883bddb67cee5d77 content_type: application/pdf creator: asandaue date_created: 2021-06-28T14:06:24Z date_updated: 2021-06-28T14:06:24Z file_id: '9613' file_name: 2021_CellReports_Contreras.pdf file_size: 7653149 relation: main_file success: 1 file_date_updated: 2021-06-28T14:06:24Z has_accepted_license: '1' intvolume: ' 35' isi: 1 issue: '12' language: - iso: eng month: '06' oa: 1 oa_version: Published Version project: - _id: 2625A13E-B435-11E9-9278-68D0E5697425 grant_number: '24812' name: Molecular Mechanisms of Radial Neuronal Migration - _id: 25D61E48-B435-11E9-9278-68D0E5697425 call_identifier: FP7 grant_number: '618444' name: Molecular Mechanisms of Cerebral Cortex Development - _id: 260018B0-B435-11E9-9278-68D0E5697425 call_identifier: H2020 grant_number: '725780' name: Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development publication: Cell Reports publication_identifier: eissn: - '22111247' publication_status: published publisher: Cell Press quality_controlled: '1' related_material: link: - description: News on IST Homepage relation: press_release url: https://ist.ac.at/en/news/boost-for-mouse-genetic-analysis/ scopus_import: '1' status: public title: A genome-wide library of MADM mice for single-cell genetic mosaic analysis 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: 4359f0d1-fa6c-11eb-b949-802e58b17ae8 volume: 35 year: '2021' ... --- _id: '9906' abstract: - lang: eng text: Endometriosis is a common gynecological disorder characterized by ectopic growth of endometrium outside the uterus and is associated with chronic pain and infertility. We investigated the role of the long intergenic noncoding RNA 01133 (LINC01133) in endometriosis, an lncRNA that has been implicated in several types of cancer. We found that LINC01133 is upregulated in ectopic endometriotic lesions. As expression appeared higher in the epithelial endometrial layer, we performed a siRNA knockdown of LINC01133 in an endometriosis epithelial cell line. Phenotypic assays indicated that LINC01133 may promote proliferation and suppress cellular migration, and affect the cytoskeleton and morphology of the cells. Gene ontology analysis of differentially expressed genes indicated that cell proliferation and migration pathways were affected in line with the observed phenotype. We validated upregulation of p21 and downregulation of Cyclin A at the protein level, which together with the quantification of the DNA content using fluorescence-activated cell sorting (FACS) analysis indicated that the observed effects on cellular proliferation may be due to changes in cell cycle. Further, we found testis-specific protein kinase 1 (TESK1) kinase upregulation corresponding with phosphorylation and inactivation of actin severing protein Cofilin, which could explain changes in the cytoskeleton and cellular migration. These results indicate that endometriosis is associated with LINC01133 upregulation, which may affect pathogenesis via the cellular proliferation and migration pathways. acknowledgement: "Open access funding provided by Medical University of Vienna. The authors would like to thank all the participants and health professionals involved in the present study. We want to thank our technical assistants Barbara Widmar and Matthias Witzmann-Stern for their diligent work and constant assistance. We would like to thank Simon Hippenmeyer for access to\r\nbioinformatic infrastructure and resources." article_number: '8385' article_processing_charge: Yes article_type: original author: - first_name: Iveta full_name: Yotova, Iveta last_name: Yotova - first_name: Quanah J. full_name: Hudson, Quanah J. last_name: Hudson - first_name: Florian full_name: Pauler, Florian id: 48EA0138-F248-11E8-B48F-1D18A9856A87 last_name: Pauler orcid: 0000-0002-7462-0048 - first_name: Katharina full_name: Proestling, Katharina last_name: Proestling - first_name: Isabella full_name: Haslinger, Isabella last_name: Haslinger - first_name: Lorenz full_name: Kuessel, Lorenz last_name: Kuessel - first_name: Alexandra full_name: Perricos, Alexandra last_name: Perricos - first_name: Heinrich full_name: Husslein, Heinrich last_name: Husslein - first_name: René full_name: Wenzl, René last_name: Wenzl citation: ama: Yotova I, Hudson QJ, Pauler F, et al. LINC01133 inhibits invasion and promotes proliferation in an endometriosis epithelial cell line. International Journal of Molecular Sciences. 2021;22(16). doi:10.3390/ijms22168385 apa: Yotova, I., Hudson, Q. J., Pauler, F., Proestling, K., Haslinger, I., Kuessel, L., … Wenzl, R. (2021). LINC01133 inhibits invasion and promotes proliferation in an endometriosis epithelial cell line. International Journal of Molecular Sciences. MDPI. https://doi.org/10.3390/ijms22168385 chicago: Yotova, Iveta, Quanah J. Hudson, Florian Pauler, Katharina Proestling, Isabella Haslinger, Lorenz Kuessel, Alexandra Perricos, Heinrich Husslein, and René Wenzl. “LINC01133 Inhibits Invasion and Promotes Proliferation in an Endometriosis Epithelial Cell Line.” International Journal of Molecular Sciences. MDPI, 2021. https://doi.org/10.3390/ijms22168385. ieee: I. Yotova et al., “LINC01133 inhibits invasion and promotes proliferation in an endometriosis epithelial cell line,” International Journal of Molecular Sciences, vol. 22, no. 16. MDPI, 2021. ista: Yotova I, Hudson QJ, Pauler F, Proestling K, Haslinger I, Kuessel L, Perricos A, Husslein H, Wenzl R. 2021. LINC01133 inhibits invasion and promotes proliferation in an endometriosis epithelial cell line. International Journal of Molecular Sciences. 22(16), 8385. mla: Yotova, Iveta, et al. “LINC01133 Inhibits Invasion and Promotes Proliferation in an Endometriosis Epithelial Cell Line.” International Journal of Molecular Sciences, vol. 22, no. 16, 8385, MDPI, 2021, doi:10.3390/ijms22168385. short: I. Yotova, Q.J. Hudson, F. Pauler, K. Proestling, I. Haslinger, L. Kuessel, A. Perricos, H. Husslein, R. Wenzl, International Journal of Molecular Sciences 22 (2021). date_created: 2021-08-15T22:01:27Z date_published: 2021-08-04T00:00:00Z date_updated: 2023-08-11T10:34:13Z day: '04' ddc: - '570' department: - _id: SiHi doi: 10.3390/ijms22168385 external_id: isi: - '000689147400001' file: - access_level: open_access checksum: be7f0042607ca60549cb27513c19c6af content_type: application/pdf creator: asandaue date_created: 2021-08-16T09:29:17Z date_updated: 2021-08-16T09:29:17Z file_id: '9922' file_name: 2021_InternationalJournalOfMolecularSciences_Yotova.pdf file_size: 2646018 relation: main_file success: 1 file_date_updated: 2021-08-16T09:29:17Z has_accepted_license: '1' intvolume: ' 22' isi: 1 issue: '16' language: - iso: eng month: '08' oa: 1 oa_version: Published Version publication: International Journal of Molecular Sciences publication_identifier: eissn: - '14220067' issn: - '16616596' publication_status: published publisher: MDPI quality_controlled: '1' scopus_import: '1' status: public title: LINC01133 inhibits invasion and promotes proliferation in an endometriosis epithelial cell line 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: 4359f0d1-fa6c-11eb-b949-802e58b17ae8 volume: 22 year: '2021' ... --- _id: '9073' abstract: - lang: eng text: The sensory and cognitive abilities of the mammalian neocortex are underpinned by intricate columnar and laminar circuits formed from an array of diverse neuronal populations. One approach to determining how interactions between these circuit components give rise to complex behavior is to investigate the rules by which cortical circuits are formed and acquire functionality during development. This review summarizes recent research on the development of the neocortex, from genetic determination in neural stem cells through to the dynamic role that specific neuronal populations play in the earliest circuits of neocortex, and how they contribute to emergent function and cognition. While many of these endeavors take advantage of model systems, consideration will also be given to advances in our understanding of activity in nascent human circuits. Such cross-species perspective is imperative when investigating the mechanisms underlying the dysfunction of early neocortical circuits in neurodevelopmental disorders, so that one can identify targets amenable to therapeutic intervention. acknowledgement: Work in the I.L.H.-O. laboratory was supported by European Research Council Grant ERC-2015-CoG 681577 and German Research Foundation Ha 4466/10-1, Ha4466/11-1, Ha4466/12-1, SPP 1665, and SFB 936B5. Work in the S.J.B.B. laboratory was supported by Biotechnology and Biological Sciences Research Council BB/P003796/1, Medical Research Council MR/K004387/1 and MR/T033320/1, Wellcome Trust 215199/Z/19/Z and 102386/Z/13/Z, and John Fell Fund. Work in the S.H. laboratory was supported by European Research Council Grants ERC-2016-CoG 725780 LinPro and FWF SFB F78. This work was supported by National Institutes of Health Grant NIMH 1R01MH110553 to N.V.D.M.G. Work in the J.A.C. laboratory was supported by the Ludwig Family Foundation, Simons Foundation SFARI Research Award, and National Institutes of Health/National Institute of Mental Health R01 MH102365 and R01MH113852. The B.V. laboratory was supported by Whitehall Foundation 2017-12-73, National Science Foundation 1736028, National Institutes of Health, National Institute of General Medical Sciences R01GM134363-01, and Halıcıoğlu Data Science Institute Fellowship. This work was supported by the University of California San Diego School of Medicine. article_processing_charge: No article_type: original author: - first_name: Ileana L. full_name: Hanganu-Opatz, Ileana L. last_name: Hanganu-Opatz - first_name: Simon J. B. full_name: Butt, Simon J. B. last_name: Butt - first_name: Simon full_name: Hippenmeyer, Simon id: 37B36620-F248-11E8-B48F-1D18A9856A87 last_name: Hippenmeyer orcid: 0000-0003-2279-1061 - first_name: Natalia V. full_name: De Marco García, Natalia V. last_name: De Marco García - first_name: Jessica A. full_name: Cardin, Jessica A. last_name: Cardin - first_name: Bradley full_name: Voytek, Bradley last_name: Voytek - first_name: Alysson R. full_name: Muotri, Alysson R. last_name: Muotri citation: ama: Hanganu-Opatz IL, Butt SJB, Hippenmeyer S, et al. The logic of developing neocortical circuits in health and disease. The Journal of Neuroscience. 2021;41(5):813-822. doi:10.1523/jneurosci.1655-20.2020 apa: Hanganu-Opatz, I. L., Butt, S. J. B., Hippenmeyer, S., De Marco García, N. V., Cardin, J. A., Voytek, B., & Muotri, A. R. (2021). The logic of developing neocortical circuits in health and disease. The Journal of Neuroscience. Society for Neuroscience. https://doi.org/10.1523/jneurosci.1655-20.2020 chicago: Hanganu-Opatz, Ileana L., Simon J. B. Butt, Simon Hippenmeyer, Natalia V. De Marco García, Jessica A. Cardin, Bradley Voytek, and Alysson R. Muotri. “The Logic of Developing Neocortical Circuits in Health and Disease.” The Journal of Neuroscience. Society for Neuroscience, 2021. https://doi.org/10.1523/jneurosci.1655-20.2020. ieee: I. L. Hanganu-Opatz et al., “The logic of developing neocortical circuits in health and disease,” The Journal of Neuroscience, vol. 41, no. 5. Society for Neuroscience, pp. 813–822, 2021. ista: Hanganu-Opatz IL, Butt SJB, Hippenmeyer S, De Marco García NV, Cardin JA, Voytek B, Muotri AR. 2021. The logic of developing neocortical circuits in health and disease. The Journal of Neuroscience. 41(5), 813–822. mla: Hanganu-Opatz, Ileana L., et al. “The Logic of Developing Neocortical Circuits in Health and Disease.” The Journal of Neuroscience, vol. 41, no. 5, Society for Neuroscience, 2021, pp. 813–22, doi:10.1523/jneurosci.1655-20.2020. short: I.L. Hanganu-Opatz, S.J.B. Butt, S. Hippenmeyer, N.V. De Marco García, J.A. Cardin, B. Voytek, A.R. Muotri, The Journal of Neuroscience 41 (2021) 813–822. date_created: 2021-02-03T12:23:51Z date_published: 2021-02-03T00:00:00Z date_updated: 2023-09-05T14:03:17Z day: '03' ddc: - '570' department: - _id: SiHi doi: 10.1523/jneurosci.1655-20.2020 ec_funded: 1 external_id: isi: - '000616763400002' pmid: - '33431633' file: - access_level: open_access checksum: 578fd7ed1a0aef74bce61bea2d987b33 content_type: application/pdf creator: dernst date_created: 2022-05-27T06:59:55Z date_updated: 2022-05-27T06:59:55Z file_id: '11414' file_name: 2021_JourNeuroscience_Hanganu.pdf file_size: 1031150 relation: main_file success: 1 file_date_updated: 2022-05-27T06:59:55Z has_accepted_license: '1' intvolume: ' 41' isi: 1 issue: '5' keyword: - General Neuroscience language: - iso: eng month: '02' oa: 1 oa_version: Published Version page: 813-822 pmid: 1 project: - _id: 260018B0-B435-11E9-9278-68D0E5697425 call_identifier: H2020 grant_number: '725780' name: Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development - _id: 059F6AB4-7A3F-11EA-A408-12923DDC885E grant_number: F07805 name: Molecular Mechanisms of Neural Stem Cell Lineage Progression publication: The Journal of Neuroscience publication_identifier: eissn: - 1529-2401 issn: - 0270-6474 publication_status: published publisher: Society for Neuroscience quality_controlled: '1' scopus_import: '1' status: public title: The logic of developing neocortical circuits in health and disease type: journal_article user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1 volume: 41 year: '2021' ... --- _id: '9793' abstract: - lang: eng text: Astrocytes extensively infiltrate the neuropil to regulate critical aspects of synaptic development and function. This process is regulated by transcellular interactions between astrocytes and neurons via cell adhesion molecules. How astrocytes coordinate developmental processes among one another to parse out the synaptic neuropil and form non-overlapping territories is unknown. Here we identify a molecular mechanism regulating astrocyte-astrocyte interactions during development to coordinate astrocyte morphogenesis and gap junction coupling. We show that hepaCAM, a disease-linked, astrocyte-enriched cell adhesion molecule, regulates astrocyte competition for territory and morphological complexity in the developing mouse cortex. Furthermore, conditional deletion of Hepacam from developing astrocytes significantly impairs gap junction coupling between astrocytes and disrupts the balance between synaptic excitation and inhibition. Mutations in HEPACAM cause megalencephalic leukoencephalopathy with subcortical cysts in humans. Therefore, our findings suggest that disruption of astrocyte self-organization mechanisms could be an underlying cause of neural pathology. acknowledgement: This work was supported by the National Institutes of Health (R01 DA047258 and R01 NS102237 to C.E., F32 NS100392 to K.T.B.) and the Holland-Trice Brain Research Award (to C.E.). K.T.B. was supported by postdoctoral fellowships from the Foerster-Bernstein Family and The Hartwell Foundation. The Hippenmeyer lab was supported by the European Research Council (ERC) under the European Union’s Horizon 2020 research and innovations program (725780 LinPro) to S.H. R.E. was supported by Ministerio de Ciencia y Tecnología (RTI2018-093493-B-I00). We thank the Duke Light Microscopy Core Facility, the Duke Transgenic Mouse Facility, Dr. U. Schulte for assistance with proteomic experiments, and Dr. D. Silver for critical review of the manuscript. Cartoon elements of figure panels were created using BioRender.com. article_processing_charge: No article_type: original author: - first_name: Katherine T. full_name: Baldwin, Katherine T. last_name: Baldwin - first_name: Christabel X. full_name: Tan, Christabel X. last_name: Tan - first_name: Samuel T. full_name: Strader, Samuel T. last_name: Strader - first_name: Changyu full_name: Jiang, Changyu last_name: Jiang - first_name: Justin T. full_name: Savage, Justin T. last_name: Savage - first_name: Xabier full_name: Elorza-Vidal, Xabier last_name: Elorza-Vidal - first_name: Ximena full_name: Contreras, Ximena id: 475990FE-F248-11E8-B48F-1D18A9856A87 last_name: Contreras - first_name: Thomas full_name: Rülicke, Thomas last_name: Rülicke - first_name: Simon full_name: Hippenmeyer, Simon id: 37B36620-F248-11E8-B48F-1D18A9856A87 last_name: Hippenmeyer orcid: 0000-0003-2279-1061 - first_name: Raúl full_name: Estévez, Raúl last_name: Estévez - first_name: Ru-Rong full_name: Ji, Ru-Rong last_name: Ji - first_name: Cagla full_name: Eroglu, Cagla last_name: Eroglu citation: ama: Baldwin KT, Tan CX, Strader ST, et al. HepaCAM controls astrocyte self-organization and coupling. Neuron. 2021;109(15):2427-2442.e10. doi:10.1016/j.neuron.2021.05.025 apa: Baldwin, K. T., Tan, C. X., Strader, S. T., Jiang, C., Savage, J. T., Elorza-Vidal, X., … Eroglu, C. (2021). HepaCAM controls astrocyte self-organization and coupling. Neuron. Elsevier. https://doi.org/10.1016/j.neuron.2021.05.025 chicago: Baldwin, Katherine T., Christabel X. Tan, Samuel T. Strader, Changyu Jiang, Justin T. Savage, Xabier Elorza-Vidal, Ximena Contreras, et al. “HepaCAM Controls Astrocyte Self-Organization and Coupling.” Neuron. Elsevier, 2021. https://doi.org/10.1016/j.neuron.2021.05.025. ieee: K. T. Baldwin et al., “HepaCAM controls astrocyte self-organization and coupling,” Neuron, vol. 109, no. 15. Elsevier, p. 2427–2442.e10, 2021. ista: Baldwin KT, Tan CX, Strader ST, Jiang C, Savage JT, Elorza-Vidal X, Contreras X, Rülicke T, Hippenmeyer S, Estévez R, Ji R-R, Eroglu C. 2021. HepaCAM controls astrocyte self-organization and coupling. Neuron. 109(15), 2427–2442.e10. mla: Baldwin, Katherine T., et al. “HepaCAM Controls Astrocyte Self-Organization and Coupling.” Neuron, vol. 109, no. 15, Elsevier, 2021, p. 2427–2442.e10, doi:10.1016/j.neuron.2021.05.025. short: K.T. Baldwin, C.X. Tan, S.T. Strader, C. Jiang, J.T. Savage, X. Elorza-Vidal, X. Contreras, T. Rülicke, S. Hippenmeyer, R. Estévez, R.-R. Ji, C. Eroglu, Neuron 109 (2021) 2427–2442.e10. date_created: 2021-08-06T09:08:25Z date_published: 2021-08-04T00:00:00Z date_updated: 2023-09-27T07:46:09Z day: '04' department: - _id: SiHi doi: 10.1016/j.neuron.2021.05.025 ec_funded: 1 external_id: isi: - '000692851900010' pmid: - '34171291' intvolume: ' 109' isi: 1 issue: '15' language: - iso: eng main_file_link: - open_access: '1' url: https://doi.org/10.1016/j.neuron.2021.05.025 month: '08' oa: 1 oa_version: Published Version page: 2427-2442.e10 pmid: 1 project: - _id: 260018B0-B435-11E9-9278-68D0E5697425 call_identifier: H2020 grant_number: '725780' name: Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development publication: Neuron publication_identifier: eissn: - 1097-4199 issn: - 0896-6273 publication_status: published publisher: Elsevier quality_controlled: '1' scopus_import: '1' status: public title: HepaCAM controls astrocyte self-organization and coupling type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 109 year: '2021' ... --- _id: '10655' abstract: - lang: eng text: "Adeno-associated viruses (AAVs) are widely used to deliver genetic material in vivo to distinct cell types such as neurons or glial cells, allowing for targeted manipulation. Transduction of microglia is mostly excluded from this strategy, likely due to the cells’ heterogeneous state upon environmental changes, which makes AAV design challenging. Here, we established the retina as a model system for microglial AAV validation and optimization. First, we show that AAV2/6 transduced microglia in both synaptic layers, where layer preference corresponds to the intravitreal or subretinal delivery method. Surprisingly, we observed significantly enhanced microglial transduction during photoreceptor degeneration. Thus, we modified the AAV6 capsid to reduce heparin binding by introducing four point mutations (K531E, R576Q, K493S, and K459S), resulting in increased microglial transduction in the outer plexiform layer. Finally, to improve microglial-specific transduction, we validated a Cre-dependent transgene delivery cassette for use in combination with the Cx3cr1CreERT2 mouse line. Together, our results provide a foundation for future studies optimizing AAV-mediated microglia transduction and highlight that environmental conditions influence microglial transduction efficiency.\r\n" acknowledged_ssus: - _id: Bio - _id: LifeSc - _id: PreCl acknowledgement: This project has received funding from the European Research Council (ERC) under the European Union’s Horizon 2020 research and innovation programme (grant agreement no. 715571). The research was supported by the Scientific Service Units (SSU) of IST Austria through resources provided by the Bioimaging Facility, the Life Science Facility, and the Pre-Clinical Facility, namely Sonja Haslinger and Michael Schunn for their animal colony management and support. We would also like to thank Chakrabarty Lab for sharing the plasmids for AAV2/6 production. Finally, we would like to thank the Siegert team members for discussion about the manuscript. article_processing_charge: Yes article_type: original author: - first_name: Margaret E full_name: Maes, Margaret E id: 3838F452-F248-11E8-B48F-1D18A9856A87 last_name: Maes orcid: 0000-0001-9642-1085 - first_name: Gabriele M. full_name: Wögenstein, Gabriele M. last_name: Wögenstein - first_name: Gloria full_name: Colombo, Gloria id: 3483CF6C-F248-11E8-B48F-1D18A9856A87 last_name: Colombo orcid: 0000-0001-9434-8902 - first_name: Raquel full_name: Casado Polanco, Raquel id: 15240fc1-dbcd-11ea-9d1d-ac5a786425fd last_name: Casado Polanco orcid: 0000-0001-8293-4568 - first_name: Sandra full_name: Siegert, Sandra id: 36ACD32E-F248-11E8-B48F-1D18A9856A87 last_name: Siegert orcid: 0000-0001-8635-0877 citation: ama: Maes ME, Wögenstein GM, Colombo G, Casado Polanco R, Siegert S. Optimizing AAV2/6 microglial targeting identified enhanced efficiency in the photoreceptor degenerative environment. Molecular Therapy - Methods and Clinical Development. 2021;23:210-224. doi:10.1016/j.omtm.2021.09.006 apa: Maes, M. E., Wögenstein, G. M., Colombo, G., Casado Polanco, R., & Siegert, S. (2021). Optimizing AAV2/6 microglial targeting identified enhanced efficiency in the photoreceptor degenerative environment. Molecular Therapy - Methods and Clinical Development. Elsevier. https://doi.org/10.1016/j.omtm.2021.09.006 chicago: Maes, Margaret E, Gabriele M. Wögenstein, Gloria Colombo, Raquel Casado Polanco, and Sandra Siegert. “Optimizing AAV2/6 Microglial Targeting Identified Enhanced Efficiency in the Photoreceptor Degenerative Environment.” Molecular Therapy - Methods and Clinical Development. Elsevier, 2021. https://doi.org/10.1016/j.omtm.2021.09.006. ieee: M. E. Maes, G. M. Wögenstein, G. Colombo, R. Casado Polanco, and S. Siegert, “Optimizing AAV2/6 microglial targeting identified enhanced efficiency in the photoreceptor degenerative environment,” Molecular Therapy - Methods and Clinical Development, vol. 23. Elsevier, pp. 210–224, 2021. ista: Maes ME, Wögenstein GM, Colombo G, Casado Polanco R, Siegert S. 2021. Optimizing AAV2/6 microglial targeting identified enhanced efficiency in the photoreceptor degenerative environment. Molecular Therapy - Methods and Clinical Development. 23, 210–224. mla: Maes, Margaret E., et al. “Optimizing AAV2/6 Microglial Targeting Identified Enhanced Efficiency in the Photoreceptor Degenerative Environment.” Molecular Therapy - Methods and Clinical Development, vol. 23, Elsevier, 2021, pp. 210–24, doi:10.1016/j.omtm.2021.09.006. short: M.E. Maes, G.M. Wögenstein, G. Colombo, R. Casado Polanco, S. Siegert, Molecular Therapy - Methods and Clinical Development 23 (2021) 210–224. date_created: 2022-01-23T23:01:28Z date_published: 2021-12-10T00:00:00Z date_updated: 2023-11-16T13:12:03Z day: '10' ddc: - '570' department: - _id: SaSi - _id: SiHi doi: 10.1016/j.omtm.2021.09.006 ec_funded: 1 external_id: isi: - '000748748500019' file: - access_level: open_access checksum: 77dc540e8011c5475031bdf6ccef20a6 content_type: application/pdf creator: cchlebak date_created: 2022-01-24T07:43:09Z date_updated: 2022-01-24T07:43:09Z file_id: '10657' file_name: 2021_MolTherMethodsClinDev_Maes.pdf file_size: 4794147 relation: main_file success: 1 file_date_updated: 2022-01-24T07:43:09Z has_accepted_license: '1' intvolume: ' 23' isi: 1 language: - iso: eng month: '12' oa: 1 oa_version: Published Version page: 210-224 project: - _id: 25D4A630-B435-11E9-9278-68D0E5697425 call_identifier: H2020 grant_number: '715571' name: Microglia action towards neuronal circuit formation and function in health and disease publication: Molecular Therapy - Methods and Clinical Development publication_identifier: eissn: - 2329-0501 publication_status: published publisher: Elsevier quality_controlled: '1' scopus_import: '1' status: public title: Optimizing AAV2/6 microglial targeting identified enhanced efficiency in the photoreceptor degenerative environment 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: 23 year: '2021' ... --- _id: '10321' abstract: - lang: eng text: Mosaic analysis with double markers (MADM) technology enables the generation of genetic mosaic tissue in mice. MADM enables concomitant fluorescent cell labeling and introduction of a mutation of a gene of interest with single-cell resolution. This protocol highlights major steps for the generation of genetic mosaic tissue and the isolation and processing of respective tissues for downstream histological analysis. For complete details on the use and execution of this protocol, please refer to Contreras et al. (2021). acknowledged_ssus: - _id: Bio - _id: PreCl acknowledgement: This research was supported by the Scientific Service Units (SSU) at IST Austria through resources provided by the Bioimaging (BIF) and Preclinical Facilities (PCF). We particularly thank Mohammad Goudarzi for assistance with photography of mouse perfusion and dissection. N.A. received support from FWF Firnberg-Programm (T 1031). This work was also supported by IST Austria institutional funds; FWF SFB F78 to S.H.; and the European Research Council (ERC) under the European Union’s Horizon 2020 research and innovation programme (grant agreement no. 725780 LinPro) to S.H. article_number: '100939' article_processing_charge: Yes article_type: original author: - first_name: Nicole full_name: Amberg, Nicole id: 4CD6AAC6-F248-11E8-B48F-1D18A9856A87 last_name: Amberg orcid: 0000-0002-3183-8207 - first_name: Simon full_name: Hippenmeyer, Simon id: 37B36620-F248-11E8-B48F-1D18A9856A87 last_name: Hippenmeyer orcid: 0000-0003-2279-1061 citation: ama: Amberg N, Hippenmeyer S. Genetic mosaic dissection of candidate genes in mice using mosaic analysis with double markers. STAR Protocols. 2021;2(4). doi:10.1016/j.xpro.2021.100939 apa: Amberg, N., & Hippenmeyer, S. (2021). Genetic mosaic dissection of candidate genes in mice using mosaic analysis with double markers. STAR Protocols. Cell Press. https://doi.org/10.1016/j.xpro.2021.100939 chicago: Amberg, Nicole, and Simon Hippenmeyer. “Genetic Mosaic Dissection of Candidate Genes in Mice Using Mosaic Analysis with Double Markers.” STAR Protocols. Cell Press, 2021. https://doi.org/10.1016/j.xpro.2021.100939. ieee: N. Amberg and S. Hippenmeyer, “Genetic mosaic dissection of candidate genes in mice using mosaic analysis with double markers,” STAR Protocols, vol. 2, no. 4. Cell Press, 2021. ista: Amberg N, Hippenmeyer S. 2021. Genetic mosaic dissection of candidate genes in mice using mosaic analysis with double markers. STAR Protocols. 2(4), 100939. mla: Amberg, Nicole, and Simon Hippenmeyer. “Genetic Mosaic Dissection of Candidate Genes in Mice Using Mosaic Analysis with Double Markers.” STAR Protocols, vol. 2, no. 4, 100939, Cell Press, 2021, doi:10.1016/j.xpro.2021.100939. short: N. Amberg, S. Hippenmeyer, STAR Protocols 2 (2021). date_created: 2021-11-21T23:01:28Z date_published: 2021-11-10T00:00:00Z date_updated: 2023-11-16T13:08:03Z day: '10' ddc: - '573' department: - _id: SiHi doi: 10.1016/j.xpro.2021.100939 ec_funded: 1 file: - access_level: open_access checksum: 9e3f6d06bf583e7a8b6a9e9a60500a28 content_type: application/pdf creator: cchlebak date_created: 2021-11-22T08:23:58Z date_updated: 2021-11-22T08:23:58Z file_id: '10329' file_name: 2021_STARProtocols_Amberg.pdf file_size: 7309464 relation: main_file success: 1 file_date_updated: 2021-11-22T08:23:58Z has_accepted_license: '1' intvolume: ' 2' issue: '4' language: - iso: eng month: '11' oa: 1 oa_version: Published Version project: - _id: 260018B0-B435-11E9-9278-68D0E5697425 call_identifier: H2020 grant_number: '725780' name: Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development - _id: 268F8446-B435-11E9-9278-68D0E5697425 call_identifier: FWF grant_number: T0101031 name: Role of Eed in neural stem cell lineage progression - _id: 059F6AB4-7A3F-11EA-A408-12923DDC885E grant_number: F07805 name: Molecular Mechanisms of Neural Stem Cell Lineage Progression publication: STAR Protocols publication_identifier: eissn: - 2666-1667 publication_status: published publisher: Cell Press quality_controlled: '1' scopus_import: '1' status: public title: Genetic mosaic dissection of candidate genes in mice using mosaic analysis with double markers 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: 2 year: '2021' ... --- _id: '8544' abstract: - lang: eng text: The synaptotrophic hypothesis posits that synapse formation stabilizes dendritic branches, yet this hypothesis has not been causally tested in vivo in the mammalian brain. Presynaptic ligand cerebellin-1 (Cbln1) and postsynaptic receptor GluD2 mediate synaptogenesis between granule cells and Purkinje cells in the molecular layer of the cerebellar cortex. Here we show that sparse but not global knockout of GluD2 causes under-elaboration of Purkinje cell dendrites in the deep molecular layer and overelaboration in the superficial molecular layer. Developmental, overexpression, structure-function, and genetic epistasis analyses indicate that dendrite morphogenesis defects result from competitive synaptogenesis in a Cbln1/GluD2-dependent manner. A generative model of dendritic growth based on competitive synaptogenesis largely recapitulates GluD2 sparse and global knockout phenotypes. Our results support the synaptotrophic hypothesis at initial stages of dendrite development, suggest a second mode in which cumulative synapse formation inhibits further dendrite growth, and highlight the importance of competition in dendrite morphogenesis. acknowledgement: We thank M. Mishina for GluD2fl frozen embryos, T.C. Südhof and J.I. Morgan for Cbln1fl mice, L. Anderson for help in generating the MADM alleles, W. Joo for a previously unpublished construct, M. Yuzaki, K. Shen, J. Ding, and members of the Luo lab, including J.M. Kebschull, H. Li, J. Li, T. Li, C.M. McLaughlin, D. Pederick, J. Ren, D.C. Wang and C. Xu for discussions and critiques of the manuscript, and M. Yuzaki for supporting Y.H.T. during the final phase of this project. Y.H.T. was supported by a JSPS fellowship; S.A.S. was supported by a Stanford Graduate Fellowship and an NSF Predoctoral Fellowship; L.J. is supported by a Stanford Graduate Fellowship and an NSF Predoctoral Fellowship; M.J.W. is supported by a Burroughs Wellcome Fund CASI Award. This work was supported by an NIH grant (R01-NS050538) to L.L.; the European Research Council (ERC) under the European Union's Horizon 2020 research and innovations programme (No. 725780 LinPro) to S.H.; and Simons and James S. McDonnell Foundations and an NSF CAREER award to S.G.; L.L. is an HHMI investigator. article_processing_charge: No article_type: original author: - first_name: Yukari H. full_name: Takeo, Yukari H. last_name: Takeo - first_name: S. Andrew full_name: Shuster, S. Andrew last_name: Shuster - first_name: Linnie full_name: Jiang, Linnie last_name: Jiang - first_name: Miley full_name: Hu, Miley last_name: Hu - first_name: David J. full_name: Luginbuhl, David J. last_name: Luginbuhl - first_name: Thomas full_name: Rülicke, Thomas last_name: Rülicke - first_name: Ximena full_name: Contreras, Ximena id: 475990FE-F248-11E8-B48F-1D18A9856A87 last_name: Contreras - first_name: Simon full_name: Hippenmeyer, Simon id: 37B36620-F248-11E8-B48F-1D18A9856A87 last_name: Hippenmeyer orcid: 0000-0003-2279-1061 - first_name: Mark J. full_name: Wagner, Mark J. last_name: Wagner - first_name: Surya full_name: Ganguli, Surya last_name: Ganguli - first_name: Liqun full_name: Luo, Liqun last_name: Luo citation: ama: Takeo YH, Shuster SA, Jiang L, et al. GluD2- and Cbln1-mediated competitive synaptogenesis shapes the dendritic arbors of cerebellar Purkinje cells. Neuron. 2021;109(4):P629-644.E8. doi:10.1016/j.neuron.2020.11.028 apa: Takeo, Y. H., Shuster, S. A., Jiang, L., Hu, M., Luginbuhl, D. J., Rülicke, T., … Luo, L. (2021). GluD2- and Cbln1-mediated competitive synaptogenesis shapes the dendritic arbors of cerebellar Purkinje cells. Neuron. Elsevier. https://doi.org/10.1016/j.neuron.2020.11.028 chicago: Takeo, Yukari H., S. Andrew Shuster, Linnie Jiang, Miley Hu, David J. Luginbuhl, Thomas Rülicke, Ximena Contreras, et al. “GluD2- and Cbln1-Mediated Competitive Synaptogenesis Shapes the Dendritic Arbors of Cerebellar Purkinje Cells.” Neuron. Elsevier, 2021. https://doi.org/10.1016/j.neuron.2020.11.028. ieee: Y. H. Takeo et al., “GluD2- and Cbln1-mediated competitive synaptogenesis shapes the dendritic arbors of cerebellar Purkinje cells,” Neuron, vol. 109, no. 4. Elsevier, p. P629–644.E8, 2021. ista: Takeo YH, Shuster SA, Jiang L, Hu M, Luginbuhl DJ, Rülicke T, Contreras X, Hippenmeyer S, Wagner MJ, Ganguli S, Luo L. 2021. GluD2- and Cbln1-mediated competitive synaptogenesis shapes the dendritic arbors of cerebellar Purkinje cells. Neuron. 109(4), P629–644.E8. mla: Takeo, Yukari H., et al. “GluD2- and Cbln1-Mediated Competitive Synaptogenesis Shapes the Dendritic Arbors of Cerebellar Purkinje Cells.” Neuron, vol. 109, no. 4, Elsevier, 2021, p. P629–644.E8, doi:10.1016/j.neuron.2020.11.028. short: Y.H. Takeo, S.A. Shuster, L. Jiang, M. Hu, D.J. Luginbuhl, T. Rülicke, X. Contreras, S. Hippenmeyer, M.J. Wagner, S. Ganguli, L. Luo, Neuron 109 (2021) P629–644.E8. date_created: 2020-09-21T11:59:47Z date_published: 2021-02-17T00:00:00Z date_updated: 2024-03-06T12:12:48Z day: '17' department: - _id: SiHi doi: 10.1016/j.neuron.2020.11.028 ec_funded: 1 intvolume: ' 109' issue: '4' language: - iso: eng main_file_link: - open_access: '1' url: https://doi.org/10.1101/2020.06.14.151258 month: '02' oa: 1 oa_version: Preprint page: P629-644.E8 project: - _id: 260018B0-B435-11E9-9278-68D0E5697425 call_identifier: H2020 grant_number: '725780' name: Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development publication: Neuron publication_identifier: eissn: - 1097-4199 publication_status: published publisher: Elsevier quality_controlled: '1' scopus_import: '1' status: public title: GluD2- and Cbln1-mediated competitive synaptogenesis shapes the dendritic arbors of cerebellar Purkinje cells type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 109 year: '2021' ... --- _id: '9962' abstract: - lang: eng text: The brain is one of the largest and most complex organs and it is composed of billions of neurons that communicate together enabling e.g. consciousness. The cerebral cortex is the largest site of neural integration in the central nervous system. Concerted radial migration of newly born cortical projection neurons, from their birthplace to their final position, is a key step in the assembly of the cerebral cortex. The cellular and molecular mechanisms regulating radial neuronal migration in vivo are however still unclear. Recent evidence suggests that distinct signaling cues act cell-autonomously but differentially at certain steps during the overall migration process. Moreover, functional analysis of genetic mosaics (mutant neurons present in wild-type/heterozygote environment) using the MADM (Mosaic Analysis with Double Markers) analyses in comparison to global knockout also indicate a significant degree of non-cell-autonomous and/or community effects in the control of cortical neuron migration. The interactions of cell-intrinsic (cell-autonomous) and cell-extrinsic (non-cell-autonomous) components are largely unknown. In part of this thesis work we established a MADM-based experimental strategy for the quantitative analysis of cell-autonomous gene function versus non-cell-autonomous and/or community effects. The direct comparison of mutant neurons from the genetic mosaic (cell-autonomous) to mutant neurons in the conditional and/or global knockout (cell-autonomous + non-cell-autonomous) allows to quantitatively analyze non-cell-autonomous effects. Such analysis enable the high-resolution analysis of projection neuron migration dynamics in distinct environments with concomitant isolation of genomic and proteomic profiles. Using these experimental paradigms and in combination with computational modeling we show and characterize the nature of non-cell-autonomous effects to coordinate radial neuron migration. Furthermore, this thesis discusses recent developments in neurodevelopment with focus on neuronal polarization and non-cell-autonomous mechanisms in neuronal migration. alternative_title: - ISTA Thesis article_processing_charge: No author: - first_name: Andi H full_name: Hansen, Andi H id: 38853E16-F248-11E8-B48F-1D18A9856A87 last_name: Hansen citation: ama: Hansen AH. Cell-autonomous gene function and non-cell-autonomous effects in radial projection neuron migration. 2021. doi:10.15479/at:ista:9962 apa: Hansen, A. H. (2021). Cell-autonomous gene function and non-cell-autonomous effects in radial projection neuron migration. Institute of Science and Technology Austria. https://doi.org/10.15479/at:ista:9962 chicago: Hansen, Andi H. “Cell-Autonomous Gene Function and Non-Cell-Autonomous Effects in Radial Projection Neuron Migration.” Institute of Science and Technology Austria, 2021. https://doi.org/10.15479/at:ista:9962. ieee: A. H. Hansen, “Cell-autonomous gene function and non-cell-autonomous effects in radial projection neuron migration,” Institute of Science and Technology Austria, 2021. ista: Hansen AH. 2021. Cell-autonomous gene function and non-cell-autonomous effects in radial projection neuron migration. Institute of Science and Technology Austria. mla: Hansen, Andi H. Cell-Autonomous Gene Function and Non-Cell-Autonomous Effects in Radial Projection Neuron Migration. Institute of Science and Technology Austria, 2021, doi:10.15479/at:ista:9962. short: A.H. Hansen, Cell-Autonomous Gene Function and Non-Cell-Autonomous Effects in Radial Projection Neuron Migration, Institute of Science and Technology Austria, 2021. date_created: 2021-08-29T12:36:50Z date_published: 2021-09-02T00:00:00Z date_updated: 2023-09-22T09:58:30Z day: '02' ddc: - '570' degree_awarded: PhD department: - _id: GradSch - _id: SiHi doi: 10.15479/at:ista:9962 file: - access_level: closed checksum: 66b56f5b988b233dc66a4f4b4fb2cdfe content_type: application/vnd.openxmlformats-officedocument.wordprocessingml.document creator: ahansen date_created: 2021-08-30T09:17:39Z date_updated: 2022-09-03T22:30:04Z embargo_to: open_access file_id: '9971' file_name: Thesis_Hansen.docx file_size: 10629190 relation: source_file - access_level: open_access checksum: 204fa40321a1c6289b68c473634c4bf3 content_type: application/pdf creator: ahansen date_created: 2021-08-30T09:29:44Z date_updated: 2022-09-03T22:30:04Z embargo: 2022-09-02 file_id: '9972' file_name: Thesis_Hansen_PDFA-1a.pdf file_size: 13457469 relation: main_file file_date_updated: 2022-09-03T22:30:04Z has_accepted_license: '1' keyword: - Neuronal migration - Non-cell-autonomous - Cell-autonomous - Neurodevelopmental disease language: - iso: eng month: '09' oa: 1 oa_version: Published Version page: '182' project: - _id: 2625A13E-B435-11E9-9278-68D0E5697425 grant_number: '24812' name: Molecular Mechanisms of Radial Neuronal Migration publication_identifier: issn: - 2663-337X publication_status: published publisher: Institute of Science and Technology Austria related_material: record: - id: '8569' relation: part_of_dissertation status: public - id: '960' relation: part_of_dissertation status: public status: public supervisor: - first_name: Simon full_name: Hippenmeyer, Simon id: 37B36620-F248-11E8-B48F-1D18A9856A87 last_name: Hippenmeyer orcid: 0000-0003-2279-1061 title: Cell-autonomous gene function and non-cell-autonomous effects in radial projection neuron migration 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: dissertation user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1 year: '2021' ... --- _id: '7814' abstract: - lang: eng text: 'Scientific research is to date largely restricted to wealthy laboratories in developed nations due to the necessity of complex and expensive equipment. This inequality limits the capacity of science to be used as a diplomatic channel. Maker movements use open-source technologies including additive manufacturing (3D printing) and laser cutting, together with low-cost computers for developing novel products. This movement is setting the groundwork for a revolution, allowing scientific equipment to be sourced at a fraction of the cost and has the potential to increase the availability of equipment for scientists around the world. Science education is increasingly recognized as another channel for science diplomacy. In this perspective, we introduce the idea that the Maker movement and open-source technologies have the potential to revolutionize science, technology, engineering and mathematics (STEM) education worldwide. We present an open-source STEM didactic tool called SCOPES (Sparking Curiosity through Open-source Platforms in Education and Science). SCOPES is self-contained, independent of local resources, and cost-effective. SCOPES can be adapted to communicate complex subjects from genetics to neurobiology, perform real-world biological experiments and explore digitized scientific samples. We envision such platforms will enhance science diplomacy by providing a means for scientists to share their findings with classrooms and for educators to incorporate didactic concepts into STEM lessons. By providing students the opportunity to design, perform, and share scientific experiments, students also experience firsthand the benefits of a multinational scientific community. We provide instructions on how to build and use SCOPES on our webpage: http://scopeseducation.org.' acknowledged_ssus: - _id: Bio - _id: LifeSc - _id: PreCl - _id: EM-Fac article_number: '48' article_processing_charge: No article_type: original author: - first_name: Robert J full_name: Beattie, Robert J id: 2E26DF60-F248-11E8-B48F-1D18A9856A87 last_name: Beattie orcid: 0000-0002-8483-8753 - first_name: Simon full_name: Hippenmeyer, Simon id: 37B36620-F248-11E8-B48F-1D18A9856A87 last_name: Hippenmeyer orcid: 0000-0003-2279-1061 - first_name: Florian full_name: Pauler, Florian id: 48EA0138-F248-11E8-B48F-1D18A9856A87 last_name: Pauler citation: ama: 'Beattie RJ, Hippenmeyer S, Pauler F. SCOPES: Sparking curiosity through Open-Source platforms in education and science. Frontiers in Education. 2020;5. doi:10.3389/feduc.2020.00048' apa: 'Beattie, R. J., Hippenmeyer, S., & Pauler, F. (2020). SCOPES: Sparking curiosity through Open-Source platforms in education and science. Frontiers in Education. Frontiers Media. https://doi.org/10.3389/feduc.2020.00048' chicago: 'Beattie, Robert J, Simon Hippenmeyer, and Florian Pauler. “SCOPES: Sparking Curiosity through Open-Source Platforms in Education and Science.” Frontiers in Education. Frontiers Media, 2020. https://doi.org/10.3389/feduc.2020.00048.' ieee: 'R. J. Beattie, S. Hippenmeyer, and F. Pauler, “SCOPES: Sparking curiosity through Open-Source platforms in education and science,” Frontiers in Education, vol. 5. Frontiers Media, 2020.' ista: 'Beattie RJ, Hippenmeyer S, Pauler F. 2020. SCOPES: Sparking curiosity through Open-Source platforms in education and science. Frontiers in Education. 5, 48.' mla: 'Beattie, Robert J., et al. “SCOPES: Sparking Curiosity through Open-Source Platforms in Education and Science.” Frontiers in Education, vol. 5, 48, Frontiers Media, 2020, doi:10.3389/feduc.2020.00048.' short: R.J. Beattie, S. Hippenmeyer, F. Pauler, Frontiers in Education 5 (2020). date_created: 2020-05-11T08:18:48Z date_published: 2020-05-08T00:00:00Z date_updated: 2021-01-12T08:15:42Z day: '08' ddc: - '570' department: - _id: SiHi doi: 10.3389/feduc.2020.00048 ec_funded: 1 file: - access_level: open_access checksum: a24ec24e38d843341ae620ec76c53688 content_type: application/pdf creator: dernst date_created: 2020-05-11T11:34:08Z date_updated: 2020-07-14T12:48:03Z file_id: '7818' file_name: 2020_FrontiersEduc_Beattie.pdf file_size: 1402146 relation: main_file file_date_updated: 2020-07-14T12:48:03Z has_accepted_license: '1' intvolume: ' 5' language: - iso: eng month: '05' oa: 1 oa_version: Published Version project: - _id: 264E56E2-B435-11E9-9278-68D0E5697425 call_identifier: FWF grant_number: M02416 name: Molecular Mechanisms Regulating Gliogenesis in the Cerebral Cortex - _id: 260018B0-B435-11E9-9278-68D0E5697425 call_identifier: H2020 grant_number: '725780' name: Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development publication: Frontiers in Education publication_identifier: issn: - 2504-284X publication_status: published publisher: Frontiers Media quality_controlled: '1' status: public title: 'SCOPES: Sparking curiosity through Open-Source platforms in education and science' 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: 5 year: '2020' ... --- _id: '8616' abstract: - lang: eng text: The brain vasculature supplies neurons with glucose and oxygen, but little is known about how vascular plasticity contributes to brain function. Using longitudinal in vivo imaging, we reported that a substantial proportion of blood vessels in the adult brain sporadically occluded and regressed. Their regression proceeded through sequential stages of blood-flow occlusion, endothelial cell collapse, relocation or loss of pericytes, and retraction of glial endfeet. Regressing vessels were found to be widespread in mouse, monkey and human brains. Both brief occlusions of the middle cerebral artery and lipopolysaccharide-mediated inflammation induced an increase of vessel regression. Blockage of leukocyte adhesion to endothelial cells alleviated LPS-induced vessel regression. We further revealed that blood vessel regression caused a reduction of neuronal activity due to a dysfunction in mitochondrial metabolism and glutamate production. Our results elucidate the mechanism of vessel regression and its role in neuronal function in the adult brain. acknowledgement: 'The project was initiated in the Jan lab at UCSF. We thank Lily Jan and Yuh-Nung Jan’s generous support. We thank Liqun Luo’s lab for providing MADM-7 mice and Rolf A Brekken for VEGF-antibodies. Drs. Yuanquan Song (UPenn), Zhaozhu Hu (JHU), Ji Hu (ShanghaiTech), Yang Xiang (U. Mass), Hao Wang (Zhejiang U.) and Ruikang Wang (U. Washington) for critical input, colleagues at Children’s Research Institute, Departments of Neuroscience, Neurology and Neurotherapeutics, Pediatrics from UT Southwestern, and colleagues from the Jan lab for discussion. Dr. Bridget Samuels, Sean Morrison (UT Southwestern), and Nannan Lu (Zhejiang U.) for critical reading. We acknowledge the assistance of the CIBR Imaging core. We also thank UT Southwestern Live Cell Imaging Facility, a Shared Resource of the Harold C. Simmons Cancer Center, supported in part by an NCI Cancer Center Support Grant, P30 CA142543K. This work is supported by CIBR funds and the American Heart Association AWRP Summer 2016 Innovative Research Grant (17IRG33410377) to W-P.G.; National Natural Science Foundation of China (No.81370031) to Z.Z.;National Key Research and Development Program of China (2016YFE0125400)to F.H.;National Natural Science Foundations of China (No. 81473202) to Y.L.; National Natural Science Foundation of China (No.31600839) and Shenzhen Science and Technology Research Program (JCYJ20170818163320865) to B.P.; National Natural Science Foundation of China (No. 31800864) and Westlake University start-up funds to J-M. J. NIH R01NS088627 to W.L.J.; NIH: R01 AG020670 and RF1AG054111 to H.Z.; R01 NS088555 to A.M.S., and European Research Council No.725780 to S.H.;W-P.G. was a recipient of Bugher-American Heart Association Dan Adams Thinking Outside the Box Award.' article_processing_charge: No author: - first_name: Xiaofei full_name: Gao, Xiaofei last_name: Gao - first_name: Jun-Liszt full_name: Li, Jun-Liszt last_name: Li - first_name: Xingjun full_name: Chen, Xingjun last_name: Chen - first_name: Bo full_name: Ci, Bo last_name: Ci - first_name: Fei full_name: Chen, Fei last_name: Chen - first_name: Nannan full_name: Lu, Nannan last_name: Lu - first_name: Bo full_name: Shen, Bo last_name: Shen - first_name: Lijun full_name: Zheng, Lijun last_name: Zheng - first_name: Jie-Min full_name: Jia, Jie-Min last_name: Jia - first_name: Yating full_name: Yi, Yating last_name: Yi - first_name: Shiwen full_name: Zhang, Shiwen last_name: Zhang - first_name: Ying-Chao full_name: Shi, Ying-Chao last_name: Shi - first_name: Kaibin full_name: Shi, Kaibin last_name: Shi - first_name: Nicholas E full_name: Propson, Nicholas E last_name: Propson - first_name: Yubin full_name: Huang, Yubin last_name: Huang - first_name: Katherine full_name: Poinsatte, Katherine last_name: Poinsatte - first_name: Zhaohuan full_name: Zhang, Zhaohuan last_name: Zhang - first_name: Yuanlei full_name: Yue, Yuanlei last_name: Yue - first_name: Dale B full_name: Bosco, Dale B last_name: Bosco - first_name: Ying-mei full_name: Lu, Ying-mei last_name: Lu - first_name: Shi-bing full_name: Yang, Shi-bing last_name: Yang - first_name: Ralf H. full_name: Adams, Ralf H. last_name: Adams - first_name: Volkhard full_name: Lindner, Volkhard last_name: Lindner - first_name: Fen full_name: Huang, Fen last_name: Huang - first_name: Long-Jun full_name: Wu, Long-Jun last_name: Wu - first_name: Hui full_name: Zheng, Hui last_name: Zheng - first_name: Feng full_name: Han, Feng last_name: Han - first_name: Simon full_name: Hippenmeyer, Simon id: 37B36620-F248-11E8-B48F-1D18A9856A87 last_name: Hippenmeyer orcid: 0000-0003-2279-1061 - first_name: Ann M. full_name: Stowe, Ann M. last_name: Stowe - first_name: Bo full_name: Peng, Bo last_name: Peng - first_name: Marta full_name: Margeta, Marta last_name: Margeta - first_name: Xiaoqun full_name: Wang, Xiaoqun last_name: Wang - first_name: Qiang full_name: Liu, Qiang last_name: Liu - first_name: Jakob full_name: Körbelin, Jakob last_name: Körbelin - first_name: Martin full_name: Trepel, Martin last_name: Trepel - first_name: Hui full_name: Lu, Hui last_name: Lu - first_name: Bo O. full_name: Zhou, Bo O. last_name: Zhou - first_name: Hu full_name: Zhao, Hu last_name: Zhao - first_name: Wenzhi full_name: Su, Wenzhi last_name: Su - first_name: Robert M. full_name: Bachoo, Robert M. last_name: Bachoo - first_name: Woo-ping full_name: Ge, Woo-ping last_name: Ge citation: ama: Gao X, Li J-L, Chen X, et al. Reduction of neuronal activity mediated by blood-vessel regression in the brain. bioRxiv. doi:10.1101/2020.09.15.262782 apa: Gao, X., Li, J.-L., Chen, X., Ci, B., Chen, F., Lu, N., … Ge, W. (n.d.). Reduction of neuronal activity mediated by blood-vessel regression in the brain. bioRxiv. Cold Spring Harbor Laboratory. https://doi.org/10.1101/2020.09.15.262782 chicago: Gao, Xiaofei, Jun-Liszt Li, Xingjun Chen, Bo Ci, Fei Chen, Nannan Lu, Bo Shen, et al. “Reduction of Neuronal Activity Mediated by Blood-Vessel Regression in the Brain.” BioRxiv. Cold Spring Harbor Laboratory, n.d. https://doi.org/10.1101/2020.09.15.262782. ieee: X. Gao et al., “Reduction of neuronal activity mediated by blood-vessel regression in the brain,” bioRxiv. Cold Spring Harbor Laboratory. ista: Gao X, Li J-L, Chen X, Ci B, Chen F, Lu N, Shen B, Zheng L, Jia J-M, Yi Y, Zhang S, Shi Y-C, Shi K, Propson NE, Huang Y, Poinsatte K, Zhang Z, Yue Y, Bosco DB, Lu Y, Yang S, Adams RH, Lindner V, Huang F, Wu L-J, Zheng H, Han F, Hippenmeyer S, Stowe AM, Peng B, Margeta M, Wang X, Liu Q, Körbelin J, Trepel M, Lu H, Zhou BO, Zhao H, Su W, Bachoo RM, Ge W. Reduction of neuronal activity mediated by blood-vessel regression in the brain. bioRxiv, 10.1101/2020.09.15.262782. mla: Gao, Xiaofei, et al. “Reduction of Neuronal Activity Mediated by Blood-Vessel Regression in the Brain.” BioRxiv, Cold Spring Harbor Laboratory, doi:10.1101/2020.09.15.262782. short: X. Gao, J.-L. Li, X. Chen, B. Ci, F. Chen, N. Lu, B. Shen, L. Zheng, J.-M. Jia, Y. Yi, S. Zhang, Y.-C. Shi, K. Shi, N.E. Propson, Y. Huang, K. Poinsatte, Z. Zhang, Y. Yue, D.B. Bosco, Y. Lu, S. Yang, R.H. Adams, V. Lindner, F. Huang, L.-J. Wu, H. Zheng, F. Han, S. Hippenmeyer, A.M. Stowe, B. Peng, M. Margeta, X. Wang, Q. Liu, J. Körbelin, M. Trepel, H. Lu, B.O. Zhou, H. Zhao, W. Su, R.M. Bachoo, W. Ge, BioRxiv (n.d.). date_created: 2020-10-06T08:58:59Z date_published: 2020-09-15T00:00:00Z date_updated: 2021-01-12T08:20:19Z day: '15' department: - _id: SiHi doi: 10.1101/2020.09.15.262782 ec_funded: 1 language: - iso: eng main_file_link: - open_access: '1' url: https://doi.org/10.1101/2020.09.15.262782 month: '09' oa: 1 oa_version: Preprint project: - _id: 260018B0-B435-11E9-9278-68D0E5697425 call_identifier: H2020 grant_number: '725780' name: Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development publication: bioRxiv publication_status: submitted publisher: Cold Spring Harbor Laboratory status: public title: Reduction of neuronal activity mediated by blood-vessel regression in the brain type: preprint user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 year: '2020' ... --- _id: '8978' abstract: - lang: eng text: "Mosaic analysis with double markers (MADM) technology enables concomitant fluorescent cell labeling and induction of uniparental chromosome disomy (UPD) with single-cell resolution. In UPD, imprinted genes are either overexpressed 2-fold or are not expressed. Here, the MADM platform is utilized to probe imprinting phenotypes at the transcriptional level. This protocol highlights major steps for the generation and isolation of projection neurons and astrocytes with MADM-induced UPD from mouse cerebral cortex for downstream single-cell and low-input sample RNA-sequencing experiments.\r\n\r\nFor complete details on the use and execution of this protocol, please refer to Laukoter et al. (2020b)." acknowledged_ssus: - _id: Bio - _id: PreCl acknowledgement: This research was supported by the Scientific Service Units (SSU) at IST Austria through resources provided by the Bioimaging (BIF) and Preclinical Facilities (PCF). N.A received support from the FWF Firnberg-Programm (T 1031). This work was also supported by IST Austria institutional funds; FWF SFB F78 to S.H.; NÖ Forschung und Bildung n[f+b] life science call grant (C13-002) to S.H.; the People Programme (Marie Curie Actions) of the European Union’s Seventh Framework Programme (FP7/2007-2013) under REA grant agreement no. 618444 to S.H.; and the European Research Council (ERC) under the European Union’s Horizon 2020 research and innovation programme (grant agreement no. 725780 LinPro) to S.H. article_number: '100215' article_processing_charge: No article_type: original author: - first_name: Susanne full_name: Laukoter, Susanne id: 2D6B7A9A-F248-11E8-B48F-1D18A9856A87 last_name: Laukoter - first_name: Nicole full_name: Amberg, Nicole id: 4CD6AAC6-F248-11E8-B48F-1D18A9856A87 last_name: Amberg orcid: 0000-0002-3183-8207 - first_name: Florian full_name: Pauler, Florian id: 48EA0138-F248-11E8-B48F-1D18A9856A87 last_name: Pauler - first_name: Simon full_name: Hippenmeyer, Simon id: 37B36620-F248-11E8-B48F-1D18A9856A87 last_name: Hippenmeyer orcid: 0000-0003-2279-1061 citation: ama: Laukoter S, Amberg N, Pauler F, Hippenmeyer S. Generation and isolation of single cells from mouse brain with mosaic analysis with double markers-induced uniparental chromosome disomy. STAR Protocols. 2020;1(3). doi:10.1016/j.xpro.2020.100215 apa: Laukoter, S., Amberg, N., Pauler, F., & Hippenmeyer, S. (2020). Generation and isolation of single cells from mouse brain with mosaic analysis with double markers-induced uniparental chromosome disomy. STAR Protocols. Elsevier. https://doi.org/10.1016/j.xpro.2020.100215 chicago: Laukoter, Susanne, Nicole Amberg, Florian Pauler, and Simon Hippenmeyer. “Generation and Isolation of Single Cells from Mouse Brain with Mosaic Analysis with Double Markers-Induced Uniparental Chromosome Disomy.” STAR Protocols. Elsevier, 2020. https://doi.org/10.1016/j.xpro.2020.100215. ieee: S. Laukoter, N. Amberg, F. Pauler, and S. Hippenmeyer, “Generation and isolation of single cells from mouse brain with mosaic analysis with double markers-induced uniparental chromosome disomy,” STAR Protocols, vol. 1, no. 3. Elsevier, 2020. ista: Laukoter S, Amberg N, Pauler F, Hippenmeyer S. 2020. Generation and isolation of single cells from mouse brain with mosaic analysis with double markers-induced uniparental chromosome disomy. STAR Protocols. 1(3), 100215. mla: Laukoter, Susanne, et al. “Generation and Isolation of Single Cells from Mouse Brain with Mosaic Analysis with Double Markers-Induced Uniparental Chromosome Disomy.” STAR Protocols, vol. 1, no. 3, 100215, Elsevier, 2020, doi:10.1016/j.xpro.2020.100215. short: S. Laukoter, N. Amberg, F. Pauler, S. Hippenmeyer, STAR Protocols 1 (2020). date_created: 2020-12-30T10:17:07Z date_published: 2020-12-18T00:00:00Z date_updated: 2021-01-12T08:21:36Z day: '18' ddc: - '570' department: - _id: SiHi doi: 10.1016/j.xpro.2020.100215 ec_funded: 1 external_id: pmid: - '33377108' file: - access_level: open_access checksum: f1e9a433e9cb0f41f7b6df6b76db1f6e content_type: application/pdf creator: dernst date_created: 2021-01-07T15:57:27Z date_updated: 2021-01-07T15:57:27Z file_id: '8996' file_name: 2020_STARProtocols_Laukoter.pdf file_size: 4031449 relation: main_file success: 1 file_date_updated: 2021-01-07T15:57:27Z has_accepted_license: '1' intvolume: ' 1' issue: '3' language: - iso: eng month: '12' oa: 1 oa_version: Published Version pmid: 1 project: - _id: 268F8446-B435-11E9-9278-68D0E5697425 call_identifier: FWF grant_number: T0101031 name: Role of Eed in neural stem cell lineage progression - _id: 059F6AB4-7A3F-11EA-A408-12923DDC885E grant_number: F07805 name: Molecular Mechanisms of Neural Stem Cell Lineage Progression - _id: 25D92700-B435-11E9-9278-68D0E5697425 grant_number: LS13-002 name: Mapping Cell-Type Specificity of the Genomic Imprintome in the Brain - _id: 25D61E48-B435-11E9-9278-68D0E5697425 call_identifier: FP7 grant_number: '618444' name: Molecular Mechanisms of Cerebral Cortex Development - _id: 260018B0-B435-11E9-9278-68D0E5697425 call_identifier: H2020 grant_number: '725780' name: Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development publication: STAR Protocols publication_identifier: issn: - 2666-1667 publication_status: published publisher: Elsevier quality_controlled: '1' status: public title: Generation and isolation of single cells from mouse brain with mosaic analysis with double markers-induced uniparental chromosome disomy 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: 1 year: '2020' ... --- _id: '7253' abstract: - lang: eng text: The cyclin-dependent kinase inhibitor p57KIP2 is encoded by the imprinted Cdkn1c locus, exhibits maternal expression, and is essential for cerebral cortex development. How Cdkn1c regulates corticogenesis is however not clear. To this end we employ Mosaic Analysis with Double Markers (MADM) technology to genetically dissect Cdkn1c gene function in corticogenesis at single cell resolution. We find that the previously described growth-inhibitory Cdkn1c function is a non-cell-autonomous one, acting on the whole organism. In contrast we reveal a growth-promoting cell-autonomous Cdkn1c function which at the mechanistic level mediates radial glial progenitor cell and nascent projection neuron survival. Strikingly, the growth-promoting function of Cdkn1c is highly dosage sensitive but not subject to genomic imprinting. Collectively, our results suggest that the Cdkn1c locus regulates cortical development through distinct cell-autonomous and non-cell-autonomous mechanisms. More generally, our study highlights the importance to probe the relative contributions of cell intrinsic gene function and tissue-wide mechanisms to the overall phenotype. acknowledged_ssus: - _id: PreCl article_number: '195' article_processing_charge: No article_type: original author: - first_name: Susanne full_name: Laukoter, Susanne id: 2D6B7A9A-F248-11E8-B48F-1D18A9856A87 last_name: Laukoter orcid: 0000-0002-7903-3010 - first_name: Robert J full_name: Beattie, Robert J id: 2E26DF60-F248-11E8-B48F-1D18A9856A87 last_name: Beattie orcid: 0000-0002-8483-8753 - first_name: Florian full_name: Pauler, Florian id: 48EA0138-F248-11E8-B48F-1D18A9856A87 last_name: Pauler orcid: 0000-0002-7462-0048 - first_name: Nicole full_name: Amberg, Nicole id: 4CD6AAC6-F248-11E8-B48F-1D18A9856A87 last_name: Amberg orcid: 0000-0002-3183-8207 - first_name: Keiichi I. full_name: Nakayama, Keiichi I. last_name: Nakayama - first_name: Simon full_name: Hippenmeyer, Simon id: 37B36620-F248-11E8-B48F-1D18A9856A87 last_name: Hippenmeyer orcid: 0000-0003-2279-1061 citation: ama: Laukoter S, Beattie RJ, Pauler F, Amberg N, Nakayama KI, Hippenmeyer S. Imprinted Cdkn1c genomic locus cell-autonomously promotes cell survival in cerebral cortex development. Nature Communications. 2020;11. doi:10.1038/s41467-019-14077-2 apa: Laukoter, S., Beattie, R. J., Pauler, F., Amberg, N., Nakayama, K. I., & Hippenmeyer, S. (2020). Imprinted Cdkn1c genomic locus cell-autonomously promotes cell survival in cerebral cortex development. Nature Communications. Springer Nature. https://doi.org/10.1038/s41467-019-14077-2 chicago: Laukoter, Susanne, Robert J Beattie, Florian Pauler, Nicole Amberg, Keiichi I. Nakayama, and Simon Hippenmeyer. “Imprinted Cdkn1c Genomic Locus Cell-Autonomously Promotes Cell Survival in Cerebral Cortex Development.” Nature Communications. Springer Nature, 2020. https://doi.org/10.1038/s41467-019-14077-2. ieee: S. Laukoter, R. J. Beattie, F. Pauler, N. Amberg, K. I. Nakayama, and S. Hippenmeyer, “Imprinted Cdkn1c genomic locus cell-autonomously promotes cell survival in cerebral cortex development,” Nature Communications, vol. 11. Springer Nature, 2020. ista: Laukoter S, Beattie RJ, Pauler F, Amberg N, Nakayama KI, Hippenmeyer S. 2020. Imprinted Cdkn1c genomic locus cell-autonomously promotes cell survival in cerebral cortex development. Nature Communications. 11, 195. mla: Laukoter, Susanne, et al. “Imprinted Cdkn1c Genomic Locus Cell-Autonomously Promotes Cell Survival in Cerebral Cortex Development.” Nature Communications, vol. 11, 195, Springer Nature, 2020, doi:10.1038/s41467-019-14077-2. short: S. Laukoter, R.J. Beattie, F. Pauler, N. Amberg, K.I. Nakayama, S. Hippenmeyer, Nature Communications 11 (2020). date_created: 2020-01-11T10:42:48Z date_published: 2020-01-10T00:00:00Z date_updated: 2023-08-17T14:23:41Z day: '10' ddc: - '570' department: - _id: SiHi doi: 10.1038/s41467-019-14077-2 ec_funded: 1 external_id: isi: - '000551459000005' file: - access_level: open_access checksum: ebf1ed522f4e0be8d94c939c1806a709 content_type: application/pdf creator: dernst date_created: 2020-01-13T07:42:31Z date_updated: 2020-07-14T12:47:54Z file_id: '7261' file_name: 2020_NatureComm_Laukoter.pdf file_size: 8063333 relation: main_file file_date_updated: 2020-07-14T12:47:54Z has_accepted_license: '1' intvolume: ' 11' isi: 1 language: - iso: eng month: '01' oa: 1 oa_version: Published Version project: - _id: 268F8446-B435-11E9-9278-68D0E5697425 call_identifier: FWF grant_number: T0101031 name: Role of Eed in neural stem cell lineage progression - _id: 264E56E2-B435-11E9-9278-68D0E5697425 call_identifier: FWF grant_number: M02416 name: Molecular Mechanisms Regulating Gliogenesis in the Cerebral Cortex - _id: 260018B0-B435-11E9-9278-68D0E5697425 call_identifier: H2020 grant_number: '725780' name: Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development - _id: 25D92700-B435-11E9-9278-68D0E5697425 grant_number: LS13-002 name: Mapping Cell-Type Specificity of the Genomic Imprintome in the Brain publication: Nature Communications publication_identifier: issn: - 2041-1723 publication_status: published publisher: Springer Nature quality_controlled: '1' related_material: link: - description: News on IST Homepage relation: press_release url: https://ist.ac.at/en/news/new-function-for-potential-tumour-suppressor-in-brain-development/ scopus_import: '1' status: public title: Imprinted Cdkn1c genomic locus cell-autonomously promotes cell survival in cerebral cortex development 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: 4359f0d1-fa6c-11eb-b949-802e58b17ae8 volume: 11 year: '2020' ... --- _id: '7593' abstract: - lang: eng text: Heterozygous loss of human PAFAH1B1 (coding for LIS1) results in the disruption of neurogenesis and neuronal migration via dysregulation of microtubule (MT) stability and dynein motor function/localization that alters mitotic spindle orientation, chromosomal segregation, and nuclear migration. Recently, human induced pluripotent stem cell (iPSC) models revealed an important role for LIS1 in controlling the length of terminal cell divisions of outer radial glial (oRG) progenitors, suggesting cellular functions of LIS1 in regulating neural progenitor cell (NPC) daughter cell separation. Here we examined the late mitotic stages NPCs in vivo and mouse embryonic fibroblasts (MEFs) in vitro from Pafah1b1-deficient mutants. Pafah1b1-deficient neocortical NPCs and MEFs similarly exhibited cleavage plane displacement with mislocalization of furrow-associated markers, associated with actomyosin dysfunction and cell membrane hyper-contractility. Thus, it suggests LIS1 acts as a key molecular link connecting MTs/dynein and actomyosin, ensuring that cell membrane contractility is tightly controlled to execute proper daughter cell separation. article_number: '51512' article_processing_charge: No article_type: original author: - first_name: Hyang Mi full_name: Moon, Hyang Mi last_name: Moon - 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 - first_name: Anthony full_name: Wynshaw-Boris, Anthony last_name: Wynshaw-Boris citation: ama: Moon HM, Hippenmeyer S, Luo L, Wynshaw-Boris A. LIS1 determines cleavage plane positioning by regulating actomyosin-mediated cell membrane contractility. eLife. 2020;9. doi:10.7554/elife.51512 apa: Moon, H. M., Hippenmeyer, S., Luo, L., & Wynshaw-Boris, A. (2020). LIS1 determines cleavage plane positioning by regulating actomyosin-mediated cell membrane contractility. ELife. eLife Sciences Publications. https://doi.org/10.7554/elife.51512 chicago: Moon, Hyang Mi, Simon Hippenmeyer, Liqun Luo, and Anthony Wynshaw-Boris. “LIS1 Determines Cleavage Plane Positioning by Regulating Actomyosin-Mediated Cell Membrane Contractility.” ELife. eLife Sciences Publications, 2020. https://doi.org/10.7554/elife.51512. ieee: H. M. Moon, S. Hippenmeyer, L. Luo, and A. Wynshaw-Boris, “LIS1 determines cleavage plane positioning by regulating actomyosin-mediated cell membrane contractility,” eLife, vol. 9. eLife Sciences Publications, 2020. ista: Moon HM, Hippenmeyer S, Luo L, Wynshaw-Boris A. 2020. LIS1 determines cleavage plane positioning by regulating actomyosin-mediated cell membrane contractility. eLife. 9, 51512. mla: Moon, Hyang Mi, et al. “LIS1 Determines Cleavage Plane Positioning by Regulating Actomyosin-Mediated Cell Membrane Contractility.” ELife, vol. 9, 51512, eLife Sciences Publications, 2020, doi:10.7554/elife.51512. short: H.M. Moon, S. Hippenmeyer, L. Luo, A. Wynshaw-Boris, ELife 9 (2020). date_created: 2020-03-20T13:16:41Z date_published: 2020-03-11T00:00:00Z date_updated: 2023-08-18T07:06:31Z day: '11' ddc: - '570' department: - _id: SiHi doi: 10.7554/elife.51512 external_id: isi: - '000522835800001' pmid: - '32159512' file: - access_level: open_access checksum: 396ceb2dd10b102ef4e699666b9342c3 content_type: application/pdf creator: dernst date_created: 2020-09-24T07:03:20Z date_updated: 2020-09-24T07:03:20Z file_id: '8567' file_name: 2020_elife_Moon.pdf file_size: 15089438 relation: main_file success: 1 file_date_updated: 2020-09-24T07:03:20Z has_accepted_license: '1' intvolume: ' 9' isi: 1 language: - iso: eng main_file_link: - open_access: '1' url: https://doi.org/10.1101/751958 month: '03' oa: 1 oa_version: Published Version pmid: 1 publication: eLife publication_identifier: issn: - 2050-084X publication_status: published publisher: eLife Sciences Publications quality_controlled: '1' scopus_import: '1' status: public title: LIS1 determines cleavage plane positioning by regulating actomyosin-mediated cell membrane contractility 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: 4359f0d1-fa6c-11eb-b949-802e58b17ae8 volume: 9 year: '2020' ... --- _id: '8093' abstract: - lang: eng text: "Background: The activation of the EGFR/Ras-signalling pathway in tumour cells induces a distinct chemokine repertoire, which in turn modulates the tumour microenvironment.\r\nMethods: The effects of EGFR/Ras on the expression and translation of CCL20 were analysed in a large set of epithelial cancer cell lines and tumour tissues by RT-qPCR and ELISA in vitro. CCL20 production was verified by immunohistochemistry in different tumour tissues and correlated with clinical data. The effects of CCL20 on endothelial cell migration and tumour-associated vascularisation were comprehensively analysed with chemotaxis assays in vitro and in CCR6-deficient mice in vivo.\r\nResults: Tumours facilitate progression by the EGFR/Ras-induced production of CCL20. Expression of the chemokine CCL20 in tumours correlates with advanced tumour stage, increased lymph node metastasis and decreased survival in patients. Microvascular endothelial cells abundantly express the specific CCL20 receptor CCR6. CCR6 signalling in endothelial cells induces angiogenesis. CCR6-deficient mice show significantly decreased tumour growth and tumour-associated vascularisation. The observed phenotype is dependent on CCR6 deficiency in stromal cells but not within the immune system.\r\nConclusion: We propose that the chemokine axis CCL20–CCR6 represents a novel and promising target to interfere with the tumour microenvironment, and opens an innovative multimodal strategy for cancer therapy." acknowledgement: "The authors would like to thank A. van Lierop for technical assistance. In addition, we thank C. Dullin, J. Missbach-Güntner and S. Greco for advice and assistance with fpVCT imaging. Furthermore, the authors would like to thank H. K. Horst for advice on performing matrigel plug assays. This study has also been partially presented in A. Schorr’s doctoral thesis and the funding report of the SPP 1190 ‘The tumor-vessel interface’ of the ‘Deutsche Forschungsgemeinschaft’ (DFG).\r\nThis project was funded by the SPP 1190 “The tumor-vessel interface” and HO 2092/8-1 of the ‘Deutsche Forschungsgemeinschaft’ (DFG) to B. Homey. In addition, it was supported by grants from the Austrian Science Fund (FWF, W1212 to N. Amberg and J. Klufa and I4300-B to T. Bauer), the WWTF project LS16-025 and the European Research Council (ERC) Advanced grant (ERC-2015-AdG TNT-Tumors 694883) to M. Sibilia." article_processing_charge: No article_type: original author: - first_name: Andreas full_name: Hippe, Andreas last_name: Hippe - first_name: Stephan Alexander full_name: Braun, Stephan Alexander last_name: Braun - first_name: Péter full_name: Oláh, Péter last_name: Oláh - first_name: Peter Arne full_name: Gerber, Peter Arne last_name: Gerber - first_name: Anne full_name: Schorr, Anne last_name: Schorr - first_name: Stephan full_name: Seeliger, Stephan last_name: Seeliger - first_name: Stephanie full_name: Holtz, Stephanie last_name: Holtz - first_name: Katharina full_name: Jannasch, Katharina last_name: Jannasch - first_name: Andor full_name: Pivarcsi, Andor last_name: Pivarcsi - first_name: Bettina full_name: Buhren, Bettina last_name: Buhren - first_name: Holger full_name: Schrumpf, Holger last_name: Schrumpf - first_name: Andreas full_name: Kislat, Andreas last_name: Kislat - first_name: Erich full_name: Bünemann, Erich last_name: Bünemann - first_name: Martin full_name: Steinhoff, Martin last_name: Steinhoff - first_name: Jens full_name: Fischer, Jens last_name: Fischer - first_name: Sérgio A. full_name: Lira, Sérgio A. last_name: Lira - first_name: Petra full_name: Boukamp, Petra last_name: Boukamp - first_name: Peter full_name: Hevezi, Peter last_name: Hevezi - first_name: Nikolas Hendrik full_name: Stoecklein, Nikolas Hendrik last_name: Stoecklein - first_name: Thomas full_name: Hoffmann, Thomas last_name: Hoffmann - first_name: Frauke full_name: Alves, Frauke last_name: Alves - first_name: Jonathan full_name: Sleeman, Jonathan last_name: Sleeman - first_name: Thomas full_name: Bauer, Thomas last_name: Bauer - first_name: Jörg full_name: Klufa, Jörg last_name: Klufa - first_name: Nicole full_name: Amberg, Nicole id: 4CD6AAC6-F248-11E8-B48F-1D18A9856A87 last_name: Amberg orcid: 0000-0002-3183-8207 - first_name: Maria full_name: Sibilia, Maria last_name: Sibilia - first_name: Albert full_name: Zlotnik, Albert last_name: Zlotnik - first_name: Anja full_name: Müller-Homey, Anja last_name: Müller-Homey - first_name: Bernhard full_name: Homey, Bernhard last_name: Homey citation: ama: Hippe A, Braun SA, Oláh P, et al. EGFR/Ras-induced CCL20 production modulates the tumour microenvironment. British Journal of Cancer. 2020;123:942-954. doi:10.1038/s41416-020-0943-2 apa: Hippe, A., Braun, S. A., Oláh, P., Gerber, P. A., Schorr, A., Seeliger, S., … Homey, B. (2020). EGFR/Ras-induced CCL20 production modulates the tumour microenvironment. British Journal of Cancer. Springer Nature. https://doi.org/10.1038/s41416-020-0943-2 chicago: Hippe, Andreas, Stephan Alexander Braun, Péter Oláh, Peter Arne Gerber, Anne Schorr, Stephan Seeliger, Stephanie Holtz, et al. “EGFR/Ras-Induced CCL20 Production Modulates the Tumour Microenvironment.” British Journal of Cancer. Springer Nature, 2020. https://doi.org/10.1038/s41416-020-0943-2. ieee: A. Hippe et al., “EGFR/Ras-induced CCL20 production modulates the tumour microenvironment,” British Journal of Cancer, vol. 123. Springer Nature, pp. 942–954, 2020. ista: Hippe A, Braun SA, Oláh P, Gerber PA, Schorr A, Seeliger S, Holtz S, Jannasch K, Pivarcsi A, Buhren B, Schrumpf H, Kislat A, Bünemann E, Steinhoff M, Fischer J, Lira SA, Boukamp P, Hevezi P, Stoecklein NH, Hoffmann T, Alves F, Sleeman J, Bauer T, Klufa J, Amberg N, Sibilia M, Zlotnik A, Müller-Homey A, Homey B. 2020. EGFR/Ras-induced CCL20 production modulates the tumour microenvironment. British Journal of Cancer. 123, 942–954. mla: Hippe, Andreas, et al. “EGFR/Ras-Induced CCL20 Production Modulates the Tumour Microenvironment.” British Journal of Cancer, vol. 123, Springer Nature, 2020, pp. 942–54, doi:10.1038/s41416-020-0943-2. short: A. Hippe, S.A. Braun, P. Oláh, P.A. Gerber, A. Schorr, S. Seeliger, S. Holtz, K. Jannasch, A. Pivarcsi, B. Buhren, H. Schrumpf, A. Kislat, E. Bünemann, M. Steinhoff, J. Fischer, S.A. Lira, P. Boukamp, P. Hevezi, N.H. Stoecklein, T. Hoffmann, F. Alves, J. Sleeman, T. Bauer, J. Klufa, N. Amberg, M. Sibilia, A. Zlotnik, A. Müller-Homey, B. Homey, British Journal of Cancer 123 (2020) 942–954. date_created: 2020-07-05T22:00:46Z date_published: 2020-09-15T00:00:00Z date_updated: 2023-08-22T07:51:12Z day: '15' ddc: - '610' department: - _id: SiHi doi: 10.1038/s41416-020-0943-2 external_id: isi: - '000544152500001' pmid: - '32601464' file: - access_level: open_access checksum: 05a8e65d49c3f5b8e37ac4afe68287e2 content_type: application/pdf creator: cchlebak date_created: 2021-12-02T12:35:12Z date_updated: 2021-12-02T12:35:12Z file_id: '10398' file_name: 2020_BrJournalCancer_Hippe.pdf file_size: 3620691 relation: main_file success: 1 file_date_updated: 2021-12-02T12:35:12Z has_accepted_license: '1' intvolume: ' 123' isi: 1 language: - iso: eng month: '09' oa: 1 oa_version: Published Version page: 942-954 pmid: 1 publication: British Journal of Cancer publication_identifier: eissn: - 1532-1827 issn: - 0007-0920 publication_status: published publisher: Springer Nature quality_controlled: '1' related_material: link: - relation: erratum url: https://doi.org/10.1038/s41416-021-01563-y record: - id: '10170' relation: later_version status: deleted scopus_import: '1' status: public title: EGFR/Ras-induced CCL20 production modulates the tumour microenvironment 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: 4359f0d1-fa6c-11eb-b949-802e58b17ae8 volume: 123 year: '2020' ... --- _id: '8162' abstract: - lang: eng text: In mammalian genomes, a subset of genes is regulated by genomic imprinting, resulting in silencing of one parental allele. Imprinting is essential for cerebral cortex development, but prevalence and functional impact in individual cells is unclear. Here, we determined allelic expression in cortical cell types and established a quantitative platform to interrogate imprinting in single cells. We created cells with uniparental chromosome disomy (UPD) containing two copies of either the maternal or the paternal chromosome; hence, imprinted genes will be 2-fold overexpressed or not expressed. By genetic labeling of UPD, we determined cellular phenotypes and transcriptional responses to deregulated imprinted gene expression at unprecedented single-cell resolution. We discovered an unexpected degree of cell-type specificity and a novel function of imprinting in the regulation of cortical astrocyte survival. More generally, our results suggest functional relevance of imprinted gene expression in glial astrocyte lineage and thus for generating cortical cell-type diversity. acknowledged_ssus: - _id: Bio - _id: LifeSc - _id: PreCl acknowledgement: We thank A. Heger (IST Austria Preclinical Facility), A. Sommer and C. Czepe (VBCF GmbH, NGS Unit), and A. Seitz and P. Moll (Lexogen GmbH) for technical support; G. Arque, S. Resch, C. Igler, C. Dotter, C. Yahya, Q. Hudson, and D. Andergassen for initial experiments and/or assistance; D. Barlow, O. Bell, and all members of the Hippenmeyer lab for discussion; and N. Barton, B. Vicoso, M. Sixt, and L. Luo for comments on earlier versions of the manuscript. This research was supported by the Scientific Service Units (SSU) of IST Austria through resources provided by the Bioimaging Facilities (BIF), Life Science Facilities (LSF), and Preclinical Facilities (PCF). A.H.H. is a recipient of a DOC fellowship (24812) of the Austrian Academy of Sciences. N.A. received support from the FWF Firnberg-Programm (T 1031). R.B. received support from the FWF Meitner-Programm (M 2416). This work was also supported by IST Austria institutional funds; a NÖ Forschung und Bildung n[f+b] life science call grant (C13-002) to S.H.; a program grant from the Human Frontiers Science Program (RGP0053/2014) to S.H.; the People Programme (Marie Curie Actions) of the European Union’s Seventh Framework Programme (FP7/2007-2013) under REA grant agreement 618444 to S.H.; and the European Research Council (ERC) under the European Union’s Horizon 2020 research and innovation program (grant agreement 725780 LinPro) to S.H. article_processing_charge: No article_type: original author: - first_name: Susanne full_name: Laukoter, Susanne id: 2D6B7A9A-F248-11E8-B48F-1D18A9856A87 last_name: Laukoter orcid: 0000-0002-7903-3010 - first_name: Florian full_name: Pauler, Florian id: 48EA0138-F248-11E8-B48F-1D18A9856A87 last_name: Pauler orcid: 0000-0002-7462-0048 - first_name: Robert J full_name: Beattie, Robert J id: 2E26DF60-F248-11E8-B48F-1D18A9856A87 last_name: Beattie orcid: 0000-0002-8483-8753 - first_name: Nicole full_name: Amberg, Nicole id: 4CD6AAC6-F248-11E8-B48F-1D18A9856A87 last_name: Amberg orcid: 0000-0002-3183-8207 - first_name: Andi H full_name: Hansen, Andi H id: 38853E16-F248-11E8-B48F-1D18A9856A87 last_name: Hansen - first_name: Carmen full_name: Streicher, Carmen id: 36BCB99C-F248-11E8-B48F-1D18A9856A87 last_name: Streicher - first_name: Thomas full_name: Penz, Thomas last_name: Penz - first_name: Christoph full_name: Bock, Christoph last_name: Bock orcid: 0000-0001-6091-3088 - first_name: Simon full_name: Hippenmeyer, Simon id: 37B36620-F248-11E8-B48F-1D18A9856A87 last_name: Hippenmeyer orcid: 0000-0003-2279-1061 citation: ama: Laukoter S, Pauler F, Beattie RJ, et al. Cell-type specificity of genomic imprinting in cerebral cortex. Neuron. 2020;107(6):1160-1179.e9. doi:10.1016/j.neuron.2020.06.031 apa: Laukoter, S., Pauler, F., Beattie, R. J., Amberg, N., Hansen, A. H., Streicher, C., … Hippenmeyer, S. (2020). Cell-type specificity of genomic imprinting in cerebral cortex. Neuron. Elsevier. https://doi.org/10.1016/j.neuron.2020.06.031 chicago: Laukoter, Susanne, Florian Pauler, Robert J Beattie, Nicole Amberg, Andi H Hansen, Carmen Streicher, Thomas Penz, Christoph Bock, and Simon Hippenmeyer. “Cell-Type Specificity of Genomic Imprinting in Cerebral Cortex.” Neuron. Elsevier, 2020. https://doi.org/10.1016/j.neuron.2020.06.031. ieee: S. Laukoter et al., “Cell-type specificity of genomic imprinting in cerebral cortex,” Neuron, vol. 107, no. 6. Elsevier, p. 1160–1179.e9, 2020. ista: Laukoter S, Pauler F, Beattie RJ, Amberg N, Hansen AH, Streicher C, Penz T, Bock C, Hippenmeyer S. 2020. Cell-type specificity of genomic imprinting in cerebral cortex. Neuron. 107(6), 1160–1179.e9. mla: Laukoter, Susanne, et al. “Cell-Type Specificity of Genomic Imprinting in Cerebral Cortex.” Neuron, vol. 107, no. 6, Elsevier, 2020, p. 1160–1179.e9, doi:10.1016/j.neuron.2020.06.031. short: S. Laukoter, F. Pauler, R.J. Beattie, N. Amberg, A.H. Hansen, C. Streicher, T. Penz, C. Bock, S. Hippenmeyer, Neuron 107 (2020) 1160–1179.e9. date_created: 2020-07-23T16:03:12Z date_published: 2020-09-23T00:00:00Z date_updated: 2023-08-22T08:20:11Z day: '23' ddc: - '570' department: - _id: SiHi doi: 10.1016/j.neuron.2020.06.031 ec_funded: 1 external_id: isi: - '000579698700006' file: - access_level: open_access checksum: 7becdc16a6317304304631087ae7dd7f content_type: application/pdf creator: dernst date_created: 2020-12-02T09:26:46Z date_updated: 2020-12-02T09:26:46Z file_id: '8828' file_name: 2020_Neuron_Laukoter.pdf file_size: 8911830 relation: main_file success: 1 file_date_updated: 2020-12-02T09:26:46Z has_accepted_license: '1' intvolume: ' 107' isi: 1 issue: '6' language: - iso: eng month: '09' oa: 1 oa_version: Published Version page: 1160-1179.e9 project: - _id: 2625A13E-B435-11E9-9278-68D0E5697425 grant_number: '24812' name: Molecular Mechanisms of Radial Neuronal Migration - _id: 268F8446-B435-11E9-9278-68D0E5697425 call_identifier: FWF grant_number: T0101031 name: Role of Eed in neural stem cell lineage progression - _id: 264E56E2-B435-11E9-9278-68D0E5697425 call_identifier: FWF grant_number: M02416 name: Molecular Mechanisms Regulating Gliogenesis in the Cerebral Cortex - _id: 25D92700-B435-11E9-9278-68D0E5697425 grant_number: LS13-002 name: Mapping Cell-Type Specificity of the Genomic Imprintome in the Brain - _id: 25D7962E-B435-11E9-9278-68D0E5697425 grant_number: RGP0053/2014 name: Quantitative Structure-Function Analysis of Cerebral Cortex Assembly at Clonal Level - _id: 25D61E48-B435-11E9-9278-68D0E5697425 call_identifier: FP7 grant_number: '618444' name: Molecular Mechanisms of Cerebral Cortex Development - _id: 260018B0-B435-11E9-9278-68D0E5697425 call_identifier: H2020 grant_number: '725780' name: Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development publication: Neuron publication_identifier: issn: - 0896-6273 publication_status: published publisher: Elsevier quality_controlled: '1' related_material: link: - description: News on IST Website relation: press_release url: https://ist.ac.at/en/news/cells-react-differently-to-genomic-imprinting/ scopus_import: '1' status: public title: Cell-type specificity of genomic imprinting in cerebral cortex 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: 4359f0d1-fa6c-11eb-b949-802e58b17ae8 volume: 107 year: '2020' ... --- _id: '8592' abstract: - lang: eng text: Glioblastoma is the most malignant cancer in the brain and currently incurable. It is urgent to identify effective targets for this lethal disease. Inhibition of such targets should suppress the growth of cancer cells and, ideally also precancerous cells for early prevention, but minimally affect their normal counterparts. Using genetic mouse models with neural stem cells (NSCs) or oligodendrocyte precursor cells (OPCs) as the cells‐of‐origin/mutation, it is shown that the susceptibility of cells within the development hierarchy of glioma to the knockout of insulin‐like growth factor I receptor (IGF1R) is determined not only by their oncogenic states, but also by their cell identities/states. Knockout of IGF1R selectively disrupts the growth of mutant and transformed, but not normal OPCs, or NSCs. The desirable outcome of IGF1R knockout on cell growth requires the mutant cells to commit to the OPC identity regardless of its development hierarchical status. At the molecular level, oncogenic mutations reprogram the cellular network of OPCs and force them to depend more on IGF1R for their growth. A new‐generation brain‐penetrable, orally available IGF1R inhibitor harnessing tumor OPCs in the brain is also developed. The findings reveal the cellular window of IGF1R targeting and establish IGF1R as an effective target for the prevention and treatment of glioblastoma. acknowledgement: The authors thank Drs. J. Eisen, QR. Lu, S. Duan, Z‐H. Li, W. Mo, and Q. Wu for their critical comments on the manuscript. They also thank Dr. H. Zong for providing the CKO_NG2‐CreER model. This work is supported by the National Key Research and Development Program of China, Stem Cell and Translational Research (2016YFA0101201 to C.L., 2016YFA0100303 to Y.J.W.), the National Natural Science Foundation of China (81673035 and 81972915 to C.L., 81472722 to Y.J.W.), the Science Foundation for Distinguished Young Scientists of Zhejiang Province (LR17H160001 to C.L.), Fundamental Research Funds for the Central Universities (2016QNA7023 and 2017QNA7028 to C.L.) and the Thousand Talent Program for Young Outstanding Scientists, China (to C.L.), IST Austria institutional funds (to S.H.), European Research Council (ERC) under the European Union's Horizon 2020 research and innovation programme (725780 LinPro to S.H.). C.L. is a scholar of K. C. Wong Education Foundation. article_number: '2001724' article_processing_charge: No article_type: original author: - first_name: Anhao full_name: Tian, Anhao last_name: Tian - first_name: Bo full_name: Kang, Bo last_name: Kang - first_name: Baizhou full_name: Li, Baizhou last_name: Li - first_name: Biying full_name: Qiu, Biying last_name: Qiu - first_name: Wenhong full_name: Jiang, Wenhong last_name: Jiang - first_name: Fangjie full_name: Shao, Fangjie last_name: Shao - first_name: Qingqing full_name: Gao, Qingqing last_name: Gao - first_name: Rui full_name: Liu, Rui last_name: Liu - first_name: Chengwei full_name: Cai, Chengwei last_name: Cai - first_name: Rui full_name: Jing, Rui last_name: Jing - first_name: Wei full_name: Wang, Wei last_name: Wang - first_name: Pengxiang full_name: Chen, Pengxiang last_name: Chen - first_name: Qinghui full_name: Liang, Qinghui last_name: Liang - first_name: Lili full_name: Bao, Lili last_name: Bao - first_name: Jianghong full_name: Man, Jianghong last_name: Man - first_name: Yan full_name: Wang, Yan last_name: Wang - first_name: Yu full_name: Shi, Yu last_name: Shi - first_name: Jin full_name: Li, Jin last_name: Li - first_name: Minmin full_name: Yang, Minmin last_name: Yang - first_name: Lisha full_name: Wang, Lisha last_name: Wang - first_name: Jianmin full_name: Zhang, Jianmin last_name: Zhang - first_name: Simon full_name: Hippenmeyer, Simon id: 37B36620-F248-11E8-B48F-1D18A9856A87 last_name: Hippenmeyer orcid: 0000-0003-2279-1061 - first_name: Junming full_name: Zhu, Junming last_name: Zhu - first_name: Xiuwu full_name: Bian, Xiuwu last_name: Bian - first_name: Ying‐Jie full_name: Wang, Ying‐Jie last_name: Wang - first_name: Chong full_name: Liu, Chong last_name: Liu citation: ama: Tian A, Kang B, Li B, et al. Oncogenic state and cell identity combinatorially dictate the susceptibility of cells within glioma development hierarchy to IGF1R targeting. Advanced Science. 2020;7(21). doi:10.1002/advs.202001724 apa: Tian, A., Kang, B., Li, B., Qiu, B., Jiang, W., Shao, F., … Liu, C. (2020). Oncogenic state and cell identity combinatorially dictate the susceptibility of cells within glioma development hierarchy to IGF1R targeting. Advanced Science. Wiley. https://doi.org/10.1002/advs.202001724 chicago: Tian, Anhao, Bo Kang, Baizhou Li, Biying Qiu, Wenhong Jiang, Fangjie Shao, Qingqing Gao, et al. “Oncogenic State and Cell Identity Combinatorially Dictate the Susceptibility of Cells within Glioma Development Hierarchy to IGF1R Targeting.” Advanced Science. Wiley, 2020. https://doi.org/10.1002/advs.202001724. ieee: A. Tian et al., “Oncogenic state and cell identity combinatorially dictate the susceptibility of cells within glioma development hierarchy to IGF1R targeting,” Advanced Science, vol. 7, no. 21. Wiley, 2020. ista: Tian A, Kang B, Li B, Qiu B, Jiang W, Shao F, Gao Q, Liu R, Cai C, Jing R, Wang W, Chen P, Liang Q, Bao L, Man J, Wang Y, Shi Y, Li J, Yang M, Wang L, Zhang J, Hippenmeyer S, Zhu J, Bian X, Wang Y, Liu C. 2020. Oncogenic state and cell identity combinatorially dictate the susceptibility of cells within glioma development hierarchy to IGF1R targeting. Advanced Science. 7(21), 2001724. mla: Tian, Anhao, et al. “Oncogenic State and Cell Identity Combinatorially Dictate the Susceptibility of Cells within Glioma Development Hierarchy to IGF1R Targeting.” Advanced Science, vol. 7, no. 21, 2001724, Wiley, 2020, doi:10.1002/advs.202001724. short: A. Tian, B. Kang, B. Li, B. Qiu, W. Jiang, F. Shao, Q. Gao, R. Liu, C. Cai, R. Jing, W. Wang, P. Chen, Q. Liang, L. Bao, J. Man, Y. Wang, Y. Shi, J. Li, M. Yang, L. Wang, J. Zhang, S. Hippenmeyer, J. Zhu, X. Bian, Y. Wang, C. Liu, Advanced Science 7 (2020). date_created: 2020-10-01T09:44:13Z date_published: 2020-11-04T00:00:00Z date_updated: 2023-08-22T09:53:01Z day: '04' ddc: - '570' department: - _id: SiHi doi: 10.1002/advs.202001724 ec_funded: 1 external_id: isi: - '000573860700001' file: - access_level: open_access checksum: 92818c23ecc70e35acfa671f3cfb9909 content_type: application/pdf creator: dernst date_created: 2020-12-10T14:07:24Z date_updated: 2020-12-10T14:07:24Z file_id: '8938' file_name: 2020_AdvScience_Tian.pdf file_size: 7835833 relation: main_file success: 1 file_date_updated: 2020-12-10T14:07:24Z has_accepted_license: '1' intvolume: ' 7' isi: 1 issue: '21' keyword: - General Engineering - General Physics and Astronomy - General Materials Science - Medicine (miscellaneous) - General Chemical Engineering - Biochemistry - Genetics and Molecular Biology (miscellaneous) language: - iso: eng month: '11' oa: 1 oa_version: Published Version project: - _id: 260018B0-B435-11E9-9278-68D0E5697425 call_identifier: H2020 grant_number: '725780' name: Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development publication: Advanced Science publication_identifier: issn: - 2198-3844 publication_status: published publisher: Wiley quality_controlled: '1' status: public title: Oncogenic state and cell identity combinatorially dictate the susceptibility of cells within glioma development hierarchy to IGF1R targeting 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: 4359f0d1-fa6c-11eb-b949-802e58b17ae8 volume: 7 year: '2020' ... --- _id: '8949' abstract: - lang: eng text: Development of the nervous system undergoes important transitions, including one from neurogenesis to gliogenesis which occurs late during embryonic gestation. Here we report on clonal analysis of gliogenesis in mice using Mosaic Analysis with Double Markers (MADM) with quantitative and computational methods. Results reveal that developmental gliogenesis in the cerebral cortex occurs in a fraction of earlier neurogenic clones, accelerating around E16.5, and giving rise to both astrocytes and oligodendrocytes. Moreover, MADM-based genetic deletion of the epidermal growth factor receptor (Egfr) in gliogenic clones revealed that Egfr is cell autonomously required for gliogenesis in the mouse dorsolateral cortices. A broad range in the proliferation capacity, symmetry of clones, and competitive advantage of MADM cells was evident in clones that contained one cellular lineage with double dosage of Egfr relative to their environment, while their sibling Egfr-null cells failed to generate glia. Remarkably, the total numbers of glia in MADM clones balance out regardless of significant alterations in clonal symmetries. The variability in glial clones shows stochastic patterns that we define mathematically, which are different from the deterministic patterns in neuronal clones. This study sets a foundation for studying the biological significance of stochastic and deterministic clonal principles underlying tissue development, and identifying mechanisms that differentiate between neurogenesis and gliogenesis. acknowledgement: This research was funded by grants from the National Institutes of Health to H.T.G. (R01NS098370 and R01NS089795). C.V.M. was supported by a National Science Foundation Graduate Research Fellowship (DGE-1746939). R.B. was supported by the FWF Lise-Meitner program (M 2416), and S.H. was supported by the European Research Council (ERC) under the European Union’s Horizon 2020 research and innovation programme (grant agreement No 725780 LinPro).The authors thank members of the Ghashghaei lab for discussions, technical support, and help with preparation of the manuscript. article_number: '2662' article_processing_charge: No article_type: original author: - first_name: Xuying full_name: Zhang, Xuying last_name: Zhang - first_name: Christine V. full_name: Mennicke, Christine V. last_name: Mennicke - first_name: Guanxi full_name: Xiao, Guanxi last_name: Xiao - first_name: Robert J full_name: Beattie, Robert J id: 2E26DF60-F248-11E8-B48F-1D18A9856A87 last_name: Beattie orcid: 0000-0002-8483-8753 - first_name: Mansoor full_name: Haider, Mansoor last_name: Haider - first_name: Simon full_name: Hippenmeyer, Simon id: 37B36620-F248-11E8-B48F-1D18A9856A87 last_name: Hippenmeyer orcid: 0000-0003-2279-1061 - first_name: H. Troy full_name: Ghashghaei, H. Troy last_name: Ghashghaei citation: ama: Zhang X, Mennicke CV, Xiao G, et al. Clonal analysis of gliogenesis in the cerebral cortex reveals stochastic expansion of glia and cell autonomous responses to Egfr dosage. Cells. 2020;9(12). doi:10.3390/cells9122662 apa: Zhang, X., Mennicke, C. V., Xiao, G., Beattie, R. J., Haider, M., Hippenmeyer, S., & Ghashghaei, H. T. (2020). Clonal analysis of gliogenesis in the cerebral cortex reveals stochastic expansion of glia and cell autonomous responses to Egfr dosage. Cells. MDPI. https://doi.org/10.3390/cells9122662 chicago: Zhang, Xuying, Christine V. Mennicke, Guanxi Xiao, Robert J Beattie, Mansoor Haider, Simon Hippenmeyer, and H. Troy Ghashghaei. “Clonal Analysis of Gliogenesis in the Cerebral Cortex Reveals Stochastic Expansion of Glia and Cell Autonomous Responses to Egfr Dosage.” Cells. MDPI, 2020. https://doi.org/10.3390/cells9122662. ieee: X. Zhang et al., “Clonal analysis of gliogenesis in the cerebral cortex reveals stochastic expansion of glia and cell autonomous responses to Egfr dosage,” Cells, vol. 9, no. 12. MDPI, 2020. ista: Zhang X, Mennicke CV, Xiao G, Beattie RJ, Haider M, Hippenmeyer S, Ghashghaei HT. 2020. Clonal analysis of gliogenesis in the cerebral cortex reveals stochastic expansion of glia and cell autonomous responses to Egfr dosage. Cells. 9(12), 2662. mla: Zhang, Xuying, et al. “Clonal Analysis of Gliogenesis in the Cerebral Cortex Reveals Stochastic Expansion of Glia and Cell Autonomous Responses to Egfr Dosage.” Cells, vol. 9, no. 12, 2662, MDPI, 2020, doi:10.3390/cells9122662. short: X. Zhang, C.V. Mennicke, G. Xiao, R.J. Beattie, M. Haider, S. Hippenmeyer, H.T. Ghashghaei, Cells 9 (2020). date_created: 2020-12-14T08:04:03Z date_published: 2020-12-11T00:00:00Z date_updated: 2023-08-24T10:57:48Z day: '11' ddc: - '570' department: - _id: SiHi doi: 10.3390/cells9122662 ec_funded: 1 external_id: isi: - '000601787300001' file: - access_level: open_access checksum: 5095cbdc728c9a510c5761cf60a8861c content_type: application/pdf creator: dernst date_created: 2020-12-14T08:09:43Z date_updated: 2020-12-14T08:09:43Z file_id: '8950' file_name: 2020_Cells_Zhang.pdf file_size: 3504525 relation: main_file success: 1 file_date_updated: 2020-12-14T08:09:43Z has_accepted_license: '1' intvolume: ' 9' isi: 1 issue: '12' language: - iso: eng month: '12' oa: 1 oa_version: Published Version project: - _id: 264E56E2-B435-11E9-9278-68D0E5697425 call_identifier: FWF grant_number: M02416 name: Molecular Mechanisms Regulating Gliogenesis in the Cerebral Cortex - _id: 260018B0-B435-11E9-9278-68D0E5697425 call_identifier: H2020 grant_number: '725780' name: Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development publication: Cells publication_identifier: issn: - 2073-4409 publication_status: published publisher: MDPI quality_controlled: '1' status: public title: Clonal analysis of gliogenesis in the cerebral cortex reveals stochastic expansion of glia and cell autonomous responses to Egfr dosage 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: 4359f0d1-fa6c-11eb-b949-802e58b17ae8 volume: 9 year: '2020' ... --- _id: '8813' abstract: - lang: eng text: 'In mammals, chromatin marks at imprinted genes are asymmetrically inherited to control parentally-biased gene expression. This control is thought predominantly to involve parent-specific differentially methylated regions (DMR) in genomic DNA. However, neither parent-of-origin-specific transcription nor DMRs have been comprehensively mapped. We here address this by integrating transcriptomic and epigenomic approaches in mouse preimplantation embryos (blastocysts). Transcriptome-analysis identified 71 genes expressed with previously unknown parent-of-origin-specific expression in blastocysts (nBiX: novel blastocyst-imprinted expression). Uniparental expression of nBiX genes disappeared soon after implantation. Micro-whole-genome bisulfite sequencing (μWGBS) of individual uniparental blastocysts detected 859 DMRs. Only 18% of nBiXs were associated with a DMR, whereas 60% were associated with parentally-biased H3K27me3. This suggests a major role for Polycomb-mediated imprinting in blastocysts. Five nBiX-clusters contained at least one known imprinted gene, and five novel clusters contained exclusively nBiX-genes. These data suggest a complex program of stage-specific imprinting involving different tiers of regulation.' article_processing_charge: No author: - first_name: Laura full_name: Santini, Laura last_name: Santini - first_name: Florian full_name: Halbritter, Florian last_name: Halbritter - first_name: Fabian full_name: Titz-Teixeira, Fabian last_name: Titz-Teixeira - first_name: Toru full_name: Suzuki, Toru last_name: Suzuki - first_name: Maki full_name: Asami, Maki last_name: Asami - first_name: Julia full_name: Ramesmayer, Julia last_name: Ramesmayer - first_name: Xiaoyan full_name: Ma, Xiaoyan last_name: Ma - first_name: Andreas full_name: Lackner, Andreas last_name: Lackner - first_name: Nick full_name: Warr, Nick last_name: Warr - first_name: Florian full_name: Pauler, Florian id: 48EA0138-F248-11E8-B48F-1D18A9856A87 last_name: Pauler orcid: 0000-0002-7462-0048 - first_name: Simon full_name: Hippenmeyer, Simon id: 37B36620-F248-11E8-B48F-1D18A9856A87 last_name: Hippenmeyer orcid: 0000-0003-2279-1061 - first_name: Ernest full_name: Laue, Ernest last_name: Laue - first_name: Matthias full_name: Farlik, Matthias last_name: Farlik - first_name: Christoph full_name: Bock, Christoph last_name: Bock - first_name: Andreas full_name: Beyer, Andreas last_name: Beyer - first_name: Anthony C. F. full_name: Perry, Anthony C. F. last_name: Perry - first_name: Martin full_name: Leeb, Martin last_name: Leeb citation: ama: Santini L, Halbritter F, Titz-Teixeira F, et al. Novel imprints in mouse blastocysts are predominantly DNA methylation independent. bioRxiv. doi:10.1101/2020.11.03.366948 apa: Santini, L., Halbritter, F., Titz-Teixeira, F., Suzuki, T., Asami, M., Ramesmayer, J., … Leeb, M. (n.d.). Novel imprints in mouse blastocysts are predominantly DNA methylation independent. bioRxiv. Cold Spring Harbor Laboratory. https://doi.org/10.1101/2020.11.03.366948 chicago: Santini, Laura, Florian Halbritter, Fabian Titz-Teixeira, Toru Suzuki, Maki Asami, Julia Ramesmayer, Xiaoyan Ma, et al. “Novel Imprints in Mouse Blastocysts Are Predominantly DNA Methylation Independent.” BioRxiv. Cold Spring Harbor Laboratory, n.d. https://doi.org/10.1101/2020.11.03.366948. ieee: L. Santini et al., “Novel imprints in mouse blastocysts are predominantly DNA methylation independent,” bioRxiv. Cold Spring Harbor Laboratory. ista: Santini L, Halbritter F, Titz-Teixeira F, Suzuki T, Asami M, Ramesmayer J, Ma X, Lackner A, Warr N, Pauler F, Hippenmeyer S, Laue E, Farlik M, Bock C, Beyer A, Perry ACF, Leeb M. Novel imprints in mouse blastocysts are predominantly DNA methylation independent. bioRxiv, 10.1101/2020.11.03.366948. mla: Santini, Laura, et al. “Novel Imprints in Mouse Blastocysts Are Predominantly DNA Methylation Independent.” BioRxiv, Cold Spring Harbor Laboratory, doi:10.1101/2020.11.03.366948. short: L. Santini, F. Halbritter, F. Titz-Teixeira, T. Suzuki, M. Asami, J. Ramesmayer, X. Ma, A. Lackner, N. Warr, F. Pauler, S. Hippenmeyer, E. Laue, M. Farlik, C. Bock, A. Beyer, A.C.F. Perry, M. Leeb, BioRxiv (n.d.). date_created: 2020-11-26T07:17:19Z date_published: 2020-11-05T00:00:00Z date_updated: 2023-09-12T11:05:28Z day: '05' department: - _id: SiHi doi: 10.1101/2020.11.03.366948 external_id: pmid: - 'PPR234457 ' language: - iso: eng main_file_link: - open_access: '1' url: https://doi.org/10.1101/2020.11.03.366948 month: '11' oa: 1 oa_version: Preprint pmid: 1 publication: bioRxiv publication_status: submitted publisher: Cold Spring Harbor Laboratory status: public title: Novel imprints in mouse blastocysts are predominantly DNA methylation independent type: preprint user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 year: '2020' ... --- _id: '8569' abstract: - lang: eng text: Concerted radial migration of newly born cortical projection neurons, from their birthplace to their final target lamina, is a key step in the assembly of the cerebral cortex. The cellular and molecular mechanisms regulating the specific sequential steps of radial neuronal migration in vivo are however still unclear, let alone the effects and interactions with the extracellular environment. In any in vivo context, cells will always be exposed to a complex extracellular environment consisting of (1) secreted factors acting as potential signaling cues, (2) the extracellular matrix, and (3) other cells providing cell–cell interaction through receptors and/or direct physical stimuli. Most studies so far have described and focused mainly on intrinsic cell-autonomous gene functions in neuronal migration but there is accumulating evidence that non-cell-autonomous-, local-, systemic-, and/or whole tissue-wide effects substantially contribute to the regulation of radial neuronal migration. These non-cell-autonomous effects may differentially affect cortical neuron migration in distinct cellular environments. However, the cellular and molecular natures of such non-cell-autonomous mechanisms are mostly unknown. Furthermore, physical forces due to collective migration and/or community effects (i.e., interactions with surrounding cells) may play important roles in neocortical projection neuron migration. In this concise review, we first outline distinct models of non-cell-autonomous interactions of cortical projection neurons along their radial migration trajectory during development. We then summarize experimental assays and platforms that can be utilized to visualize and potentially probe non-cell-autonomous mechanisms. Lastly, we define key questions to address in the future. acknowledgement: AH was a recipient of a DOC Fellowship (24812) of the Austrian Academy of Sciences. This work also received support from IST Austria institutional funds; the People Programme (Marie Curie Actions) of the European Union’s Seventh Framework Programme (FP7/2007–2013) under REA Grant Agreement No. 618444 to SH. article_number: '574382' article_processing_charge: Yes (via OA deal) article_type: original author: - first_name: Andi H full_name: Hansen, Andi H id: 38853E16-F248-11E8-B48F-1D18A9856A87 last_name: Hansen - first_name: Simon full_name: Hippenmeyer, Simon id: 37B36620-F248-11E8-B48F-1D18A9856A87 last_name: Hippenmeyer orcid: 0000-0003-2279-1061 citation: ama: Hansen AH, Hippenmeyer S. Non-cell-autonomous mechanisms in radial projection neuron migration in the developing cerebral cortex. Frontiers in Cell and Developmental Biology. 2020;8(9). doi:10.3389/fcell.2020.574382 apa: Hansen, A. H., & Hippenmeyer, S. (2020). Non-cell-autonomous mechanisms in radial projection neuron migration in the developing cerebral cortex. Frontiers in Cell and Developmental Biology. Frontiers. https://doi.org/10.3389/fcell.2020.574382 chicago: Hansen, Andi H, and Simon Hippenmeyer. “Non-Cell-Autonomous Mechanisms in Radial Projection Neuron Migration in the Developing Cerebral Cortex.” Frontiers in Cell and Developmental Biology. Frontiers, 2020. https://doi.org/10.3389/fcell.2020.574382. ieee: A. H. Hansen and S. Hippenmeyer, “Non-cell-autonomous mechanisms in radial projection neuron migration in the developing cerebral cortex,” Frontiers in Cell and Developmental Biology, vol. 8, no. 9. Frontiers, 2020. ista: Hansen AH, Hippenmeyer S. 2020. Non-cell-autonomous mechanisms in radial projection neuron migration in the developing cerebral cortex. Frontiers in Cell and Developmental Biology. 8(9), 574382. mla: Hansen, Andi H., and Simon Hippenmeyer. “Non-Cell-Autonomous Mechanisms in Radial Projection Neuron Migration in the Developing Cerebral Cortex.” Frontiers in Cell and Developmental Biology, vol. 8, no. 9, 574382, Frontiers, 2020, doi:10.3389/fcell.2020.574382. short: A.H. Hansen, S. Hippenmeyer, Frontiers in Cell and Developmental Biology 8 (2020). date_created: 2020-09-26T06:11:07Z date_published: 2020-09-25T00:00:00Z date_updated: 2024-03-28T23:30:41Z day: '25' ddc: - '570' department: - _id: SiHi doi: 10.3389/fcell.2020.574382 ec_funded: 1 external_id: isi: - '000577915900001' pmid: - '33102480' file: - access_level: open_access checksum: 01f731824194c94c81a5da360d997073 content_type: application/pdf creator: dernst date_created: 2020-09-28T13:11:17Z date_updated: 2020-09-28T13:11:17Z file_id: '8584' file_name: 2020_Frontiers_Hansen.pdf file_size: 5527139 relation: main_file success: 1 file_date_updated: 2020-09-28T13:11:17Z has_accepted_license: '1' intvolume: ' 8' isi: 1 issue: '9' language: - iso: eng month: '09' oa: 1 oa_version: Published Version pmid: 1 project: - _id: 2625A13E-B435-11E9-9278-68D0E5697425 grant_number: '24812' name: Molecular Mechanisms of Radial Neuronal Migration - _id: 25D61E48-B435-11E9-9278-68D0E5697425 call_identifier: FP7 grant_number: '618444' name: Molecular Mechanisms of Cerebral Cortex Development publication: Frontiers in Cell and Developmental Biology publication_identifier: issn: - 2296-634X publication_status: published publisher: Frontiers quality_controlled: '1' related_material: record: - id: '9962' relation: dissertation_contains status: public scopus_import: '1' status: public title: Non-cell-autonomous mechanisms in radial projection neuron migration in the developing cerebral cortex 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: 4359f0d1-fa6c-11eb-b949-802e58b17ae8 volume: 8 year: '2020' ... --- _id: '7815' abstract: - lang: eng text: Beginning from a limited pool of progenitors, the mammalian cerebral cortex forms highly organized functional neural circuits. However, the underlying cellular and molecular mechanisms regulating lineage transitions of neural stem cells (NSCs) and eventual production of neurons and glia in the developing neuroepithelium remains unclear. Methods to trace NSC division patterns and map the lineage of clonally related cells have advanced dramatically. However, many contemporary lineage tracing techniques suffer from the lack of cellular resolution of progeny cell fate, which is essential for deciphering progenitor cell division patterns. Presented is a protocol using mosaic analysis with double markers (MADM) to perform in vivo clonal analysis. MADM concomitantly manipulates individual progenitor cells and visualizes precise division patterns and lineage progression at unprecedented single cell resolution. MADM-based interchromosomal recombination events during the G2-X phase of mitosis, together with temporally inducible CreERT2, provide exact information on the birth dates of clones and their division patterns. Thus, MADM lineage tracing provides unprecedented qualitative and quantitative optical readouts of the proliferation mode of stem cell progenitors at the single cell level. MADM also allows for examination of the mechanisms and functional requirements of candidate genes in NSC lineage progression. This method is unique in that comparative analysis of control and mutant subclones can be performed in the same tissue environment in vivo. Here, the protocol is described in detail, and experimental paradigms to employ MADM for clonal analysis and lineage tracing in the developing cerebral cortex are demonstrated. Importantly, this protocol can be adapted to perform MADM clonal analysis in any murine stem cell niche, as long as the CreERT2 driver is present. acknowledged_ssus: - _id: Bio - _id: LifeSc - _id: PreCl article_number: e61147 article_processing_charge: No article_type: original author: - first_name: Robert J full_name: Beattie, Robert J id: 2E26DF60-F248-11E8-B48F-1D18A9856A87 last_name: Beattie orcid: 0000-0002-8483-8753 - first_name: Carmen full_name: Streicher, Carmen id: 36BCB99C-F248-11E8-B48F-1D18A9856A87 last_name: Streicher - first_name: Nicole full_name: Amberg, Nicole id: 4CD6AAC6-F248-11E8-B48F-1D18A9856A87 last_name: Amberg orcid: 0000-0002-3183-8207 - first_name: Giselle T full_name: Cheung, Giselle T id: 471195F6-F248-11E8-B48F-1D18A9856A87 last_name: Cheung orcid: 0000-0001-8457-2572 - first_name: Ximena full_name: Contreras, Ximena id: 475990FE-F248-11E8-B48F-1D18A9856A87 last_name: Contreras - first_name: Andi H full_name: Hansen, Andi H id: 38853E16-F248-11E8-B48F-1D18A9856A87 last_name: Hansen - first_name: Simon full_name: Hippenmeyer, Simon id: 37B36620-F248-11E8-B48F-1D18A9856A87 last_name: Hippenmeyer orcid: 0000-0003-2279-1061 citation: ama: Beattie RJ, Streicher C, Amberg N, et al. Lineage tracing and clonal analysis in developing cerebral cortex using mosaic analysis with double markers (MADM). Journal of Visual Experiments. 2020;(159). doi:10.3791/61147 apa: Beattie, R. J., Streicher, C., Amberg, N., Cheung, G. T., Contreras, X., Hansen, A. H., & Hippenmeyer, S. (2020). Lineage tracing and clonal analysis in developing cerebral cortex using mosaic analysis with double markers (MADM). Journal of Visual Experiments. MyJove Corporation. https://doi.org/10.3791/61147 chicago: Beattie, Robert J, Carmen Streicher, Nicole Amberg, Giselle T Cheung, Ximena Contreras, Andi H Hansen, and Simon Hippenmeyer. “Lineage Tracing and Clonal Analysis in Developing Cerebral Cortex Using Mosaic Analysis with Double Markers (MADM).” Journal of Visual Experiments. MyJove Corporation, 2020. https://doi.org/10.3791/61147. ieee: R. J. Beattie et al., “Lineage tracing and clonal analysis in developing cerebral cortex using mosaic analysis with double markers (MADM),” Journal of Visual Experiments, no. 159. MyJove Corporation, 2020. ista: Beattie RJ, Streicher C, Amberg N, Cheung GT, Contreras X, Hansen AH, Hippenmeyer S. 2020. Lineage tracing and clonal analysis in developing cerebral cortex using mosaic analysis with double markers (MADM). Journal of Visual Experiments. (159), e61147. mla: Beattie, Robert J., et al. “Lineage Tracing and Clonal Analysis in Developing Cerebral Cortex Using Mosaic Analysis with Double Markers (MADM).” Journal of Visual Experiments, no. 159, e61147, MyJove Corporation, 2020, doi:10.3791/61147. short: R.J. Beattie, C. Streicher, N. Amberg, G.T. Cheung, X. Contreras, A.H. Hansen, S. Hippenmeyer, Journal of Visual Experiments (2020). date_created: 2020-05-11T08:31:20Z date_published: 2020-05-08T00:00:00Z date_updated: 2024-03-28T23:30:42Z day: '08' ddc: - '570' department: - _id: SiHi doi: 10.3791/61147 ec_funded: 1 external_id: isi: - '000546406600043' file: - access_level: open_access checksum: 3154ea7f90b9fb45e084cd1c2770597d content_type: application/pdf creator: rbeattie date_created: 2020-05-11T08:28:38Z date_updated: 2020-07-14T12:48:03Z file_id: '7816' file_name: jove-protocol-61147-lineage-tracing-clonal-analysis-developing-cerebral-cortex-using.pdf file_size: 1352186 relation: main_file file_date_updated: 2020-07-14T12:48:03Z has_accepted_license: '1' isi: 1 issue: '159' language: - iso: eng month: '05' oa: 1 oa_version: Published Version project: - _id: 264E56E2-B435-11E9-9278-68D0E5697425 call_identifier: FWF grant_number: M02416 name: Molecular Mechanisms Regulating Gliogenesis in the Cerebral Cortex - _id: 268F8446-B435-11E9-9278-68D0E5697425 call_identifier: FWF grant_number: T0101031 name: Role of Eed in neural stem cell lineage progression - _id: 260C2330-B435-11E9-9278-68D0E5697425 call_identifier: H2020 grant_number: '754411' name: ISTplus - Postdoctoral Fellowships - _id: 2625A13E-B435-11E9-9278-68D0E5697425 grant_number: '24812' name: Molecular Mechanisms of Radial Neuronal Migration - _id: 260018B0-B435-11E9-9278-68D0E5697425 call_identifier: H2020 grant_number: '725780' name: Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development publication: Journal of Visual Experiments publication_identifier: issn: - 1940-087X publication_status: published publisher: MyJove Corporation quality_controlled: '1' related_material: record: - id: '7902' relation: part_of_dissertation status: public scopus_import: '1' status: public title: Lineage tracing and clonal analysis in developing cerebral cortex using mosaic analysis with double markers (MADM) 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 year: '2020' ... --- _id: '7902' abstract: - lang: eng text: "Mosaic genetic analysis has been widely used in different model organisms such as the fruit fly to study gene-function in a cell-autonomous or tissue-specific fashion. More recently, and less easily conducted, mosaic genetic analysis in mice has also been enabled with the ambition to shed light on human gene function and disease. These genetic tools are of particular interest, but not restricted to, the study of the brain. Notably, the MADM technology offers a genetic approach in mice to visualize and concomitantly manipulate small subsets of genetically defined cells at a clonal level and single cell resolution. MADM-based analysis has already advanced the study of genetic mechanisms regulating brain development and is expected that further MADM-based analysis of genetic alterations will continue to reveal important insights on the fundamental principles of development and disease to potentially assist in the development of new therapies or treatments.\r\nIn summary, this work completed and characterized the necessary genome-wide genetic tools to perform MADM-based analysis at single cell level of the vast majority of mouse genes in virtually any cell type and provided a protocol to perform lineage tracing using the novel MADM resource. Importantly, this work also explored and revealed novel aspects of biologically relevant events in an in vivo context, such as the chromosome-specific bias of chromatid sister segregation pattern, the generation of cell-type diversity in the cerebral cortex and in the cerebellum and finally, the relevance of the interplay between the cell-autonomous gene function and cell-non-autonomous (community) effects in radial glial progenitor lineage progression.\r\nThis work provides a foundation and opens the door to further elucidating the molecular mechanisms underlying neuronal diversity and astrocyte generation." acknowledged_ssus: - _id: PreCl - _id: Bio alternative_title: - ISTA Thesis article_processing_charge: No author: - first_name: Ximena full_name: Contreras, Ximena id: 475990FE-F248-11E8-B48F-1D18A9856A87 last_name: Contreras citation: ama: Contreras X. Genetic dissection of neural development in health and disease at single cell resolution. 2020. doi:10.15479/AT:ISTA:7902 apa: Contreras, X. (2020). Genetic dissection of neural development in health and disease at single cell resolution. Institute of Science and Technology Austria. https://doi.org/10.15479/AT:ISTA:7902 chicago: Contreras, Ximena. “Genetic Dissection of Neural Development in Health and Disease at Single Cell Resolution.” Institute of Science and Technology Austria, 2020. https://doi.org/10.15479/AT:ISTA:7902. ieee: X. Contreras, “Genetic dissection of neural development in health and disease at single cell resolution,” Institute of Science and Technology Austria, 2020. ista: Contreras X. 2020. Genetic dissection of neural development in health and disease at single cell resolution. Institute of Science and Technology Austria. mla: Contreras, Ximena. Genetic Dissection of Neural Development in Health and Disease at Single Cell Resolution. Institute of Science and Technology Austria, 2020, doi:10.15479/AT:ISTA:7902. short: X. Contreras, Genetic Dissection of Neural Development in Health and Disease at Single Cell Resolution, Institute of Science and Technology Austria, 2020. date_created: 2020-05-29T08:27:32Z date_published: 2020-06-05T00:00:00Z date_updated: 2023-10-18T08:45:16Z day: '05' ddc: - '570' degree_awarded: PhD department: - _id: SiHi doi: 10.15479/AT:ISTA:7902 ec_funded: 1 file: - access_level: closed checksum: 43c172bf006c95b65992d473c7240d13 content_type: application/vnd.openxmlformats-officedocument.wordprocessingml.document creator: xcontreras date_created: 2020-06-05T08:18:08Z date_updated: 2021-06-07T22:30:03Z embargo_to: open_access file_id: '7927' file_name: PhDThesis_Contreras.docx file_size: 53134142 relation: source_file - access_level: open_access checksum: addfed9128271be05cae3608e03a6ec0 content_type: application/pdf creator: xcontreras date_created: 2020-06-05T08:18:07Z date_updated: 2021-06-07T22:30:03Z embargo: 2021-06-06 file_id: '7928' file_name: PhDThesis_Contreras.pdf file_size: 35117191 relation: main_file file_date_updated: 2021-06-07T22:30:03Z has_accepted_license: '1' language: - iso: eng month: '06' oa: 1 oa_version: Published Version page: '214' project: - _id: 260018B0-B435-11E9-9278-68D0E5697425 call_identifier: H2020 grant_number: '725780' name: Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development publication_identifier: issn: - 2663-337X publication_status: published publisher: Institute of Science and Technology Austria related_material: record: - id: '6830' relation: dissertation_contains status: public - id: '28' relation: dissertation_contains status: public - id: '7815' relation: dissertation_contains status: public status: public supervisor: - first_name: Simon full_name: Hippenmeyer, Simon id: 37B36620-F248-11E8-B48F-1D18A9856A87 last_name: Hippenmeyer orcid: 0000-0003-2279-1061 title: Genetic dissection of neural development in health and disease at single cell resolution type: dissertation user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 year: '2020' ... --- _id: '6091' abstract: - lang: eng text: Cortical networks are characterized by sparse connectivity, with synapses found at only a subset of axo-dendritic contacts. Yet within these networks, neurons can exhibit high connection probabilities, suggesting that cell-intrinsic factors, not proximity, determine connectivity. Here, we identify ephrin-B3 (eB3) as a factor that determines synapse density by mediating a cell-cell competition that requires ephrin-B-EphB signaling. In a microisland culture system designed to isolate cell-cell competition, we find that eB3 determines winning and losing neurons in a contest for synapses. In a Mosaic Analysis with Double Markers (MADM) genetic mouse model system in vivo the relative levels of eB3 control spine density in layer 5 and 6 neurons. MADM cortical neurons in vitro reveal that eB3 controls synapse density independently of action potential-driven activity. Our findings illustrate a new class of competitive mechanism mediated by trans-synaptic organizing proteins which control the number of synapses neurons receive relative to neighboring neurons. article_number: e41563 article_processing_charge: No author: - first_name: Nathan T. full_name: Henderson, Nathan T. last_name: Henderson - first_name: Sylvain J. full_name: Le Marchand, Sylvain J. last_name: Le Marchand - first_name: Martin full_name: Hruska, Martin last_name: Hruska - 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 - first_name: Matthew B. full_name: Dalva, Matthew B. last_name: Dalva citation: ama: Henderson NT, Le Marchand SJ, Hruska M, Hippenmeyer S, Luo L, Dalva MB. Ephrin-B3 controls excitatory synapse density through cell-cell competition for EphBs. eLife. 2019;8. doi:10.7554/eLife.41563 apa: Henderson, N. T., Le Marchand, S. J., Hruska, M., Hippenmeyer, S., Luo, L., & Dalva, M. B. (2019). Ephrin-B3 controls excitatory synapse density through cell-cell competition for EphBs. ELife. eLife Sciences Publications. https://doi.org/10.7554/eLife.41563 chicago: Henderson, Nathan T., Sylvain J. Le Marchand, Martin Hruska, Simon Hippenmeyer, Liqun Luo, and Matthew B. Dalva. “Ephrin-B3 Controls Excitatory Synapse Density through Cell-Cell Competition for EphBs.” ELife. eLife Sciences Publications, 2019. https://doi.org/10.7554/eLife.41563. ieee: N. T. Henderson, S. J. Le Marchand, M. Hruska, S. Hippenmeyer, L. Luo, and M. B. Dalva, “Ephrin-B3 controls excitatory synapse density through cell-cell competition for EphBs,” eLife, vol. 8. eLife Sciences Publications, 2019. ista: Henderson NT, Le Marchand SJ, Hruska M, Hippenmeyer S, Luo L, Dalva MB. 2019. Ephrin-B3 controls excitatory synapse density through cell-cell competition for EphBs. eLife. 8, e41563. mla: Henderson, Nathan T., et al. “Ephrin-B3 Controls Excitatory Synapse Density through Cell-Cell Competition for EphBs.” ELife, vol. 8, e41563, eLife Sciences Publications, 2019, doi:10.7554/eLife.41563. short: N.T. Henderson, S.J. Le Marchand, M. Hruska, S. Hippenmeyer, L. Luo, M.B. Dalva, ELife 8 (2019). date_created: 2019-03-10T22:59:20Z date_published: 2019-02-21T00:00:00Z date_updated: 2023-08-24T14:50:50Z day: '21' ddc: - '570' department: - _id: SiHi doi: 10.7554/eLife.41563 external_id: isi: - '000459380600001' pmid: - '30789343' file: - access_level: open_access checksum: 7b0800d003f14cd06b1802dea0c52941 content_type: application/pdf creator: dernst date_created: 2019-03-11T16:15:37Z date_updated: 2020-07-14T12:47:19Z file_id: '6098' file_name: 2019_eLife_Henderson.pdf file_size: 7260753 relation: main_file file_date_updated: 2020-07-14T12:47:19Z has_accepted_license: '1' intvolume: ' 8' isi: 1 language: - iso: eng month: '02' oa: 1 oa_version: Published Version pmid: 1 publication: eLife publication_status: published publisher: eLife Sciences Publications quality_controlled: '1' scopus_import: '1' status: public title: Ephrin-B3 controls excitatory synapse density through cell-cell competition for EphBs 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: 4359f0d1-fa6c-11eb-b949-802e58b17ae8 volume: 8 year: '2019' ... --- _id: '6844' abstract: - lang: eng text: Studying the progression of the proliferative and differentiative patterns of neural stem cells at the individual cell level is crucial to the understanding of cortex development and how the disruption of such patterns can lead to malformations and neurodevelopmental diseases. However, our understanding of the precise lineage progression programme at single-cell resolution is still incomplete due to the technical variations in lineage- tracing approaches. One of the key challenges involves developing a robust theoretical framework in which we can integrate experimental observations and introduce correction factors to obtain a reliable and representative description of the temporal modulation of proliferation and differentiation. In order to obtain more conclusive insights, we carry out virtual clonal analysis using mathematical modelling and compare our results against experimental data. Using a dataset obtained with Mosaic Analysis with Double Markers, we illustrate how the theoretical description can be exploited to interpret and reconcile the disparity between virtual and experimental results. article_processing_charge: No article_type: original author: - first_name: Noemi full_name: Picco, Noemi last_name: Picco - first_name: Simon full_name: Hippenmeyer, Simon id: 37B36620-F248-11E8-B48F-1D18A9856A87 last_name: Hippenmeyer orcid: 0000-0003-2279-1061 - first_name: Julio full_name: Rodarte, Julio id: 3C70A038-F248-11E8-B48F-1D18A9856A87 last_name: Rodarte - first_name: Carmen full_name: Streicher, Carmen id: 36BCB99C-F248-11E8-B48F-1D18A9856A87 last_name: Streicher - first_name: Zoltán full_name: Molnár, Zoltán last_name: Molnár - first_name: Philip K. full_name: Maini, Philip K. last_name: Maini - first_name: Thomas E. full_name: Woolley, Thomas E. last_name: Woolley citation: ama: Picco N, Hippenmeyer S, Rodarte J, et al. A mathematical insight into cell labelling experiments for clonal analysis. Journal of Anatomy. 2019;235(3):686-696. doi:10.1111/joa.13001 apa: Picco, N., Hippenmeyer, S., Rodarte, J., Streicher, C., Molnár, Z., Maini, P. K., & Woolley, T. E. (2019). A mathematical insight into cell labelling experiments for clonal analysis. Journal of Anatomy. Wiley. https://doi.org/10.1111/joa.13001 chicago: Picco, Noemi, Simon Hippenmeyer, Julio Rodarte, Carmen Streicher, Zoltán Molnár, Philip K. Maini, and Thomas E. Woolley. “A Mathematical Insight into Cell Labelling Experiments for Clonal Analysis.” Journal of Anatomy. Wiley, 2019. https://doi.org/10.1111/joa.13001. ieee: N. Picco et al., “A mathematical insight into cell labelling experiments for clonal analysis,” Journal of Anatomy, vol. 235, no. 3. Wiley, pp. 686–696, 2019. ista: Picco N, Hippenmeyer S, Rodarte J, Streicher C, Molnár Z, Maini PK, Woolley TE. 2019. A mathematical insight into cell labelling experiments for clonal analysis. Journal of Anatomy. 235(3), 686–696. mla: Picco, Noemi, et al. “A Mathematical Insight into Cell Labelling Experiments for Clonal Analysis.” Journal of Anatomy, vol. 235, no. 3, Wiley, 2019, pp. 686–96, doi:10.1111/joa.13001. short: N. Picco, S. Hippenmeyer, J. Rodarte, C. Streicher, Z. Molnár, P.K. Maini, T.E. Woolley, Journal of Anatomy 235 (2019) 686–696. date_created: 2019-09-02T11:57:28Z date_published: 2019-09-01T00:00:00Z date_updated: 2023-08-29T07:19:39Z day: '01' ddc: - '570' department: - _id: SiHi doi: 10.1111/joa.13001 ec_funded: 1 external_id: isi: - '000482426800017' file: - access_level: open_access checksum: 160f960844b204057f20896e0e1f8ee7 content_type: application/pdf creator: dernst date_created: 2019-09-02T12:05:18Z date_updated: 2020-07-14T12:47:42Z file_id: '6845' file_name: 2019_JournalAnatomy_Picco.pdf file_size: 1192994 relation: main_file file_date_updated: 2020-07-14T12:47:42Z has_accepted_license: '1' intvolume: ' 235' isi: 1 issue: '3' language: - iso: eng license: https://creativecommons.org/licenses/by-nc/4.0/ month: '09' oa: 1 oa_version: Published Version page: 686-696 project: - _id: 260018B0-B435-11E9-9278-68D0E5697425 call_identifier: H2020 grant_number: '725780' name: Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development publication: Journal of Anatomy publication_identifier: eissn: - 1469-7580 issn: - 0021-8782 publication_status: published publisher: Wiley quality_controlled: '1' scopus_import: '1' status: public title: A mathematical insight into cell labelling experiments for clonal analysis tmp: image: /images/cc_by_nc.png legal_code_url: https://creativecommons.org/licenses/by-nc/4.0/legalcode name: Creative Commons Attribution-NonCommercial 4.0 International (CC BY-NC 4.0) short: CC BY-NC (4.0) type: journal_article user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8 volume: 235 year: '2019' ... --- _id: '7005' abstract: - lang: eng text: Activity-dependent bulk endocytosis generates synaptic vesicles (SVs) during intense neuronal activity via a two-step process. First, bulk endosomes are formed direct from the plasma membrane from which SVs are then generated. SV generation from bulk endosomes requires the efflux of previously accumulated calcium and activation of the protein phosphatase calcineurin. However, it is still unknown how calcineurin mediates SV generation. We addressed this question using a series of acute interventions that decoupled the generation of SVs from bulk endosomes in rat primary neuronal culture. This was achieved by either disruption of protein–protein interactions via delivery of competitive peptides, or inhibition of enzyme activity by known inhibitors. SV generation was monitored using either a morphological horseradish peroxidase assay or an optical assay that monitors the replenishment of the reserve SV pool. We found that SV generation was inhibited by, (i) peptides that disrupt calcineurin interactions, (ii) an inhibitor of dynamin I GTPase activity and (iii) peptides that disrupt the phosphorylation-dependent dynamin I–syndapin I interaction. Peptides that disrupted syndapin I interactions with eps15 homology domain-containing proteins had no effect. This revealed that (i) calcineurin must be localized at bulk endosomes to mediate its effect, (ii) dynamin I GTPase activity is essential for SV fission and (iii) the calcineurin-dependent interaction between dynamin I and syndapin I is essential for SV generation. We therefore propose that a calcineurin-dependent dephosphorylation cascade that requires both dynamin I GTPase and syndapin I lipid-deforming activity is essential for SV generation from bulk endosomes. article_processing_charge: No article_type: original author: - first_name: Giselle T full_name: Cheung, Giselle T id: 471195F6-F248-11E8-B48F-1D18A9856A87 last_name: Cheung orcid: 0000-0001-8457-2572 - first_name: Michael A. full_name: Cousin, Michael A. last_name: Cousin citation: ama: Cheung GT, Cousin MA. Synaptic vesicle generation from activity‐dependent bulk endosomes requires a dephosphorylation‐dependent dynamin–syndapin interaction. Journal of Neurochemistry. 2019;151(5):570-583. doi:10.1111/jnc.14862 apa: Cheung, G. T., & Cousin, M. A. (2019). Synaptic vesicle generation from activity‐dependent bulk endosomes requires a dephosphorylation‐dependent dynamin–syndapin interaction. Journal of Neurochemistry. Wiley. https://doi.org/10.1111/jnc.14862 chicago: Cheung, Giselle T, and Michael A. Cousin. “Synaptic Vesicle Generation from Activity‐dependent Bulk Endosomes Requires a Dephosphorylation‐dependent Dynamin–Syndapin Interaction.” Journal of Neurochemistry. Wiley, 2019. https://doi.org/10.1111/jnc.14862. ieee: G. T. Cheung and M. A. Cousin, “Synaptic vesicle generation from activity‐dependent bulk endosomes requires a dephosphorylation‐dependent dynamin–syndapin interaction,” Journal of Neurochemistry, vol. 151, no. 5. Wiley, pp. 570–583, 2019. ista: Cheung GT, Cousin MA. 2019. Synaptic vesicle generation from activity‐dependent bulk endosomes requires a dephosphorylation‐dependent dynamin–syndapin interaction. Journal of Neurochemistry. 151(5), 570–583. mla: Cheung, Giselle T., and Michael A. Cousin. “Synaptic Vesicle Generation from Activity‐dependent Bulk Endosomes Requires a Dephosphorylation‐dependent Dynamin–Syndapin Interaction.” Journal of Neurochemistry, vol. 151, no. 5, Wiley, 2019, pp. 570–83, doi:10.1111/jnc.14862. short: G.T. Cheung, M.A. Cousin, Journal of Neurochemistry 151 (2019) 570–583. date_created: 2019-11-12T14:37:08Z date_published: 2019-12-01T00:00:00Z date_updated: 2023-08-30T07:21:50Z day: '01' ddc: - '570' department: - _id: SiHi doi: 10.1111/jnc.14862 external_id: isi: - '000490703100001' pmid: - '31479508' file: - access_level: open_access checksum: ec1fb2aebb874009bc309adaada6e1d7 content_type: application/pdf creator: dernst date_created: 2020-02-05T10:30:02Z date_updated: 2020-07-14T12:47:47Z file_id: '7452' file_name: 2019_JournNeurochemistry_Cheung.pdf file_size: 4334962 relation: main_file file_date_updated: 2020-07-14T12:47:47Z has_accepted_license: '1' intvolume: ' 151' isi: 1 issue: '5' language: - iso: eng month: '12' oa: 1 oa_version: Published Version page: 570-583 pmid: 1 publication: Journal of Neurochemistry publication_identifier: eissn: - 1471-4159 issn: - 0022-3042 publication_status: published publisher: Wiley quality_controlled: '1' scopus_import: '1' status: public title: Synaptic vesicle generation from activity‐dependent bulk endosomes requires a dephosphorylation‐dependent dynamin–syndapin interaction 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: 4359f0d1-fa6c-11eb-b949-802e58b17ae8 volume: 151 year: '2019' ... --- _id: '6455' abstract: - lang: eng text: During corticogenesis, distinct subtypes of neurons are sequentially born from ventricular zone progenitors. How these cells are molecularly temporally patterned is poorly understood. We used single-cell RNA sequencing at high temporal resolution to trace the lineage of the molecular identities of successive generations of apical progenitors (APs) and their daughter neurons in mouse embryos. We identified a core set of evolutionarily conserved, temporally patterned genes that drive APs from internally driven to more exteroceptive states. We found that the Polycomb repressor complex 2 (PRC2) epigenetically regulates AP temporal progression. Embryonic age–dependent AP molecular states are transmitted to their progeny as successive ground states, onto which essentially conserved early postmitotic differentiation programs are applied, and are complemented by later-occurring environment-dependent signals. Thus, epigenetically regulated temporal molecular birthmarks present in progenitors act in their postmitotic progeny to seed adult neuronal diversity. article_number: eaav2522 article_processing_charge: No article_type: original author: - first_name: L full_name: Telley, L last_name: Telley - first_name: G full_name: Agirman, G last_name: Agirman - first_name: J full_name: Prados, J last_name: Prados - first_name: Nicole full_name: Amberg, Nicole id: 4CD6AAC6-F248-11E8-B48F-1D18A9856A87 last_name: Amberg orcid: 0000-0002-3183-8207 - first_name: S full_name: Fièvre, S last_name: Fièvre - first_name: P full_name: Oberst, P last_name: Oberst - first_name: G full_name: Bartolini, G last_name: Bartolini - first_name: I full_name: Vitali, I last_name: Vitali - first_name: C full_name: Cadilhac, C last_name: Cadilhac - first_name: Simon full_name: Hippenmeyer, Simon id: 37B36620-F248-11E8-B48F-1D18A9856A87 last_name: Hippenmeyer orcid: 0000-0003-2279-1061 - first_name: L full_name: Nguyen, L last_name: Nguyen - first_name: A full_name: Dayer, A last_name: Dayer - first_name: D full_name: Jabaudon, D last_name: Jabaudon citation: ama: Telley L, Agirman G, Prados J, et al. Temporal patterning of apical progenitors and their daughter neurons in the developing neocortex. Science. 2019;364(6440). doi:10.1126/science.aav2522 apa: Telley, L., Agirman, G., Prados, J., Amberg, N., Fièvre, S., Oberst, P., … Jabaudon, D. (2019). Temporal patterning of apical progenitors and their daughter neurons in the developing neocortex. Science. AAAS. https://doi.org/10.1126/science.aav2522 chicago: Telley, L, G Agirman, J Prados, Nicole Amberg, S Fièvre, P Oberst, G Bartolini, et al. “Temporal Patterning of Apical Progenitors and Their Daughter Neurons in the Developing Neocortex.” Science. AAAS, 2019. https://doi.org/10.1126/science.aav2522. ieee: L. Telley et al., “Temporal patterning of apical progenitors and their daughter neurons in the developing neocortex,” Science, vol. 364, no. 6440. AAAS, 2019. ista: Telley L, Agirman G, Prados J, Amberg N, Fièvre S, Oberst P, Bartolini G, Vitali I, Cadilhac C, Hippenmeyer S, Nguyen L, Dayer A, Jabaudon D. 2019. Temporal patterning of apical progenitors and their daughter neurons in the developing neocortex. Science. 364(6440), eaav2522. mla: Telley, L., et al. “Temporal Patterning of Apical Progenitors and Their Daughter Neurons in the Developing Neocortex.” Science, vol. 364, no. 6440, eaav2522, AAAS, 2019, doi:10.1126/science.aav2522. short: L. Telley, G. Agirman, J. Prados, N. Amberg, S. Fièvre, P. Oberst, G. Bartolini, I. Vitali, C. Cadilhac, S. Hippenmeyer, L. Nguyen, A. Dayer, D. Jabaudon, Science 364 (2019). date_created: 2019-05-14T13:07:47Z date_published: 2019-05-10T00:00:00Z date_updated: 2023-09-05T11:51:09Z day: '10' department: - _id: SiHi doi: 10.1126/science.aav2522 ec_funded: 1 external_id: isi: - '000467631800034' pmid: - '31073041' intvolume: ' 364' isi: 1 issue: '6440' language: - iso: eng main_file_link: - open_access: '1' url: https://orbi.uliege.be/bitstream/2268/239604/1/Telley_Agirman_Science2019.pdf month: '05' oa: 1 oa_version: Published Version pmid: 1 project: - _id: 260018B0-B435-11E9-9278-68D0E5697425 call_identifier: H2020 grant_number: '725780' name: Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development - _id: 268F8446-B435-11E9-9278-68D0E5697425 call_identifier: FWF grant_number: T0101031 name: Role of Eed in neural stem cell lineage progression publication: Science publication_identifier: eissn: - 1095-9203 issn: - 0036-8075 publication_status: published publisher: AAAS quality_controlled: '1' related_material: link: - description: News on IST Homepage relation: press_release url: https://ist.ac.at/en/news/how-to-generate-a-brain-of-correct-size-and-composition/ scopus_import: '1' status: public title: Temporal patterning of apical progenitors and their daughter neurons in the developing neocortex type: journal_article user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1 volume: 364 year: '2019' ... --- _id: '6454' abstract: - lang: eng text: 'Adult neural stem cells and multiciliated ependymalcells are glial cells essential for neurological func-tions. Together, they make up the adult neurogenicniche. Using both high-throughput clonal analysisand single-cell resolution of progenitor division pat-terns and fate, we show that these two componentsof the neurogenic niche are lineally related: adult neu-ral stem cells are sister cells to ependymal cells,whereas most ependymal cells arise from the termi-nal symmetric divisions of the lineage. Unexpectedly,we found that the antagonist regulators of DNA repli-cation, GemC1 and Geminin, can tune the proportionof neural stem cells and ependymal cells. Our find-ings reveal the controlled dynamic of the neurogenicniche ontogeny and identify the Geminin familymembers as key regulators of the initial pool of adultneural stem cells.' article_processing_charge: No author: - first_name: G full_name: Ortiz-Álvarez, G last_name: Ortiz-Álvarez - first_name: M full_name: Daclin, M last_name: Daclin - first_name: A full_name: Shihavuddin, A last_name: Shihavuddin - first_name: P full_name: Lansade, P last_name: Lansade - first_name: A full_name: Fortoul, A last_name: Fortoul - first_name: M full_name: Faucourt, M last_name: Faucourt - first_name: S full_name: Clavreul, S last_name: Clavreul - first_name: ME full_name: Lalioti, ME last_name: Lalioti - first_name: S full_name: Taraviras, S last_name: Taraviras - first_name: Simon full_name: Hippenmeyer, Simon id: 37B36620-F248-11E8-B48F-1D18A9856A87 last_name: Hippenmeyer orcid: 0000-0003-2279-1061 - first_name: J full_name: Livet, J last_name: Livet - first_name: A full_name: Meunier, A last_name: Meunier - first_name: A full_name: Genovesio, A last_name: Genovesio - first_name: N full_name: Spassky, N last_name: Spassky citation: ama: Ortiz-Álvarez G, Daclin M, Shihavuddin A, et al. Adult neural stem cells and multiciliated ependymal cells share a common lineage regulated by the Geminin family members. Neuron. 2019;102(1):159-172.e7. doi:10.1016/j.neuron.2019.01.051 apa: Ortiz-Álvarez, G., Daclin, M., Shihavuddin, A., Lansade, P., Fortoul, A., Faucourt, M., … Spassky, N. (2019). Adult neural stem cells and multiciliated ependymal cells share a common lineage regulated by the Geminin family members. Neuron. Elsevier. https://doi.org/10.1016/j.neuron.2019.01.051 chicago: Ortiz-Álvarez, G, M Daclin, A Shihavuddin, P Lansade, A Fortoul, M Faucourt, S Clavreul, et al. “Adult Neural Stem Cells and Multiciliated Ependymal Cells Share a Common Lineage Regulated by the Geminin Family Members.” Neuron. Elsevier, 2019. https://doi.org/10.1016/j.neuron.2019.01.051. ieee: G. Ortiz-Álvarez et al., “Adult neural stem cells and multiciliated ependymal cells share a common lineage regulated by the Geminin family members,” Neuron, vol. 102, no. 1. Elsevier, p. 159–172.e7, 2019. ista: Ortiz-Álvarez G, Daclin M, Shihavuddin A, Lansade P, Fortoul A, Faucourt M, Clavreul S, Lalioti M, Taraviras S, Hippenmeyer S, Livet J, Meunier A, Genovesio A, Spassky N. 2019. Adult neural stem cells and multiciliated ependymal cells share a common lineage regulated by the Geminin family members. Neuron. 102(1), 159–172.e7. mla: Ortiz-Álvarez, G., et al. “Adult Neural Stem Cells and Multiciliated Ependymal Cells Share a Common Lineage Regulated by the Geminin Family Members.” Neuron, vol. 102, no. 1, Elsevier, 2019, p. 159–172.e7, doi:10.1016/j.neuron.2019.01.051. short: G. Ortiz-Álvarez, M. Daclin, A. Shihavuddin, P. Lansade, A. Fortoul, M. Faucourt, S. Clavreul, M. Lalioti, S. Taraviras, S. Hippenmeyer, J. Livet, A. Meunier, A. Genovesio, N. Spassky, Neuron 102 (2019) 159–172.e7. date_created: 2019-05-14T13:06:30Z date_published: 2019-04-03T00:00:00Z date_updated: 2023-09-05T13:02:21Z day: '03' ddc: - '570' department: - _id: SiHi doi: 10.1016/j.neuron.2019.01.051 ec_funded: 1 external_id: isi: - '000463337900018' pmid: - '30824354' file: - access_level: open_access checksum: 1fb6e195c583eb0c5cabf26f69ff6675 content_type: application/pdf creator: dernst date_created: 2019-05-15T09:28:41Z date_updated: 2020-07-14T12:47:30Z file_id: '6457' file_name: 2019_Neuron_Ortiz.pdf file_size: 7288572 relation: main_file file_date_updated: 2020-07-14T12:47:30Z has_accepted_license: '1' intvolume: ' 102' isi: 1 issue: '1' language: - iso: eng month: '04' oa: 1 oa_version: Published Version page: 159-172.e7 pmid: 1 project: - _id: 260018B0-B435-11E9-9278-68D0E5697425 call_identifier: H2020 grant_number: '725780' name: Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development publication: Neuron publication_identifier: eissn: - 1097-4199 issn: - 0896-6273 publication_status: published publisher: Elsevier quality_controlled: '1' scopus_import: '1' status: public title: Adult neural stem cells and multiciliated ependymal cells share a common lineage regulated by the Geminin family members 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: c635000d-4b10-11ee-a964-aac5a93f6ac1 volume: 102 year: '2019' ...