--- _id: '14826' abstract: - lang: eng text: The plant-signaling molecule auxin triggers fast and slow cellular responses across land plants and algae. The nuclear auxin pathway mediates gene expression and controls growth and development in land plants, but this pathway is absent from algal sister groups. Several components of rapid responses have been identified in Arabidopsis, but it is unknown if these are part of a conserved mechanism. We recently identified a fast, proteome-wide phosphorylation response to auxin. Here, we show that this response occurs across 5 land plant and algal species and converges on a core group of shared targets. We found conserved rapid physiological responses to auxin in the same species and identified rapidly accelerated fibrosarcoma (RAF)-like protein kinases as central mediators of auxin-triggered phosphorylation across species. Genetic analysis connects this kinase to both auxin-triggered protein phosphorylation and rapid cellular response, thus identifying an ancient mechanism for fast auxin responses in the green lineage. acknowledgement: 'We are grateful to Asuka Shitaku and Eri Koide for generating and sharing the Marchantia PRAF-mCitrine line and Peng-Cheng Wang for sharing the Arabidopsis raf mutant. We are grateful to our team members for discussions and helpful advice. This work was supported by funding from the Netherlands Organization for Scientific Research (NWO): VICI grant 865.14.001 and ENW-KLEIN OCENW.KLEIN.027 grants to D.W.; VENI grant VI.VENI.212.003 to A.K.; the European Research Council AdG DIRNDL (contract number 833867) to D.W.; CoG CATCH to J.S.; StG CELLONGATE (contract 803048) to M.F.; and AdG ETAP (contract 742985) to J.F.; MEXT KAKENHI grant number JP19H05675 to T.K.; JSPS KAKENHI grant number JP20H03275 to R.N.; Takeda Science Foundation to R.N.; and the Austrian Science Fund (FWF, P29988) to J.F.' article_processing_charge: Yes (in subscription journal) article_type: original author: - first_name: Andre full_name: Kuhn, Andre last_name: Kuhn - first_name: Mark full_name: Roosjen, Mark last_name: Roosjen - first_name: Sumanth full_name: Mutte, Sumanth last_name: Mutte - first_name: Shiv Mani full_name: Dubey, Shiv Mani last_name: Dubey - first_name: Vanessa Polet full_name: Carrillo Carrasco, Vanessa Polet last_name: Carrillo Carrasco - first_name: Sjef full_name: Boeren, Sjef last_name: Boeren - first_name: Aline full_name: Monzer, Aline id: 2DB5D88C-D7B3-11E9-B8FD-7907E6697425 last_name: Monzer - first_name: Jasper full_name: Koehorst, Jasper last_name: Koehorst - first_name: Takayuki full_name: Kohchi, Takayuki last_name: Kohchi - first_name: Ryuichi full_name: Nishihama, Ryuichi last_name: Nishihama - first_name: Matyas full_name: Fendrych, Matyas id: 43905548-F248-11E8-B48F-1D18A9856A87 last_name: Fendrych orcid: 0000-0002-9767-8699 - first_name: Joris full_name: Sprakel, Joris last_name: Sprakel - first_name: Jiří full_name: Friml, Jiří id: 4159519E-F248-11E8-B48F-1D18A9856A87 last_name: Friml orcid: 0000-0002-8302-7596 - first_name: Dolf full_name: Weijers, Dolf last_name: Weijers citation: ama: Kuhn A, Roosjen M, Mutte S, et al. RAF-like protein kinases mediate a deeply conserved, rapid auxin response. Cell. 2024;187(1):130-148.e17. doi:10.1016/j.cell.2023.11.021 apa: Kuhn, A., Roosjen, M., Mutte, S., Dubey, S. M., Carrillo Carrasco, V. P., Boeren, S., … Weijers, D. (2024). RAF-like protein kinases mediate a deeply conserved, rapid auxin response. Cell. Elsevier. https://doi.org/10.1016/j.cell.2023.11.021 chicago: Kuhn, Andre, Mark Roosjen, Sumanth Mutte, Shiv Mani Dubey, Vanessa Polet Carrillo Carrasco, Sjef Boeren, Aline Monzer, et al. “RAF-like Protein Kinases Mediate a Deeply Conserved, Rapid Auxin Response.” Cell. Elsevier, 2024. https://doi.org/10.1016/j.cell.2023.11.021. ieee: A. Kuhn et al., “RAF-like protein kinases mediate a deeply conserved, rapid auxin response,” Cell, vol. 187, no. 1. Elsevier, p. 130–148.e17, 2024. ista: Kuhn A, Roosjen M, Mutte S, Dubey SM, Carrillo Carrasco VP, Boeren S, Monzer A, Koehorst J, Kohchi T, Nishihama R, Fendrych M, Sprakel J, Friml J, Weijers D. 2024. RAF-like protein kinases mediate a deeply conserved, rapid auxin response. Cell. 187(1), 130–148.e17. mla: Kuhn, Andre, et al. “RAF-like Protein Kinases Mediate a Deeply Conserved, Rapid Auxin Response.” Cell, vol. 187, no. 1, Elsevier, 2024, p. 130–148.e17, doi:10.1016/j.cell.2023.11.021. short: A. Kuhn, M. Roosjen, S. Mutte, S.M. Dubey, V.P. Carrillo Carrasco, S. Boeren, A. Monzer, J. Koehorst, T. Kohchi, R. Nishihama, M. Fendrych, J. Sprakel, J. Friml, D. Weijers, Cell 187 (2024) 130–148.e17. date_created: 2024-01-17T12:45:40Z date_published: 2024-01-04T00:00:00Z date_updated: 2024-01-22T13:43:40Z day: '04' ddc: - '580' department: - _id: JiFr doi: 10.1016/j.cell.2023.11.021 ec_funded: 1 external_id: pmid: - '38128538' file: - access_level: open_access checksum: 06fd236a9ee0b46ccb05f44695bfc34b content_type: application/pdf creator: dernst date_created: 2024-01-22T13:41:41Z date_updated: 2024-01-22T13:41:41Z file_id: '14874' file_name: 2024_Cell_Kuhn.pdf file_size: 13194060 relation: main_file success: 1 file_date_updated: 2024-01-22T13:41:41Z has_accepted_license: '1' intvolume: ' 187' issue: '1' keyword: - General Biochemistry - Genetics and Molecular Biology language: - iso: eng license: https://creativecommons.org/licenses/by-nc/4.0/ month: '01' oa: 1 oa_version: Published Version page: 130-148.e17 pmid: 1 project: - _id: 261099A6-B435-11E9-9278-68D0E5697425 call_identifier: H2020 grant_number: '742985' name: Tracing Evolution of Auxin Transport and Polarity in Plants - _id: 262EF96E-B435-11E9-9278-68D0E5697425 call_identifier: FWF grant_number: P29988 name: RNA-directed DNA methylation in plant development publication: Cell publication_identifier: eissn: - 1097-4172 issn: - 0092-8674 publication_status: published publisher: Elsevier quality_controlled: '1' scopus_import: '1' status: public title: RAF-like protein kinases mediate a deeply conserved, rapid auxin response 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: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 187 year: '2024' ... --- _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 license: https://creativecommons.org/licenses/by/4.0/ 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: '10573' abstract: - lang: eng text: How tissues acquire complex shapes is a fundamental question in biology and regenerative medicine. Zebrafish semicircular canals form from invaginations in the otic epithelium (buds) that extend and fuse to form the hubs of each canal. We find that conventional actomyosin-driven behaviors are not required. Instead, local secretion of hyaluronan, made by the enzymes uridine 5′-diphosphate dehydrogenase (ugdh) and hyaluronan synthase 3 (has3), drives canal morphogenesis. Charged hyaluronate polymers osmotically swell with water and generate isotropic extracellular pressure to deform the overlying epithelium into buds. The mechanical anisotropy needed to shape buds into tubes is conferred by a polarized distribution of actomyosin and E-cadherin-rich membrane tethers, which we term cytocinches. Most work on tissue morphogenesis ascribes actomyosin contractility as the driving force, while the extracellular matrix shapes tissues through differential stiffness. Our work inverts this expectation. Hyaluronate pressure shaped by anisotropic tissue stiffness may be a widespread mechanism for powering morphological change in organogenesis and tissue engineering. acknowledgement: We thank Ian Swinburne, Sandy Nandagopal, and Toru Kawanishi for support, discussions, and reagents. We thank Vanessa Barone, Joseph Nasser, and members of the Megason lab for useful comments on the manuscript and general feedback. We are grateful to the Heisenberg and Knaut labs for transgenic fish. Diagrams on the right in the graphical abstract were created using BioRender. This work was supported by NIH R01DC015478 and NIH R01GM107733 to S.G.M. A.M. was supported by Human Frontiers Science Program LTF and NIH K99HD098918. article_processing_charge: No article_type: original author: - first_name: Akankshi full_name: Munjal, Akankshi last_name: Munjal - 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: Tony Y.C. full_name: Tsai, Tony Y.C. last_name: Tsai - first_name: Timothy J. full_name: Mitchison, Timothy J. last_name: Mitchison - first_name: Sean G. full_name: Megason, Sean G. last_name: Megason citation: ama: Munjal A, Hannezo EB, Tsai TYC, Mitchison TJ, Megason SG. Extracellular hyaluronate pressure shaped by cellular tethers drives tissue morphogenesis. Cell. 2021;184(26):6313-6325.e18. doi:10.1016/j.cell.2021.11.025 apa: Munjal, A., Hannezo, E. B., Tsai, T. Y. C., Mitchison, T. J., & Megason, S. G. (2021). Extracellular hyaluronate pressure shaped by cellular tethers drives tissue morphogenesis. Cell. Elsevier ; Cell Press. https://doi.org/10.1016/j.cell.2021.11.025 chicago: Munjal, Akankshi, Edouard B Hannezo, Tony Y.C. Tsai, Timothy J. Mitchison, and Sean G. Megason. “Extracellular Hyaluronate Pressure Shaped by Cellular Tethers Drives Tissue Morphogenesis.” Cell. Elsevier ; Cell Press, 2021. https://doi.org/10.1016/j.cell.2021.11.025. ieee: A. Munjal, E. B. Hannezo, T. Y. C. Tsai, T. J. Mitchison, and S. G. Megason, “Extracellular hyaluronate pressure shaped by cellular tethers drives tissue morphogenesis,” Cell, vol. 184, no. 26. Elsevier ; Cell Press, p. 6313–6325.e18, 2021. ista: Munjal A, Hannezo EB, Tsai TYC, Mitchison TJ, Megason SG. 2021. Extracellular hyaluronate pressure shaped by cellular tethers drives tissue morphogenesis. Cell. 184(26), 6313–6325.e18. mla: Munjal, Akankshi, et al. “Extracellular Hyaluronate Pressure Shaped by Cellular Tethers Drives Tissue Morphogenesis.” Cell, vol. 184, no. 26, Elsevier ; Cell Press, 2021, p. 6313–6325.e18, doi:10.1016/j.cell.2021.11.025. short: A. Munjal, E.B. Hannezo, T.Y.C. Tsai, T.J. Mitchison, S.G. Megason, Cell 184 (2021) 6313–6325.e18. date_created: 2021-12-26T23:01:26Z date_published: 2021-12-22T00:00:00Z date_updated: 2023-08-17T06:28:25Z day: '22' department: - _id: EdHa doi: 10.1016/j.cell.2021.11.025 external_id: isi: - '000735387500002' intvolume: ' 184' isi: 1 issue: '26' language: - iso: eng main_file_link: - open_access: '1' url: https://www.biorxiv.org/content/10.1101/2020.09.28.316042 month: '12' oa: 1 oa_version: Preprint page: 6313-6325.e18 publication: Cell publication_identifier: eissn: - 1097-4172 issn: - 0092-8674 publication_status: published publisher: Elsevier ; Cell Press quality_controlled: '1' scopus_import: '1' status: public title: Extracellular hyaluronate pressure shaped by cellular tethers drives tissue morphogenesis type: journal_article user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8 volume: 184 year: '2021' ... --- _id: '15151' abstract: - lang: eng text: Eukaryotic DNA-binding proteins operate in the context of chromatin, where nucleosomes are the elementary building blocks. Nucleosomal DNA is wrapped around a histone core, thereby rendering a large fraction of the DNA surface inaccessible to DNA-binding proteins. Nevertheless, first responders in DNA repair and sequence-specific transcription factors bind DNA target sites obstructed by chromatin. While early studies examined protein binding to histone-free DNA, it is only now beginning to emerge how DNA sequences are interrogated on nucleosomes. These readout strategies range from the release of nucleosomal DNA from histones, to rotational/translation register shifts of the DNA motif, and nucleosome-specific DNA binding modes that differ from those observed on naked DNA. Since DNA motif engagement on nucleosomes strongly depends on position and orientation, we argue that motif location and nucleosome positioning co-determine protein access to DNA in transcription and DNA repair. article_processing_charge: No article_type: review author: - first_name: Alicia full_name: Michael, Alicia id: 6437c950-2a03-11ee-914d-d6476dd7b75c last_name: Michael orcid: 0000-0002-6080-839X - first_name: Nicolas H. full_name: Thomä, Nicolas H. last_name: Thomä citation: ama: Michael AK, Thomä NH. Reading the chromatinized genome. Cell. 2021;184(14):3599-3611. doi:10.1016/j.cell.2021.05.029 apa: Michael, A. K., & Thomä, N. H. (2021). Reading the chromatinized genome. Cell. Elsevier. https://doi.org/10.1016/j.cell.2021.05.029 chicago: Michael, Alicia K., and Nicolas H. Thomä. “Reading the Chromatinized Genome.” Cell. Elsevier, 2021. https://doi.org/10.1016/j.cell.2021.05.029. ieee: A. K. Michael and N. H. Thomä, “Reading the chromatinized genome,” Cell, vol. 184, no. 14. Elsevier, pp. 3599–3611, 2021. ista: Michael AK, Thomä NH. 2021. Reading the chromatinized genome. Cell. 184(14), 3599–3611. mla: Michael, Alicia K., and Nicolas H. Thomä. “Reading the Chromatinized Genome.” Cell, vol. 184, no. 14, Elsevier, 2021, pp. 3599–611, doi:10.1016/j.cell.2021.05.029. short: A.K. Michael, N.H. Thomä, Cell 184 (2021) 3599–3611. date_created: 2024-03-21T07:54:19Z date_published: 2021-07-08T00:00:00Z date_updated: 2024-03-25T12:31:39Z day: '08' doi: 10.1016/j.cell.2021.05.029 extern: '1' intvolume: ' 184' issue: '14' keyword: - General Biochemistry - Genetics and Molecular Biology language: - iso: eng main_file_link: - open_access: '1' url: https://doi.org/10.1016/j.cell.2021.05.029 month: '07' oa: 1 oa_version: Published Version page: 3599-3611 publication: Cell publication_identifier: issn: - 0092-8674 publication_status: published publisher: Elsevier quality_controlled: '1' scopus_import: '1' status: public title: Reading the chromatinized genome type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 184 year: '2021' ... --- _id: '10348' abstract: - lang: eng text: The endosomal sorting complex required for transport-III (ESCRT-III) catalyzes membrane fission from within membrane necks, a process that is essential for many cellular functions, from cell division to lysosome degradation and autophagy. How it breaks membranes, though, remains unknown. Here, we characterize a sequential polymerization of ESCRT-III subunits that, driven by a recruitment cascade and by continuous subunit-turnover powered by the ATPase Vps4, induces membrane deformation and fission. During this process, the exchange of Vps24 for Did2 induces a tilt in the polymer-membrane interface, which triggers transition from flat spiral polymers to helical filament to drive the formation of membrane protrusions, and ends with the formation of a highly constricted Did2-Ist1 co-polymer that we show is competent to promote fission when bound on the inside of membrane necks. Overall, our results suggest a mechanism of stepwise changes in ESCRT-III filament structure and mechanical properties via exchange of the filament subunits to catalyze ESCRT-III activity. acknowledgement: The authors thank Nicolas Chiaruttini, Jean Gruenberg, and Lena Harker-Kirschneck for careful correction of this manuscript and helpful discussions. The authors want to thank the NCCR Chemical Biology for constant support during this project. A.R. acknowledges funding from the Swiss National Fund for Research (31003A_130520, 31003A_149975, and 31003A_173087) and the European Research Council Consolidator (311536). A.Š. acknowledges the European Research Council (802960). B.B. thanks the BBSRC (BB/K009001/1) and Wellcome Trust (203276/Z/16/Z) for support. J.M.v.F. acknowledges funding through an EMBO Long-Term Fellowship (ALTF 1065-2015), the European Commission FP7 (Marie Curie Actions, LTFCOFUND2013, and GA-2013-609409), and a Transitional Postdoc fellowship (2015/345) from the Swiss SystemsX.ch initiative, evaluated by the Swiss National Science Foundation and Swiss National Science Foundation Research (SNSF SINERGIA 160728/1 [leader, Sophie Martin]). article_processing_charge: No article_type: original author: - first_name: Anna-Katharina full_name: Pfitzner, Anna-Katharina last_name: Pfitzner - first_name: Vincent full_name: Mercier, Vincent last_name: Mercier - first_name: Xiuyun full_name: Jiang, Xiuyun last_name: Jiang - first_name: Joachim full_name: Moser von Filseck, Joachim last_name: Moser von Filseck - first_name: Buzz full_name: Baum, Buzz last_name: Baum - first_name: Anđela full_name: Šarić, Anđela id: bf63d406-f056-11eb-b41d-f263a6566d8b last_name: Šarić orcid: 0000-0002-7854-2139 - first_name: Aurélien full_name: Roux, Aurélien last_name: Roux citation: ama: Pfitzner A-K, Mercier V, Jiang X, et al. An ESCRT-III polymerization sequence drives membrane deformation and fission. Cell. 2020;182(5):1140-1155.e18. doi:10.1016/j.cell.2020.07.021 apa: Pfitzner, A.-K., Mercier, V., Jiang, X., Moser von Filseck, J., Baum, B., Šarić, A., & Roux, A. (2020). An ESCRT-III polymerization sequence drives membrane deformation and fission. Cell. Elsevier. https://doi.org/10.1016/j.cell.2020.07.021 chicago: Pfitzner, Anna-Katharina, Vincent Mercier, Xiuyun Jiang, Joachim Moser von Filseck, Buzz Baum, Anđela Šarić, and Aurélien Roux. “An ESCRT-III Polymerization Sequence Drives Membrane Deformation and Fission.” Cell. Elsevier, 2020. https://doi.org/10.1016/j.cell.2020.07.021. ieee: A.-K. Pfitzner et al., “An ESCRT-III polymerization sequence drives membrane deformation and fission,” Cell, vol. 182, no. 5. Elsevier, p. 1140–1155.e18, 2020. ista: Pfitzner A-K, Mercier V, Jiang X, Moser von Filseck J, Baum B, Šarić A, Roux A. 2020. An ESCRT-III polymerization sequence drives membrane deformation and fission. Cell. 182(5), 1140–1155.e18. mla: Pfitzner, Anna-Katharina, et al. “An ESCRT-III Polymerization Sequence Drives Membrane Deformation and Fission.” Cell, vol. 182, no. 5, Elsevier, 2020, p. 1140–1155.e18, doi:10.1016/j.cell.2020.07.021. short: A.-K. Pfitzner, V. Mercier, X. Jiang, J. Moser von Filseck, B. Baum, A. Šarić, A. Roux, Cell 182 (2020) 1140–1155.e18. date_created: 2021-11-26T08:02:27Z date_published: 2020-08-18T00:00:00Z date_updated: 2021-11-26T08:58:37Z day: '18' doi: 10.1016/j.cell.2020.07.021 extern: '1' external_id: pmid: - '32814015' intvolume: ' 182' issue: '5' keyword: - general biochemistry - genetics and molecular biology language: - iso: eng main_file_link: - open_access: '1' url: https://www.sciencedirect.com/science/article/pii/S0092867420309296 month: '08' oa: 1 oa_version: Published Version page: 1140-1155.e18 pmid: 1 publication: Cell publication_identifier: issn: - 0092-8674 publication_status: published publisher: Elsevier quality_controlled: '1' scopus_import: '1' status: public title: An ESCRT-III polymerization sequence drives membrane deformation and fission type: journal_article user_id: 8b945eb4-e2f2-11eb-945a-df72226e66a9 volume: 182 year: '2020' ... --- _id: '7001' acknowledged_ssus: - _id: PreCl - _id: Bio article_processing_charge: No article_type: original author: - first_name: Cornelia full_name: Schwayer, Cornelia id: 3436488C-F248-11E8-B48F-1D18A9856A87 last_name: Schwayer orcid: 0000-0001-5130-2226 - first_name: Shayan full_name: Shamipour, Shayan id: 40B34FE2-F248-11E8-B48F-1D18A9856A87 last_name: Shamipour - first_name: Kornelija full_name: Pranjic-Ferscha, Kornelija id: 4362B3C2-F248-11E8-B48F-1D18A9856A87 last_name: Pranjic-Ferscha - first_name: Alexandra full_name: Schauer, Alexandra id: 30A536BA-F248-11E8-B48F-1D18A9856A87 last_name: Schauer orcid: 0000-0001-7659-9142 - first_name: M full_name: Balda, M last_name: Balda - first_name: M full_name: Tada, M last_name: Tada - first_name: K full_name: Matter, K last_name: Matter - 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 citation: ama: Schwayer C, Shamipour S, Pranjic-Ferscha K, et al. Mechanosensation of tight junctions depends on ZO-1 phase separation and flow. Cell. 2019;179(4):937-952.e18. doi:10.1016/j.cell.2019.10.006 apa: Schwayer, C., Shamipour, S., Pranjic-Ferscha, K., Schauer, A., Balda, M., Tada, M., … Heisenberg, C.-P. J. (2019). Mechanosensation of tight junctions depends on ZO-1 phase separation and flow. Cell. Cell Press. https://doi.org/10.1016/j.cell.2019.10.006 chicago: Schwayer, Cornelia, Shayan Shamipour, Kornelija Pranjic-Ferscha, Alexandra Schauer, M Balda, M Tada, K Matter, and Carl-Philipp J Heisenberg. “Mechanosensation of Tight Junctions Depends on ZO-1 Phase Separation and Flow.” Cell. Cell Press, 2019. https://doi.org/10.1016/j.cell.2019.10.006. ieee: C. Schwayer et al., “Mechanosensation of tight junctions depends on ZO-1 phase separation and flow,” Cell, vol. 179, no. 4. Cell Press, p. 937–952.e18, 2019. ista: Schwayer C, Shamipour S, Pranjic-Ferscha K, Schauer A, Balda M, Tada M, Matter K, Heisenberg C-PJ. 2019. Mechanosensation of tight junctions depends on ZO-1 phase separation and flow. Cell. 179(4), 937–952.e18. mla: Schwayer, Cornelia, et al. “Mechanosensation of Tight Junctions Depends on ZO-1 Phase Separation and Flow.” Cell, vol. 179, no. 4, Cell Press, 2019, p. 937–952.e18, doi:10.1016/j.cell.2019.10.006. short: C. Schwayer, S. Shamipour, K. Pranjic-Ferscha, A. Schauer, M. Balda, M. Tada, K. Matter, C.-P.J. Heisenberg, Cell 179 (2019) 937–952.e18. date_created: 2019-11-12T12:51:06Z date_published: 2019-10-31T00:00:00Z date_updated: 2024-03-27T23:30:38Z day: '31' ddc: - '570' department: - _id: CaHe - _id: BjHo doi: 10.1016/j.cell.2019.10.006 ec_funded: 1 external_id: isi: - '000493898000012' pmid: - '31675500' file: - access_level: open_access checksum: 33dac4bb77ee630e2666e936b4d57980 content_type: application/pdf creator: dernst date_created: 2020-10-21T07:09:45Z date_updated: 2020-10-21T07:09:45Z file_id: '8684' file_name: 2019_Cell_Schwayer_accepted.pdf file_size: 8805878 relation: main_file success: 1 file_date_updated: 2020-10-21T07:09:45Z has_accepted_license: '1' intvolume: ' 179' isi: 1 issue: '4' language: - iso: eng month: '10' oa: 1 oa_version: Submitted Version page: 937-952.e18 pmid: 1 project: - _id: 260F1432-B435-11E9-9278-68D0E5697425 call_identifier: H2020 grant_number: '742573' name: Interaction and feedback between cell mechanics and fate specification in vertebrate gastrulation publication: Cell publication_identifier: eissn: - 1097-4172 issn: - 0092-8674 publication_status: published publisher: Cell Press quality_controlled: '1' related_material: link: - description: News auf IST Website relation: press_release url: https://ist.ac.at/en/news/biochemistry-meets-mechanics-the-sensitive-nature-of-cell-cell-contact-formation-in-embryo-development/ record: - id: '7186' relation: dissertation_contains status: public - id: '8350' relation: dissertation_contains status: public scopus_import: '1' status: public title: Mechanosensation of tight junctions depends on ZO-1 phase separation and flow type: journal_article user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8 volume: 179 year: '2019' ... --- _id: '6877' article_processing_charge: No article_type: original author: - first_name: Aglaja full_name: Kopf, Aglaja id: 31DAC7B6-F248-11E8-B48F-1D18A9856A87 last_name: Kopf orcid: 0000-0002-2187-6656 - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 citation: ama: Kopf A, Sixt MK. The neural crest pitches in to remove apoptotic debris. Cell. 2019;179(1):51-53. doi:10.1016/j.cell.2019.08.047 apa: Kopf, A., & Sixt, M. K. (2019). The neural crest pitches in to remove apoptotic debris. Cell. Elsevier. https://doi.org/10.1016/j.cell.2019.08.047 chicago: Kopf, Aglaja, and Michael K Sixt. “The Neural Crest Pitches in to Remove Apoptotic Debris.” Cell. Elsevier, 2019. https://doi.org/10.1016/j.cell.2019.08.047. ieee: A. Kopf and M. K. Sixt, “The neural crest pitches in to remove apoptotic debris,” Cell, vol. 179, no. 1. Elsevier, pp. 51–53, 2019. ista: Kopf A, Sixt MK. 2019. The neural crest pitches in to remove apoptotic debris. Cell. 179(1), 51–53. mla: Kopf, Aglaja, and Michael K. Sixt. “The Neural Crest Pitches in to Remove Apoptotic Debris.” Cell, vol. 179, no. 1, Elsevier, 2019, pp. 51–53, doi:10.1016/j.cell.2019.08.047. short: A. Kopf, M.K. Sixt, Cell 179 (2019) 51–53. date_created: 2019-09-15T22:00:46Z date_published: 2019-09-19T00:00:00Z date_updated: 2024-03-27T23:30:40Z day: '19' department: - _id: MiSi doi: 10.1016/j.cell.2019.08.047 external_id: isi: - '000486618500011' pmid: - '31539498' intvolume: ' 179' isi: 1 issue: '1' language: - iso: eng month: '09' oa_version: None page: 51-53 pmid: 1 publication: Cell publication_identifier: eissn: - 1097-4172 issn: - 0092-8674 publication_status: published publisher: Elsevier quality_controlled: '1' related_material: record: - id: '6891' relation: dissertation_contains status: public scopus_import: '1' status: public title: The neural crest pitches in to remove apoptotic debris type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 179 year: '2019' ... --- _id: '8436' abstract: - lang: eng text: The exchange of metabolites between the mitochondrial matrix and the cytosol depends on β-barrel channels in the outer membrane and α-helical carrier proteins in the inner membrane. The essential translocase of the inner membrane (TIM) chaperones escort these proteins through the intermembrane space, but the structural and mechanistic details remain elusive. We have used an integrated structural biology approach to reveal the functional principle of TIM chaperones. Multiple clamp-like binding sites hold the mitochondrial membrane proteins in a translocation-competent elongated form, thus mimicking characteristics of co-translational membrane insertion. The bound preprotein undergoes conformational dynamics within the chaperone binding clefts, pointing to a multitude of dynamic local binding events. Mutations in these binding sites cause cell death or growth defects associated with impairment of carrier and β-barrel protein biogenesis. Our work reveals how a single mitochondrial “transfer-chaperone” system is able to guide α-helical and β-barrel membrane proteins in a “nascent chain-like” conformation through a ribosome-free compartment. article_processing_charge: No article_type: original author: - first_name: Katharina full_name: Weinhäupl, Katharina last_name: Weinhäupl - first_name: Caroline full_name: Lindau, Caroline last_name: Lindau - first_name: Audrey full_name: Hessel, Audrey last_name: Hessel - first_name: Yong full_name: Wang, Yong last_name: Wang - first_name: Conny full_name: Schütze, Conny last_name: Schütze - first_name: Tobias full_name: Jores, Tobias last_name: Jores - first_name: Laura full_name: Melchionda, Laura last_name: Melchionda - first_name: Birgit full_name: Schönfisch, Birgit last_name: Schönfisch - first_name: Hubert full_name: Kalbacher, Hubert last_name: Kalbacher - first_name: Beate full_name: Bersch, Beate last_name: Bersch - first_name: Doron full_name: Rapaport, Doron last_name: Rapaport - first_name: Martha full_name: Brennich, Martha last_name: Brennich - first_name: Kresten full_name: Lindorff-Larsen, Kresten last_name: Lindorff-Larsen - first_name: Nils full_name: Wiedemann, Nils last_name: Wiedemann - first_name: Paul full_name: Schanda, Paul id: 7B541462-FAF6-11E9-A490-E8DFE5697425 last_name: Schanda orcid: 0000-0002-9350-7606 citation: ama: Weinhäupl K, Lindau C, Hessel A, et al. Structural basis of membrane protein chaperoning through the mitochondrial intermembrane space. Cell. 2018;175(5):1365-1379.e25. doi:10.1016/j.cell.2018.10.039 apa: Weinhäupl, K., Lindau, C., Hessel, A., Wang, Y., Schütze, C., Jores, T., … Schanda, P. (2018). Structural basis of membrane protein chaperoning through the mitochondrial intermembrane space. Cell. Elsevier. https://doi.org/10.1016/j.cell.2018.10.039 chicago: Weinhäupl, Katharina, Caroline Lindau, Audrey Hessel, Yong Wang, Conny Schütze, Tobias Jores, Laura Melchionda, et al. “Structural Basis of Membrane Protein Chaperoning through the Mitochondrial Intermembrane Space.” Cell. Elsevier, 2018. https://doi.org/10.1016/j.cell.2018.10.039. ieee: K. Weinhäupl et al., “Structural basis of membrane protein chaperoning through the mitochondrial intermembrane space,” Cell, vol. 175, no. 5. Elsevier, p. 1365–1379.e25, 2018. ista: Weinhäupl K, Lindau C, Hessel A, Wang Y, Schütze C, Jores T, Melchionda L, Schönfisch B, Kalbacher H, Bersch B, Rapaport D, Brennich M, Lindorff-Larsen K, Wiedemann N, Schanda P. 2018. Structural basis of membrane protein chaperoning through the mitochondrial intermembrane space. Cell. 175(5), 1365–1379.e25. mla: Weinhäupl, Katharina, et al. “Structural Basis of Membrane Protein Chaperoning through the Mitochondrial Intermembrane Space.” Cell, vol. 175, no. 5, Elsevier, 2018, p. 1365–1379.e25, doi:10.1016/j.cell.2018.10.039. short: K. Weinhäupl, C. Lindau, A. Hessel, Y. Wang, C. Schütze, T. Jores, L. Melchionda, B. Schönfisch, H. Kalbacher, B. Bersch, D. Rapaport, M. Brennich, K. Lindorff-Larsen, N. Wiedemann, P. Schanda, Cell 175 (2018) 1365–1379.e25. date_created: 2020-09-18T10:04:39Z date_published: 2018-11-15T00:00:00Z date_updated: 2021-01-12T08:19:15Z day: '15' doi: 10.1016/j.cell.2018.10.039 extern: '1' intvolume: ' 175' issue: '5' keyword: - General Biochemistry - Genetics and Molecular Biology language: - iso: eng month: '11' oa_version: None page: 1365-1379.e25 publication: Cell publication_identifier: issn: - 0092-8674 publication_status: published publisher: Elsevier quality_controlled: '1' status: public title: Structural basis of membrane protein chaperoning through the mitochondrial intermembrane space type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 175 year: '2018' ... --- _id: '11073' abstract: - lang: eng text: Human cancer cells bear complex chromosome rearrangements that can be potential drivers of cancer development. However, the molecular mechanisms underlying these rearrangements have been unclear. Zhang et al. use a new technique combining live-cell imaging and single-cell sequencing to demonstrate that chromosomes mis-segregated to micronuclei frequently undergo chromothripsis-like rearrangements in the subsequent cell cycle. article_processing_charge: No article_type: original author: - first_name: Emily M. full_name: Hatch, Emily M. last_name: Hatch - first_name: Martin W full_name: HETZER, Martin W id: 86c0d31b-b4eb-11ec-ac5a-eae7b2e135ed last_name: HETZER orcid: 0000-0002-2111-992X citation: ama: Hatch EM, Hetzer M. Linking micronuclei to chromosome fragmentation. Cell. 2015;161(7):1502-1504. doi:10.1016/j.cell.2015.06.005 apa: Hatch, E. M., & Hetzer, M. (2015). Linking micronuclei to chromosome fragmentation. Cell. Elsevier. https://doi.org/10.1016/j.cell.2015.06.005 chicago: Hatch, Emily M., and Martin Hetzer. “Linking Micronuclei to Chromosome Fragmentation.” Cell. Elsevier, 2015. https://doi.org/10.1016/j.cell.2015.06.005. ieee: E. M. Hatch and M. Hetzer, “Linking micronuclei to chromosome fragmentation,” Cell, vol. 161, no. 7. Elsevier, pp. 1502–1504, 2015. ista: Hatch EM, Hetzer M. 2015. Linking micronuclei to chromosome fragmentation. Cell. 161(7), 1502–1504. mla: Hatch, Emily M., and Martin Hetzer. “Linking Micronuclei to Chromosome Fragmentation.” Cell, vol. 161, no. 7, Elsevier, 2015, pp. 1502–04, doi:10.1016/j.cell.2015.06.005. short: E.M. Hatch, M. Hetzer, Cell 161 (2015) 1502–1504. date_created: 2022-04-07T07:48:49Z date_published: 2015-06-18T00:00:00Z date_updated: 2022-07-18T08:34:33Z day: '18' doi: 10.1016/j.cell.2015.06.005 extern: '1' external_id: pmid: - '26091034' intvolume: ' 161' issue: '7' keyword: - General Biochemistry - Genetics and Molecular Biology language: - iso: eng main_file_link: - open_access: '1' url: https://doi.org/10.1016/j.cell.2015.06.005 month: '06' oa: 1 oa_version: Published Version page: 1502-1504 pmid: 1 publication: Cell publication_identifier: issn: - 0092-8674 publication_status: published publisher: Elsevier quality_controlled: '1' scopus_import: '1' status: public title: Linking micronuclei to chromosome fragmentation type: journal_article user_id: 72615eeb-f1f3-11ec-aa25-d4573ddc34fd volume: 161 year: '2015' ... --- _id: '11080' abstract: - lang: eng text: The spindle assembly checkpoint prevents separation of sister chromatids until each kinetochore is attached to the mitotic spindle. Rodriguez-Bravo et al. report that the nuclear pore complex scaffolds spindle assembly checkpoint signaling in interphase, providing a store of inhibitory signals that limits the speed of the subsequent mitosis. article_processing_charge: No article_type: original author: - first_name: Abigail full_name: Buchwalter, Abigail last_name: Buchwalter - first_name: Martin W full_name: HETZER, Martin W id: 86c0d31b-b4eb-11ec-ac5a-eae7b2e135ed last_name: HETZER orcid: 0000-0002-2111-992X citation: ama: Buchwalter A, Hetzer M. Nuclear pores set the speed limit for mitosis. Cell. 2014;156(5):868-869. doi:10.1016/j.cell.2014.02.004 apa: Buchwalter, A., & Hetzer, M. (2014). Nuclear pores set the speed limit for mitosis. Cell. Elsevier. https://doi.org/10.1016/j.cell.2014.02.004 chicago: Buchwalter, Abigail, and Martin Hetzer. “Nuclear Pores Set the Speed Limit for Mitosis.” Cell. Elsevier, 2014. https://doi.org/10.1016/j.cell.2014.02.004. ieee: A. Buchwalter and M. Hetzer, “Nuclear pores set the speed limit for mitosis,” Cell, vol. 156, no. 5. Elsevier, pp. 868–869, 2014. ista: Buchwalter A, Hetzer M. 2014. Nuclear pores set the speed limit for mitosis. Cell. 156(5), 868–869. mla: Buchwalter, Abigail, and Martin Hetzer. “Nuclear Pores Set the Speed Limit for Mitosis.” Cell, vol. 156, no. 5, Elsevier, 2014, pp. 868–69, doi:10.1016/j.cell.2014.02.004. short: A. Buchwalter, M. Hetzer, Cell 156 (2014) 868–869. date_created: 2022-04-07T07:50:04Z date_published: 2014-02-27T00:00:00Z date_updated: 2022-07-18T08:44:33Z day: '27' doi: 10.1016/j.cell.2014.02.004 extern: '1' external_id: pmid: - '24581486' intvolume: ' 156' issue: '5' keyword: - General Biochemistry - Genetics and Molecular Biology language: - iso: eng main_file_link: - open_access: '1' url: https://doi.org/10.1016/j.cell.2014.02.004 month: '02' oa: 1 oa_version: Published Version page: 868-869 pmid: 1 publication: Cell publication_identifier: issn: - 0092-8674 publication_status: published publisher: Elsevier quality_controlled: '1' scopus_import: '1' status: public title: Nuclear pores set the speed limit for mitosis type: journal_article user_id: 72615eeb-f1f3-11ec-aa25-d4573ddc34fd volume: 156 year: '2014' ... --- _id: '6122' author: - first_name: Gerit A. full_name: Linneweber, Gerit A. last_name: Linneweber - first_name: Jake full_name: Jacobson, Jake last_name: Jacobson - first_name: Karl Emanuel full_name: Busch, Karl Emanuel last_name: Busch - first_name: Bruno full_name: Hudry, Bruno last_name: Hudry - first_name: Christo P. full_name: Christov, Christo P. last_name: Christov - first_name: Dirk full_name: Dormann, Dirk last_name: Dormann - first_name: Michaela full_name: Yuan, Michaela last_name: Yuan - first_name: Tomoki full_name: Otani, Tomoki last_name: Otani - first_name: Elisabeth full_name: Knust, Elisabeth last_name: Knust - first_name: Mario full_name: de Bono, Mario id: 4E3FF80E-F248-11E8-B48F-1D18A9856A87 last_name: de Bono orcid: 0000-0001-8347-0443 - first_name: Irene full_name: Miguel-Aliaga, Irene last_name: Miguel-Aliaga citation: ama: Linneweber GA, Jacobson J, Busch KE, et al. Neuronal control of metabolism through nutrient-dependent modulation of tracheal branching. Cell. 2014;156(1-2):69-83. doi:10.1016/j.cell.2013.12.008 apa: Linneweber, G. A., Jacobson, J., Busch, K. E., Hudry, B., Christov, C. P., Dormann, D., … Miguel-Aliaga, I. (2014). Neuronal control of metabolism through nutrient-dependent modulation of tracheal branching. Cell. Elsevier. https://doi.org/10.1016/j.cell.2013.12.008 chicago: Linneweber, Gerit A., Jake Jacobson, Karl Emanuel Busch, Bruno Hudry, Christo P. Christov, Dirk Dormann, Michaela Yuan, et al. “Neuronal Control of Metabolism through Nutrient-Dependent Modulation of Tracheal Branching.” Cell. Elsevier, 2014. https://doi.org/10.1016/j.cell.2013.12.008. ieee: G. A. Linneweber et al., “Neuronal control of metabolism through nutrient-dependent modulation of tracheal branching,” Cell, vol. 156, no. 1–2. Elsevier, pp. 69–83, 2014. ista: Linneweber GA, Jacobson J, Busch KE, Hudry B, Christov CP, Dormann D, Yuan M, Otani T, Knust E, de Bono M, Miguel-Aliaga I. 2014. Neuronal control of metabolism through nutrient-dependent modulation of tracheal branching. Cell. 156(1–2), 69–83. mla: Linneweber, Gerit A., et al. “Neuronal Control of Metabolism through Nutrient-Dependent Modulation of Tracheal Branching.” Cell, vol. 156, no. 1–2, Elsevier, 2014, pp. 69–83, doi:10.1016/j.cell.2013.12.008. short: G.A. Linneweber, J. Jacobson, K.E. Busch, B. Hudry, C.P. Christov, D. Dormann, M. Yuan, T. Otani, E. Knust, M. de Bono, I. Miguel-Aliaga, Cell 156 (2014) 69–83. date_created: 2019-03-19T14:35:30Z date_published: 2014-01-16T00:00:00Z date_updated: 2021-01-12T08:06:13Z day: '16' ddc: - '570' doi: 10.1016/j.cell.2013.12.008 extern: '1' external_id: pmid: - '24439370' file: - access_level: open_access checksum: ad6ef68f37fb711d9abcd97fc06ad316 content_type: application/pdf creator: kschuh date_created: 2019-03-19T14:40:38Z date_updated: 2020-07-14T12:47:20Z file_id: '6123' file_name: 2014_Elsevier_Linneweber.pdf file_size: 5020084 relation: main_file file_date_updated: 2020-07-14T12:47:20Z has_accepted_license: '1' intvolume: ' 156' issue: 1-2 language: - iso: eng month: '01' oa: 1 oa_version: Published Version page: 69-83 pmid: 1 publication: Cell publication_identifier: issn: - 0092-8674 publication_status: published publisher: Elsevier quality_controlled: '1' status: public title: Neuronal control of metabolism through nutrient-dependent modulation of tracheal branching 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: 156 year: '2014' ... --- _id: '9458' abstract: - lang: eng text: Dnmt1 epigenetically propagates symmetrical CG methylation in many eukaryotes. Their genomes are typically depleted of CG dinucleotides because of imperfect repair of deaminated methylcytosines. Here, we extensively survey diverse species lacking Dnmt1 and show that, surprisingly, symmetrical CG methylation is nonetheless frequently present and catalyzed by a different DNA methyltransferase family, Dnmt5. Numerous Dnmt5-containing organisms that diverged more than a billion years ago exhibit clustered methylation, specifically in nucleosome linkers. Clustered methylation occurs at unprecedented densities and directly disfavors nucleosomes, contributing to nucleosome positioning between clusters. Dense methylation is enabled by a regime of genomic sequence evolution that enriches CG dinucleotides and drives the highest CG frequencies known. Species with linker methylation have small, transcriptionally active nuclei that approach the physical limits of chromatin compaction. These features constitute a previously unappreciated genome architecture, in which dense methylation influences nucleosome positions, likely facilitating nuclear processes under extreme spatial constraints. article_processing_charge: No article_type: original author: - first_name: Jason T. full_name: Huff, Jason T. last_name: Huff - first_name: Daniel full_name: Zilberman, Daniel id: 6973db13-dd5f-11ea-814e-b3e5455e9ed1 last_name: Zilberman orcid: 0000-0002-0123-8649 citation: ama: Huff JT, Zilberman D. Dnmt1-independent CG methylation contributes to nucleosome positioning in diverse eukaryotes. Cell. 2014;156(6):1286-1297. doi:10.1016/j.cell.2014.01.029 apa: Huff, J. T., & Zilberman, D. (2014). Dnmt1-independent CG methylation contributes to nucleosome positioning in diverse eukaryotes. Cell. Elsevier. https://doi.org/10.1016/j.cell.2014.01.029 chicago: Huff, Jason T., and Daniel Zilberman. “Dnmt1-Independent CG Methylation Contributes to Nucleosome Positioning in Diverse Eukaryotes.” Cell. Elsevier, 2014. https://doi.org/10.1016/j.cell.2014.01.029. ieee: J. T. Huff and D. Zilberman, “Dnmt1-independent CG methylation contributes to nucleosome positioning in diverse eukaryotes,” Cell, vol. 156, no. 6. Elsevier, pp. 1286–1297, 2014. ista: Huff JT, Zilberman D. 2014. Dnmt1-independent CG methylation contributes to nucleosome positioning in diverse eukaryotes. Cell. 156(6), 1286–1297. mla: Huff, Jason T., and Daniel Zilberman. “Dnmt1-Independent CG Methylation Contributes to Nucleosome Positioning in Diverse Eukaryotes.” Cell, vol. 156, no. 6, Elsevier, 2014, pp. 1286–97, doi:10.1016/j.cell.2014.01.029. short: J.T. Huff, D. Zilberman, Cell 156 (2014) 1286–1297. date_created: 2021-06-04T12:00:16Z date_published: 2014-03-13T00:00:00Z date_updated: 2021-12-14T08:22:36Z day: '13' department: - _id: DaZi doi: 10.1016/j.cell.2014.01.029 extern: '1' external_id: pmid: - '24630728' intvolume: ' 156' issue: '6' language: - iso: eng main_file_link: - open_access: '1' url: https://doi.org/10.1016/j.cell.2014.01.029 month: '03' oa: 1 oa_version: Published Version page: 1286-1297 pmid: 1 publication: Cell publication_identifier: eissn: - 1097-4172 issn: - 0092-8674 publication_status: published publisher: Elsevier quality_controlled: '1' scopus_import: '1' status: public title: Dnmt1-independent CG methylation contributes to nucleosome positioning in diverse eukaryotes type: journal_article user_id: 8b945eb4-e2f2-11eb-945a-df72226e66a9 volume: 156 year: '2014' ... --- _id: '11087' abstract: - lang: eng text: Intracellular proteins with long lifespans have recently been linked to age-dependent defects, ranging from decreased fertility to the functional decline of neurons. Why long-lived proteins exist in metabolically active cellular environments and how they are maintained over time remains poorly understood. Here, we provide a system-wide identification of proteins with exceptional lifespans in the rat brain. These proteins are inefficiently replenished despite being translated robustly throughout adulthood. Using nucleoporins as a paradigm for long-term protein persistence, we found that nuclear pore complexes (NPCs) are maintained over a cell’s life through slow but finite exchange of even its most stable subcomplexes. This maintenance is limited, however, as some nucleoporin levels decrease during aging, providing a rationale for the previously observed age-dependent deterioration of NPC function. Our identification of a long-lived proteome reveals cellular components that are at increased risk for damage accumulation, linking long-term protein persistence to the cellular aging process. article_processing_charge: No article_type: original author: - first_name: Brandon H. full_name: Toyama, Brandon H. last_name: Toyama - first_name: Jeffrey N. full_name: Savas, Jeffrey N. last_name: Savas - first_name: Sung Kyu full_name: Park, Sung Kyu last_name: Park - first_name: Michael S. full_name: Harris, Michael S. last_name: Harris - first_name: Nicholas T. full_name: Ingolia, Nicholas T. last_name: Ingolia - first_name: John R. full_name: Yates, John R. last_name: Yates - first_name: Martin W full_name: HETZER, Martin W id: 86c0d31b-b4eb-11ec-ac5a-eae7b2e135ed last_name: HETZER orcid: 0000-0002-2111-992X citation: ama: Toyama BH, Savas JN, Park SK, et al. Identification of long-lived proteins reveals exceptional stability of essential cellular structures. Cell. 2013;154(5):971-982. doi:10.1016/j.cell.2013.07.037 apa: Toyama, B. H., Savas, J. N., Park, S. K., Harris, M. S., Ingolia, N. T., Yates, J. R., & Hetzer, M. (2013). Identification of long-lived proteins reveals exceptional stability of essential cellular structures. Cell. Elsevier. https://doi.org/10.1016/j.cell.2013.07.037 chicago: Toyama, Brandon H., Jeffrey N. Savas, Sung Kyu Park, Michael S. Harris, Nicholas T. Ingolia, John R. Yates, and Martin Hetzer. “Identification of Long-Lived Proteins Reveals Exceptional Stability of Essential Cellular Structures.” Cell. Elsevier, 2013. https://doi.org/10.1016/j.cell.2013.07.037. ieee: B. H. Toyama et al., “Identification of long-lived proteins reveals exceptional stability of essential cellular structures,” Cell, vol. 154, no. 5. Elsevier, pp. 971–982, 2013. ista: Toyama BH, Savas JN, Park SK, Harris MS, Ingolia NT, Yates JR, Hetzer M. 2013. Identification of long-lived proteins reveals exceptional stability of essential cellular structures. Cell. 154(5), 971–982. mla: Toyama, Brandon H., et al. “Identification of Long-Lived Proteins Reveals Exceptional Stability of Essential Cellular Structures.” Cell, vol. 154, no. 5, Elsevier, 2013, pp. 971–82, doi:10.1016/j.cell.2013.07.037. short: B.H. Toyama, J.N. Savas, S.K. Park, M.S. Harris, N.T. Ingolia, J.R. Yates, M. Hetzer, Cell 154 (2013) 971–982. date_created: 2022-04-07T07:51:08Z date_published: 2013-08-29T00:00:00Z date_updated: 2022-07-18T08:50:47Z day: '29' doi: 10.1016/j.cell.2013.07.037 extern: '1' external_id: pmid: - '23993091' intvolume: ' 154' issue: '5' keyword: - General Biochemistry - Genetics and Molecular Biology language: - iso: eng main_file_link: - open_access: '1' url: https://doi.org/10.1016/j.cell.2013.07.037 month: '08' oa: 1 oa_version: Published Version page: 971-982 pmid: 1 publication: Cell publication_identifier: issn: - 0092-8674 publication_status: published publisher: Elsevier quality_controlled: '1' scopus_import: '1' status: public title: Identification of long-lived proteins reveals exceptional stability of essential cellular structures type: journal_article user_id: 72615eeb-f1f3-11ec-aa25-d4573ddc34fd volume: 154 year: '2013' ... --- _id: '11085' abstract: - lang: eng text: During mitotic exit, missegregated chromosomes can recruit their own nuclear envelope (NE) to form micronuclei (MN). MN have reduced functioning compared to primary nuclei in the same cell, although the two compartments appear to be structurally comparable. Here we show that over 60% of MN undergo an irreversible loss of compartmentalization during interphase due to NE collapse. This disruption of the MN, which is induced by defects in nuclear lamina assembly, drastically reduces nuclear functions and can trigger massive DNA damage. MN disruption is associated with chromatin compaction and invasion of endoplasmic reticulum (ER) tubules into the chromatin. We identified disrupted MN in both major subtypes of human non-small-cell lung cancer, suggesting that disrupted MN could be a useful objective biomarker for genomic instability in solid tumors. Our study shows that NE collapse is a key event underlying MN dysfunction and establishes a link between aberrant NE organization and aneuploidy. article_processing_charge: No article_type: original author: - first_name: Emily M. full_name: Hatch, Emily M. last_name: Hatch - first_name: Andrew H. full_name: Fischer, Andrew H. last_name: Fischer - first_name: Thomas J. full_name: Deerinck, Thomas J. last_name: Deerinck - first_name: Martin W full_name: HETZER, Martin W id: 86c0d31b-b4eb-11ec-ac5a-eae7b2e135ed last_name: HETZER orcid: 0000-0002-2111-992X citation: ama: Hatch EM, Fischer AH, Deerinck TJ, Hetzer M. Catastrophic nuclear envelope collapse in cancer cell micronuclei. Cell. 2013;154(1):47-60. doi:10.1016/j.cell.2013.06.007 apa: Hatch, E. M., Fischer, A. H., Deerinck, T. J., & Hetzer, M. (2013). Catastrophic nuclear envelope collapse in cancer cell micronuclei. Cell. Elsevier. https://doi.org/10.1016/j.cell.2013.06.007 chicago: Hatch, Emily M., Andrew H. Fischer, Thomas J. Deerinck, and Martin Hetzer. “Catastrophic Nuclear Envelope Collapse in Cancer Cell Micronuclei.” Cell. Elsevier, 2013. https://doi.org/10.1016/j.cell.2013.06.007. ieee: E. M. Hatch, A. H. Fischer, T. J. Deerinck, and M. Hetzer, “Catastrophic nuclear envelope collapse in cancer cell micronuclei,” Cell, vol. 154, no. 1. Elsevier, pp. 47–60, 2013. ista: Hatch EM, Fischer AH, Deerinck TJ, Hetzer M. 2013. Catastrophic nuclear envelope collapse in cancer cell micronuclei. Cell. 154(1), 47–60. mla: Hatch, Emily M., et al. “Catastrophic Nuclear Envelope Collapse in Cancer Cell Micronuclei.” Cell, vol. 154, no. 1, Elsevier, 2013, pp. 47–60, doi:10.1016/j.cell.2013.06.007. short: E.M. Hatch, A.H. Fischer, T.J. Deerinck, M. Hetzer, Cell 154 (2013) 47–60. date_created: 2022-04-07T07:50:51Z date_published: 2013-07-03T00:00:00Z date_updated: 2022-07-18T08:45:47Z day: '03' doi: 10.1016/j.cell.2013.06.007 extern: '1' external_id: pmid: - '23827674' intvolume: ' 154' issue: '1' keyword: - General Biochemistry - Genetics and Molecular Biology language: - iso: eng main_file_link: - open_access: '1' url: https://doi.org/10.1016/j.cell.2013.06.007 month: '07' oa: 1 oa_version: Published Version page: 47-60 pmid: 1 publication: Cell publication_identifier: issn: - 0092-8674 publication_status: published publisher: Elsevier quality_controlled: '1' scopus_import: '1' status: public title: Catastrophic nuclear envelope collapse in cancer cell micronuclei type: journal_article user_id: 72615eeb-f1f3-11ec-aa25-d4573ddc34fd volume: 154 year: '2013' ... --- _id: '9459' abstract: - lang: eng text: Nucleosome remodelers of the DDM1/Lsh family are required for DNA methylation of transposable elements, but the reason for this is unknown. How DDM1 interacts with other methylation pathways, such as small-RNA-directed DNA methylation (RdDM), which is thought to mediate plant asymmetric methylation through DRM enzymes, is also unclear. Here, we show that most asymmetric methylation is facilitated by DDM1 and mediated by the methyltransferase CMT2 separately from RdDM. We find that heterochromatic sequences preferentially require DDM1 for DNA methylation and that this preference depends on linker histone H1. RdDM is instead inhibited by heterochromatin and absolutely requires the nucleosome remodeler DRD1. Together, DDM1 and RdDM mediate nearly all transposon methylation and collaborate to repress transposition and regulate the methylation and expression of genes. Our results indicate that DDM1 provides DNA methyltransferases access to H1-containing heterochromatin to allow stable silencing of transposable elements in cooperation with the RdDM pathway. article_processing_charge: No article_type: original author: - first_name: Assaf full_name: Zemach, Assaf last_name: Zemach - first_name: M. Yvonne full_name: Kim, M. Yvonne last_name: Kim - first_name: Ping-Hung full_name: Hsieh, Ping-Hung last_name: Hsieh - first_name: Devin full_name: Coleman-Derr, Devin last_name: Coleman-Derr - first_name: Leor full_name: Eshed-Williams, Leor last_name: Eshed-Williams - first_name: Ka full_name: Thao, Ka last_name: Thao - first_name: Stacey L. full_name: Harmer, Stacey L. last_name: Harmer - first_name: Daniel full_name: Zilberman, Daniel id: 6973db13-dd5f-11ea-814e-b3e5455e9ed1 last_name: Zilberman orcid: 0000-0002-0123-8649 citation: ama: Zemach A, Kim MY, Hsieh P-H, et al. The Arabidopsis nucleosome remodeler DDM1 allows DNA methyltransferases to access H1-containing heterochromatin. Cell. 2013;153(1):193-205. doi:10.1016/j.cell.2013.02.033 apa: Zemach, A., Kim, M. Y., Hsieh, P.-H., Coleman-Derr, D., Eshed-Williams, L., Thao, K., … Zilberman, D. (2013). The Arabidopsis nucleosome remodeler DDM1 allows DNA methyltransferases to access H1-containing heterochromatin. Cell. Elsevier. https://doi.org/10.1016/j.cell.2013.02.033 chicago: Zemach, Assaf, M. Yvonne Kim, Ping-Hung Hsieh, Devin Coleman-Derr, Leor Eshed-Williams, Ka Thao, Stacey L. Harmer, and Daniel Zilberman. “The Arabidopsis Nucleosome Remodeler DDM1 Allows DNA Methyltransferases to Access H1-Containing Heterochromatin.” Cell. Elsevier, 2013. https://doi.org/10.1016/j.cell.2013.02.033. ieee: A. Zemach et al., “The Arabidopsis nucleosome remodeler DDM1 allows DNA methyltransferases to access H1-containing heterochromatin,” Cell, vol. 153, no. 1. Elsevier, pp. 193–205, 2013. ista: Zemach A, Kim MY, Hsieh P-H, Coleman-Derr D, Eshed-Williams L, Thao K, Harmer SL, Zilberman D. 2013. The Arabidopsis nucleosome remodeler DDM1 allows DNA methyltransferases to access H1-containing heterochromatin. Cell. 153(1), 193–205. mla: Zemach, Assaf, et al. “The Arabidopsis Nucleosome Remodeler DDM1 Allows DNA Methyltransferases to Access H1-Containing Heterochromatin.” Cell, vol. 153, no. 1, Elsevier, 2013, pp. 193–205, doi:10.1016/j.cell.2013.02.033. short: A. Zemach, M.Y. Kim, P.-H. Hsieh, D. Coleman-Derr, L. Eshed-Williams, K. Thao, S.L. Harmer, D. Zilberman, Cell 153 (2013) 193–205. date_created: 2021-06-04T12:23:28Z date_published: 2013-03-28T00:00:00Z date_updated: 2021-12-14T08:25:35Z day: '28' department: - _id: DaZi doi: 10.1016/j.cell.2013.02.033 extern: '1' external_id: pmid: - '23540698' intvolume: ' 153' issue: '1' language: - iso: eng main_file_link: - open_access: '1' url: https://doi.org/10.1016/j.cell.2013.02.033 month: '03' oa: 1 oa_version: Published Version page: 193-205 pmid: 1 publication: Cell publication_identifier: eissn: - 1097-4172 issn: - 0092-8674 publication_status: published publisher: Elsevier quality_controlled: '1' scopus_import: '1' status: public title: The Arabidopsis nucleosome remodeler DDM1 allows DNA methyltransferases to access H1-containing heterochromatin type: journal_article user_id: 8b945eb4-e2f2-11eb-945a-df72226e66a9 volume: 153 year: '2013' ... --- _id: '11090' abstract: - lang: eng text: Nuclear export of mRNAs is thought to occur exclusively through nuclear pore complexes. In this issue of Cell, Speese et al. identify an alternate pathway for mRNA export in muscle cells where ribonucleoprotein complexes involved in forming neuromuscular junctions transit the nuclear envelope by fusing with and budding through the nuclear membrane. article_processing_charge: No article_type: letter_note author: - first_name: Emily M. full_name: Hatch, Emily M. last_name: Hatch - first_name: Martin W full_name: HETZER, Martin W id: 86c0d31b-b4eb-11ec-ac5a-eae7b2e135ed last_name: HETZER orcid: 0000-0002-2111-992X citation: ama: Hatch EM, Hetzer M. RNP export by nuclear envelope budding. Cell. 2012;149(4):733-735. doi:10.1016/j.cell.2012.04.018 apa: Hatch, E. M., & Hetzer, M. (2012). RNP export by nuclear envelope budding. Cell. Elsevier. https://doi.org/10.1016/j.cell.2012.04.018 chicago: Hatch, Emily M., and Martin Hetzer. “RNP Export by Nuclear Envelope Budding.” Cell. Elsevier, 2012. https://doi.org/10.1016/j.cell.2012.04.018. ieee: E. M. Hatch and M. Hetzer, “RNP export by nuclear envelope budding,” Cell, vol. 149, no. 4. Elsevier, pp. 733–735, 2012. ista: Hatch EM, Hetzer M. 2012. RNP export by nuclear envelope budding. Cell. 149(4), 733–735. mla: Hatch, Emily M., and Martin Hetzer. “RNP Export by Nuclear Envelope Budding.” Cell, vol. 149, no. 4, Elsevier, 2012, pp. 733–35, doi:10.1016/j.cell.2012.04.018. short: E.M. Hatch, M. Hetzer, Cell 149 (2012) 733–735. date_created: 2022-04-07T07:51:45Z date_published: 2012-05-11T00:00:00Z date_updated: 2022-07-18T08:58:48Z day: '11' doi: 10.1016/j.cell.2012.04.018 extern: '1' external_id: pmid: - '22579277' intvolume: ' 149' issue: '4' keyword: - General Biochemistry - Genetics and Molecular Biology language: - iso: eng main_file_link: - open_access: '1' url: https://doi.org/10.1016/j.cell.2012.04.018 month: '05' oa: 1 oa_version: Published Version page: 733-735 pmid: 1 publication: Cell publication_identifier: issn: - 0092-8674 publication_status: published publisher: Elsevier quality_controlled: '1' scopus_import: '1' status: public title: RNP export by nuclear envelope budding type: journal_article user_id: 72615eeb-f1f3-11ec-aa25-d4573ddc34fd volume: 149 year: '2012' ... --- _id: '11102' abstract: - lang: eng text: Nuclear pore complexes have recently been shown to play roles in gene activation; however their potential involvement in metazoan transcription remains unclear. Here we show that the nucleoporins Sec13, Nup98, and Nup88, as well as a group of FG-repeat nucleoporins, bind to the Drosophila genome at functionally distinct loci that often do not represent nuclear envelope contact sites. Whereas Nup88 localizes to silent loci, Sec13, Nup98, and a subset of FG-repeat nucleoporins bind to developmentally regulated genes undergoing transcription induction. Strikingly, RNAi-mediated knockdown of intranuclear Sec13 and Nup98 specifically inhibits transcription of their target genes and prevents efficient reactivation of transcription after heat shock, suggesting an essential role of NPC components in regulating complex gene expression programs of multicellular organisms. article_processing_charge: No article_type: original author: - first_name: Maya full_name: Capelson, Maya last_name: Capelson - first_name: Yun full_name: Liang, Yun last_name: Liang - first_name: Roberta full_name: Schulte, Roberta last_name: Schulte - first_name: William full_name: Mair, William last_name: Mair - first_name: Ulrich full_name: Wagner, Ulrich last_name: Wagner - first_name: Martin W full_name: HETZER, Martin W id: 86c0d31b-b4eb-11ec-ac5a-eae7b2e135ed last_name: HETZER orcid: 0000-0002-2111-992X citation: ama: Capelson M, Liang Y, Schulte R, Mair W, Wagner U, Hetzer M. Chromatin-bound nuclear pore components regulate gene expression in higher eukaryotes. Cell. 2010;140(3):372-383. doi:10.1016/j.cell.2009.12.054 apa: Capelson, M., Liang, Y., Schulte, R., Mair, W., Wagner, U., & Hetzer, M. (2010). Chromatin-bound nuclear pore components regulate gene expression in higher eukaryotes. Cell. Elsevier. https://doi.org/10.1016/j.cell.2009.12.054 chicago: Capelson, Maya, Yun Liang, Roberta Schulte, William Mair, Ulrich Wagner, and Martin Hetzer. “Chromatin-Bound Nuclear Pore Components Regulate Gene Expression in Higher Eukaryotes.” Cell. Elsevier, 2010. https://doi.org/10.1016/j.cell.2009.12.054. ieee: M. Capelson, Y. Liang, R. Schulte, W. Mair, U. Wagner, and M. Hetzer, “Chromatin-bound nuclear pore components regulate gene expression in higher eukaryotes,” Cell, vol. 140, no. 3. Elsevier, pp. 372–383, 2010. ista: Capelson M, Liang Y, Schulte R, Mair W, Wagner U, Hetzer M. 2010. Chromatin-bound nuclear pore components regulate gene expression in higher eukaryotes. Cell. 140(3), 372–383. mla: Capelson, Maya, et al. “Chromatin-Bound Nuclear Pore Components Regulate Gene Expression in Higher Eukaryotes.” Cell, vol. 140, no. 3, Elsevier, 2010, pp. 372–83, doi:10.1016/j.cell.2009.12.054. short: M. Capelson, Y. Liang, R. Schulte, W. Mair, U. Wagner, M. Hetzer, Cell 140 (2010) 372–383. date_created: 2022-04-07T07:53:36Z date_published: 2010-02-05T00:00:00Z date_updated: 2022-07-18T08:55:03Z day: '05' doi: 10.1016/j.cell.2009.12.054 extern: '1' external_id: pmid: - '20144761' intvolume: ' 140' issue: '3' keyword: - General Biochemistry - Genetics and Molecular Biology language: - iso: eng main_file_link: - open_access: '1' url: https://doi.org/10.1016/j.cell.2009.12.054 month: '02' oa: 1 oa_version: Published Version page: 372-383 pmid: 1 publication: Cell publication_identifier: issn: - 0092-8674 publication_status: published publisher: Elsevier quality_controlled: '1' scopus_import: '1' status: public title: Chromatin-bound nuclear pore components regulate gene expression in higher eukaryotes type: journal_article user_id: 72615eeb-f1f3-11ec-aa25-d4573ddc34fd volume: 140 year: '2010' ... --- _id: '11101' abstract: - lang: eng text: In metazoa, nuclear pore complexes (NPCs) assemble from disassembled precursors into a reforming nuclear envelope (NE) at the end of mitosis and into growing intact NEs during interphase. Here, we show via RNAi-mediated knockdown that ELYS, a nucleoporin critical for the recruitment of the essential Nup107/160 complex to chromatin, is required for NPC assembly at the end of mitosis but not during interphase. Conversely, the transmembrane nucleoporin POM121 is critical for the incorporation of the Nup107/160 complex into new assembly sites specifically during interphase. Strikingly, recruitment of the Nup107/160 complex to an intact NE involves a membrane curvature-sensing domain of its constituent Nup133, which is not required for postmitotic NPC formation. Our results suggest that in organisms with open mitosis, NPCs assemble via two distinct mechanisms to accommodate cell cycle-dependent differences in NE topology. article_processing_charge: No article_type: original author: - first_name: Christine M. full_name: Doucet, Christine M. last_name: Doucet - first_name: Jessica A. full_name: Talamas, Jessica A. last_name: Talamas - first_name: Martin W full_name: HETZER, Martin W id: 86c0d31b-b4eb-11ec-ac5a-eae7b2e135ed last_name: HETZER orcid: 0000-0002-2111-992X citation: ama: Doucet CM, Talamas JA, Hetzer M. Cell cycle-dependent differences in nuclear pore complex assembly in metazoa. Cell. 2010;141(6):1030-1041. doi:10.1016/j.cell.2010.04.036 apa: Doucet, C. M., Talamas, J. A., & Hetzer, M. (2010). Cell cycle-dependent differences in nuclear pore complex assembly in metazoa. Cell. Elsevier. https://doi.org/10.1016/j.cell.2010.04.036 chicago: Doucet, Christine M., Jessica A. Talamas, and Martin Hetzer. “Cell Cycle-Dependent Differences in Nuclear Pore Complex Assembly in Metazoa.” Cell. Elsevier, 2010. https://doi.org/10.1016/j.cell.2010.04.036. ieee: C. M. Doucet, J. A. Talamas, and M. Hetzer, “Cell cycle-dependent differences in nuclear pore complex assembly in metazoa,” Cell, vol. 141, no. 6. Elsevier, pp. 1030–1041, 2010. ista: Doucet CM, Talamas JA, Hetzer M. 2010. Cell cycle-dependent differences in nuclear pore complex assembly in metazoa. Cell. 141(6), 1030–1041. mla: Doucet, Christine M., et al. “Cell Cycle-Dependent Differences in Nuclear Pore Complex Assembly in Metazoa.” Cell, vol. 141, no. 6, Elsevier, 2010, pp. 1030–41, doi:10.1016/j.cell.2010.04.036. short: C.M. Doucet, J.A. Talamas, M. Hetzer, Cell 141 (2010) 1030–1041. date_created: 2022-04-07T07:53:29Z date_published: 2010-06-11T00:00:00Z date_updated: 2022-07-18T08:54:52Z day: '11' doi: 10.1016/j.cell.2010.04.036 extern: '1' external_id: pmid: - '20550937' intvolume: ' 141' issue: '6' keyword: - General Biochemistry - Genetics and Molecular Biology language: - iso: eng main_file_link: - open_access: '1' url: https://doi.org/10.1016/j.cell.2010.04.036 month: '06' oa: 1 oa_version: Published Version page: 1030-1041 pmid: 1 publication: Cell publication_identifier: issn: - 0092-8674 publication_status: published publisher: Elsevier quality_controlled: '1' scopus_import: '1' status: public title: Cell cycle-dependent differences in nuclear pore complex assembly in metazoa type: journal_article user_id: 72615eeb-f1f3-11ec-aa25-d4573ddc34fd volume: 141 year: '2010' ... --- _id: '7703' abstract: - lang: eng text: By combining gene expression profiling with image registration, Tomer et al. (2010) find that the mushroom body of the segmented worm Platynereis dumerilii shares many features with the mammalian cerebral cortex. The authors propose that the mushroom body and cortex evolved from the same structure in the common ancestor of vertebrates and invertebrates. article_processing_charge: No article_type: original author: - first_name: Lora Beatrice Jaeger full_name: Sweeney, Lora Beatrice Jaeger id: 56BE8254-C4F0-11E9-8E45-0B23E6697425 last_name: Sweeney orcid: 0000-0001-9242-5601 - first_name: Liqun full_name: Luo, Liqun last_name: Luo citation: ama: 'Sweeney LB, Luo L. ‘Fore brain: A hint of the ancestral cortex. Cell. 2010;142(5):679-681. doi:10.1016/j.cell.2010.08.024' apa: 'Sweeney, L. B., & Luo, L. (2010). ‘Fore brain: A hint of the ancestral cortex. Cell. Elsevier. https://doi.org/10.1016/j.cell.2010.08.024' chicago: 'Sweeney, Lora B., and Liqun Luo. “‘Fore Brain: A Hint of the Ancestral Cortex.” Cell. Elsevier, 2010. https://doi.org/10.1016/j.cell.2010.08.024.' ieee: 'L. B. Sweeney and L. Luo, “‘Fore brain: A hint of the ancestral cortex,” Cell, vol. 142, no. 5. Elsevier, pp. 679–681, 2010.' ista: 'Sweeney LB, Luo L. 2010. ‘Fore brain: A hint of the ancestral cortex. Cell. 142(5), 679–681.' mla: 'Sweeney, Lora B., and Liqun Luo. “‘Fore Brain: A Hint of the Ancestral Cortex.” Cell, vol. 142, no. 5, Elsevier, 2010, pp. 679–81, doi:10.1016/j.cell.2010.08.024.' short: L.B. Sweeney, L. Luo, Cell 142 (2010) 679–681. date_created: 2020-04-30T10:36:52Z date_published: 2010-09-03T00:00:00Z date_updated: 2024-01-31T10:14:59Z day: '03' doi: 10.1016/j.cell.2010.08.024 extern: '1' intvolume: ' 142' issue: '5' language: - iso: eng month: '09' oa_version: None page: 679-681 publication: Cell publication_identifier: issn: - 0092-8674 publication_status: published publisher: Elsevier quality_controlled: '1' status: public title: '‘Fore brain: A hint of the ancestral cortex' type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 142 year: '2010' ... --- _id: '11108' abstract: - lang: eng text: In dividing cells, nuclear pore complexes (NPCs) disassemble during mitosis and reassemble into the newly forming nuclei. However, the fate of nuclear pores in postmitotic cells is unknown. Here, we show that NPCs, unlike other nuclear structures, do not turn over in differentiated cells. While a subset of NPC components, like Nup153 and Nup50, are continuously exchanged, scaffold nucleoporins, like the Nup107/160 complex, are extremely long-lived and remain incorporated in the nuclear membrane during the entire cellular life span. Besides the lack of nucleoporin expression and NPC turnover, we discovered an age-related deterioration of NPCs, leading to an increase in nuclear permeability and the leaking of cytoplasmic proteins into the nucleus. Our finding that nuclear “leakiness” is dramatically accelerated during aging and that a subset of nucleoporins is oxidatively damaged in old cells suggests that the accumulation of damage at the NPC might be a crucial aging event. article_processing_charge: No article_type: original author: - first_name: Maximiliano A. full_name: D'Angelo, Maximiliano A. last_name: D'Angelo - first_name: Marcela full_name: Raices, Marcela last_name: Raices - first_name: Siler H. full_name: Panowski, Siler H. last_name: Panowski - first_name: Martin W full_name: HETZER, Martin W id: 86c0d31b-b4eb-11ec-ac5a-eae7b2e135ed last_name: HETZER orcid: 0000-0002-2111-992X citation: ama: D’Angelo MA, Raices M, Panowski SH, Hetzer M. Age-dependent deterioration of nuclear pore complexes causes a loss of nuclear integrity in postmitotic cells. Cell. 2009;136(2):284-295. doi:10.1016/j.cell.2008.11.037 apa: D’Angelo, M. A., Raices, M., Panowski, S. H., & Hetzer, M. (2009). Age-dependent deterioration of nuclear pore complexes causes a loss of nuclear integrity in postmitotic cells. Cell. Elsevier. https://doi.org/10.1016/j.cell.2008.11.037 chicago: D’Angelo, Maximiliano A., Marcela Raices, Siler H. Panowski, and Martin Hetzer. “Age-Dependent Deterioration of Nuclear Pore Complexes Causes a Loss of Nuclear Integrity in Postmitotic Cells.” Cell. Elsevier, 2009. https://doi.org/10.1016/j.cell.2008.11.037. ieee: M. A. D’Angelo, M. Raices, S. H. Panowski, and M. Hetzer, “Age-dependent deterioration of nuclear pore complexes causes a loss of nuclear integrity in postmitotic cells,” Cell, vol. 136, no. 2. Elsevier, pp. 284–295, 2009. ista: D’Angelo MA, Raices M, Panowski SH, Hetzer M. 2009. Age-dependent deterioration of nuclear pore complexes causes a loss of nuclear integrity in postmitotic cells. Cell. 136(2), 284–295. mla: D’Angelo, Maximiliano A., et al. “Age-Dependent Deterioration of Nuclear Pore Complexes Causes a Loss of Nuclear Integrity in Postmitotic Cells.” Cell, vol. 136, no. 2, Elsevier, 2009, pp. 284–95, doi:10.1016/j.cell.2008.11.037. short: M.A. D’Angelo, M. Raices, S.H. Panowski, M. Hetzer, Cell 136 (2009) 284–295. date_created: 2022-04-07T07:54:52Z date_published: 2009-01-23T00:00:00Z date_updated: 2022-07-18T08:55:29Z day: '23' doi: 10.1016/j.cell.2008.11.037 extern: '1' external_id: pmid: - '19167330' intvolume: ' 136' issue: '2' keyword: - General Biochemistry - Genetics and Molecular Biology language: - iso: eng main_file_link: - open_access: '1' url: https://doi.org/10.1016/j.cell.2008.11.037 month: '01' oa: 1 oa_version: Published Version page: 284-295 pmid: 1 publication: Cell publication_identifier: issn: - 0092-8674 publication_status: published publisher: Elsevier quality_controlled: '1' scopus_import: '1' status: public title: Age-dependent deterioration of nuclear pore complexes causes a loss of nuclear integrity in postmitotic cells type: journal_article user_id: 72615eeb-f1f3-11ec-aa25-d4573ddc34fd volume: 136 year: '2009' ... --- _id: '7704' abstract: - lang: eng text: Gradients of axon guidance molecules instruct the formation of continuous neural maps, such as the retinotopic map in the vertebrate visual system. Here we show that molecular gradients can also instruct the formation of a discrete neural map. In the fly olfactory system, axons of 50 classes of olfactory receptor neurons (ORNs) and dendrites of 50 classes of projection neurons (PNs) form one-to-one connections at discrete units called glomeruli. We provide expression, loss- and gain-of-function data to demonstrate that the levels of transmembrane Semaphorin-1a (Sema-1a), acting cell-autonomously as a receptor or part of a receptor complex, direct the dendritic targeting of PNs along the dorsolateral to ventromedial axis of the antennal lobe. Sema-1a also regulates PN axon targeting in higher olfactory centers. Thus, graded expression of Sema-1a contributes to connection specificity from ORNs to PNs and then to higher brain centers, ensuring proper representation of olfactory information in the brain. article_processing_charge: No article_type: original author: - first_name: Takaki full_name: Komiyama, Takaki last_name: Komiyama - first_name: Lora Beatrice Jaeger full_name: Sweeney, Lora Beatrice Jaeger id: 56BE8254-C4F0-11E9-8E45-0B23E6697425 last_name: Sweeney orcid: 0000-0001-9242-5601 - first_name: Oren full_name: Schuldiner, Oren last_name: Schuldiner - first_name: K. Christopher full_name: Garcia, K. Christopher last_name: Garcia - first_name: Liqun full_name: Luo, Liqun last_name: Luo citation: ama: Komiyama T, Sweeney LB, Schuldiner O, Garcia KC, Luo L. Graded expression of semaphorin-1a cell-autonomously directs dendritic targeting of olfactory projection neurons. Cell. 2007;128(2):399-410. doi:10.1016/j.cell.2006.12.028 apa: Komiyama, T., Sweeney, L. B., Schuldiner, O., Garcia, K. C., & Luo, L. (2007). Graded expression of semaphorin-1a cell-autonomously directs dendritic targeting of olfactory projection neurons. Cell. Elsevier. https://doi.org/10.1016/j.cell.2006.12.028 chicago: Komiyama, Takaki, Lora B. Sweeney, Oren Schuldiner, K. Christopher Garcia, and Liqun Luo. “Graded Expression of Semaphorin-1a Cell-Autonomously Directs Dendritic Targeting of Olfactory Projection Neurons.” Cell. Elsevier, 2007. https://doi.org/10.1016/j.cell.2006.12.028. ieee: T. Komiyama, L. B. Sweeney, O. Schuldiner, K. C. Garcia, and L. Luo, “Graded expression of semaphorin-1a cell-autonomously directs dendritic targeting of olfactory projection neurons,” Cell, vol. 128, no. 2. Elsevier, pp. 399–410, 2007. ista: Komiyama T, Sweeney LB, Schuldiner O, Garcia KC, Luo L. 2007. Graded expression of semaphorin-1a cell-autonomously directs dendritic targeting of olfactory projection neurons. Cell. 128(2), 399–410. mla: Komiyama, Takaki, et al. “Graded Expression of Semaphorin-1a Cell-Autonomously Directs Dendritic Targeting of Olfactory Projection Neurons.” Cell, vol. 128, no. 2, Elsevier, 2007, pp. 399–410, doi:10.1016/j.cell.2006.12.028. short: T. Komiyama, L.B. Sweeney, O. Schuldiner, K.C. Garcia, L. Luo, Cell 128 (2007) 399–410. date_created: 2020-04-30T10:37:08Z date_published: 2007-01-26T00:00:00Z date_updated: 2024-01-31T10:14:48Z day: '26' doi: 10.1016/j.cell.2006.12.028 extern: '1' intvolume: ' 128' issue: '2' language: - iso: eng month: '01' oa_version: None page: 399-410 publication: Cell publication_identifier: issn: - 0092-8674 publication_status: published publisher: Elsevier quality_controlled: '1' status: public title: Graded expression of semaphorin-1a cell-autonomously directs dendritic targeting of olfactory projection neurons type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 128 year: '2007' ... --- _id: '11122' abstract: - lang: eng text: Nuclear pore complexes (NPCs) are large multiprotein assemblies that allow traffic between the cytoplasm and the nucleus. During mitosis in higher eukaryotes, the Nuclear Envelope (NE) breaks down and NPCs disassemble. How NPCs reassemble and incorporate into the NE upon mitotic exit is poorly understood. We demonstrate a function for the conserved Nup107-160 complex in this process. Partial in vivo depletion of Nup133 or Nup107 via RNAi in HeLa cells resulted in reduced levels of multiple nucleoporins and decreased NPC density in the NE. Immunodepletion of the entire Nup107-160 complex from in vitro nuclear assembly reactions produced nuclei with a continuous NE but no NPCs. This phenotype was reversible only if Nup107-160 complex was readded before closed NE formation. Depletion also prevented association of FG-repeat nucleoporins with chromatin. We propose a stepwise model in which postmitotic NPC assembly initiates on chromatin via early recruitment of the Nup107-160 complex. article_processing_charge: No article_type: original author: - first_name: Tobias C. full_name: Walther, Tobias C. last_name: Walther - first_name: Annabelle full_name: Alves, Annabelle last_name: Alves - first_name: Helen full_name: Pickersgill, Helen last_name: Pickersgill - first_name: Isabelle full_name: Loı̈odice, Isabelle last_name: Loı̈odice - first_name: Martin W full_name: HETZER, Martin W id: 86c0d31b-b4eb-11ec-ac5a-eae7b2e135ed last_name: HETZER orcid: 0000-0002-2111-992X - first_name: Vincent full_name: Galy, Vincent last_name: Galy - first_name: Bastian B. full_name: Hülsmann, Bastian B. last_name: Hülsmann - first_name: Thomas full_name: Köcher, Thomas last_name: Köcher - first_name: Matthias full_name: Wilm, Matthias last_name: Wilm - first_name: Terry full_name: Allen, Terry last_name: Allen - first_name: Iain W. full_name: Mattaj, Iain W. last_name: Mattaj - first_name: Valérie full_name: Doye, Valérie last_name: Doye citation: ama: Walther TC, Alves A, Pickersgill H, et al. The conserved Nup107-160 complex is critical for nuclear pore complex assembly. Cell. 2003;113(2):195-206. doi:10.1016/s0092-8674(03)00235-6 apa: Walther, T. C., Alves, A., Pickersgill, H., Loı̈odice, I., Hetzer, M., Galy, V., … Doye, V. (2003). The conserved Nup107-160 complex is critical for nuclear pore complex assembly. Cell. Elsevier. https://doi.org/10.1016/s0092-8674(03)00235-6 chicago: Walther, Tobias C., Annabelle Alves, Helen Pickersgill, Isabelle Loı̈odice, Martin Hetzer, Vincent Galy, Bastian B. Hülsmann, et al. “The Conserved Nup107-160 Complex Is Critical for Nuclear Pore Complex Assembly.” Cell. Elsevier, 2003. https://doi.org/10.1016/s0092-8674(03)00235-6. ieee: T. C. Walther et al., “The conserved Nup107-160 complex is critical for nuclear pore complex assembly,” Cell, vol. 113, no. 2. Elsevier, pp. 195–206, 2003. ista: Walther TC, Alves A, Pickersgill H, Loı̈odice I, Hetzer M, Galy V, Hülsmann BB, Köcher T, Wilm M, Allen T, Mattaj IW, Doye V. 2003. The conserved Nup107-160 complex is critical for nuclear pore complex assembly. Cell. 113(2), 195–206. mla: Walther, Tobias C., et al. “The Conserved Nup107-160 Complex Is Critical for Nuclear Pore Complex Assembly.” Cell, vol. 113, no. 2, Elsevier, 2003, pp. 195–206, doi:10.1016/s0092-8674(03)00235-6. short: T.C. Walther, A. Alves, H. Pickersgill, I. Loı̈odice, M. Hetzer, V. Galy, B.B. Hülsmann, T. Köcher, M. Wilm, T. Allen, I.W. Mattaj, V. Doye, Cell 113 (2003) 195–206. date_created: 2022-04-07T07:57:10Z date_published: 2003-04-17T00:00:00Z date_updated: 2022-07-18T08:57:42Z day: '17' doi: 10.1016/s0092-8674(03)00235-6 extern: '1' external_id: pmid: - '12705868' intvolume: ' 113' issue: '2' keyword: - General Biochemistry - Genetics and Molecular Biology language: - iso: eng month: '04' oa_version: Published Version page: 195-206 pmid: 1 publication: Cell publication_identifier: issn: - 0092-8674 publication_status: published publisher: Elsevier quality_controlled: '1' scopus_import: '1' status: public title: The conserved Nup107-160 complex is critical for nuclear pore complex assembly type: journal_article user_id: 72615eeb-f1f3-11ec-aa25-d4573ddc34fd volume: 113 year: '2003' ... --- _id: '2989' abstract: - lang: eng text: In contrast to animals, little is known about pattern formation in plants. Physiological and genetic data suggest the involvement of the phytohormone auxin in this process. Here, we characterize a novel member of the PIN family of putative auxin efflux carriers, Arabidopsis PIN4, that is localized in developing and mature root meristems. Atpin4 mutants are defective in establishment and maintenance of endogenous auxin gradients, fail to canalize externally applied auxin, and display various patterning defects in both embryonic and seedling roots. We propose a role for AtPIN4 in generating a sink for auxin below the quiescent center of the root meristem that is essential for auxin distribution and patterning. acknowledgement: We thank Petra Tänzler, Michaela Lehnen, and Thomas Steinmann for technical help. We acknowledge the Arabidopsis Biological Resource Center (Columbus, OH) and Thomas Altman for providing material. We also gratefully acknowledge the ADIS service group for DNA sequencing and ZIGIA (Center for Functional Genomics in Arabidopsis) for the En lines. We are grateful to our colleagues, particularly Leo Gälweiler, Niko Geldner, Matthias Godde, and Kathrin Schrick for critical reading of the manuscript. This work was supported by a fellowship of the Deutscher Akademischer Austauschdienset (J.F.), the Deutsche Forschungsgemeinschaft (Schwerpunktprogramm Phytohormone), the European Communities Biotechnology Programs, the Fonds der Chemischen Industrie, and the INCO-Copernicus Program. article_processing_charge: No article_type: original author: - first_name: Jirí full_name: Friml, Jirí id: 4159519E-F248-11E8-B48F-1D18A9856A87 last_name: Friml orcid: 0000-0002-8302-7596 - first_name: Eva full_name: Benková, Eva id: 38F4F166-F248-11E8-B48F-1D18A9856A87 last_name: Benková orcid: 0000-0002-8510-9739 - first_name: Ikram full_name: Blilou, Ikram last_name: Blilou - first_name: Justyna full_name: Wiśniewska, Justyna last_name: Wiśniewska - first_name: Thorsten full_name: Hamann, Thorsten last_name: Hamann - first_name: Karin full_name: Ljung, Karin last_name: Ljung - first_name: Scott full_name: Woody, Scott last_name: Woody - first_name: Göran full_name: Sandberg, Göran last_name: Sandberg - first_name: Ben full_name: Scheres, Ben last_name: Scheres - first_name: Gerd full_name: Jürgens, Gerd last_name: Jürgens - first_name: Klaus full_name: Palme, Klaus last_name: Palme citation: ama: Friml J, Benková E, Blilou I, et al. AtPIN4 mediates sink-driven auxin gradients and root patterning in Arabidopsis. Cell. 2002;108(5):661-673. doi:10.1016/S0092-8674(02)00656-6 apa: Friml, J., Benková, E., Blilou, I., Wiśniewska, J., Hamann, T., Ljung, K., … Palme, K. (2002). AtPIN4 mediates sink-driven auxin gradients and root patterning in Arabidopsis. Cell. Cell Press. https://doi.org/10.1016/S0092-8674(02)00656-6 chicago: Friml, Jiří, Eva Benková, Ikram Blilou, Justyna Wiśniewska, Thorsten Hamann, Karin Ljung, Scott Woody, et al. “AtPIN4 Mediates Sink-Driven Auxin Gradients and Root Patterning in Arabidopsis.” Cell. Cell Press, 2002. https://doi.org/10.1016/S0092-8674(02)00656-6. ieee: J. Friml et al., “AtPIN4 mediates sink-driven auxin gradients and root patterning in Arabidopsis,” Cell, vol. 108, no. 5. Cell Press, pp. 661–673, 2002. ista: Friml J, Benková E, Blilou I, Wiśniewska J, Hamann T, Ljung K, Woody S, Sandberg G, Scheres B, Jürgens G, Palme K. 2002. AtPIN4 mediates sink-driven auxin gradients and root patterning in Arabidopsis. Cell. 108(5), 661–673. mla: Friml, Jiří, et al. “AtPIN4 Mediates Sink-Driven Auxin Gradients and Root Patterning in Arabidopsis.” Cell, vol. 108, no. 5, Cell Press, 2002, pp. 661–73, doi:10.1016/S0092-8674(02)00656-6. short: J. Friml, E. Benková, I. Blilou, J. Wiśniewska, T. Hamann, K. Ljung, S. Woody, G. Sandberg, B. Scheres, G. Jürgens, K. Palme, Cell 108 (2002) 661–673. date_created: 2018-12-11T12:00:43Z date_published: 2002-03-08T00:00:00Z date_updated: 2023-07-17T11:57:40Z day: '08' doi: 10.1016/S0092-8674(02)00656-6 extern: '1' external_id: pmid: - '11893337' intvolume: ' 108' issue: '5' language: - iso: eng month: '03' oa_version: None page: 661 - 673 pmid: 1 publication: Cell publication_identifier: issn: - 0092-8674 publication_status: published publisher: Cell Press publist_id: '3713' quality_controlled: '1' scopus_import: '1' status: public title: AtPIN4 mediates sink-driven auxin gradients and root patterning in Arabidopsis type: journal_article user_id: ea97e931-d5af-11eb-85d4-e6957dddbf17 volume: 108 year: '2002' ... --- _id: '2586' abstract: - lang: eng text: The role of inhibitory Golgi cells in cerebellar function was investigated by selectively ablating Golgi cells expressing human interleukin-2 receptor α subunit in transgenic mice, using the immunotoxin- mediated cell targeting technique. Golgi cell disruption caused severe acute motor disorders. These mice showed gradual recovery but retained a continuing inability to perform compound movements. Optical and electrical recordings combined with immunocytological analysis indicated that elimination of Golgi cells not only reduces GABA-mediated inhibition but also attenuates functional NMDA receptors in granule cells. These results demonstrate that synaptic integration involving both GABA inhibition and NMDA receptor activation is essential for compound motor coordination. Furthermore, this integration can adapt after Golgi cell elimination so as not to evoke overexcitation by the reduction of NMDA receptors. acknowledgement: "We thank Kumlesh K Dev for careful reading of this manuscript, Peter Somogyi and Hirohide Sawada for invaluable advice, and Akira Uesugi for photographic assistance. This work was supported in part by research grants from the Ministry of Education, Science and Culture of Japan. the Sankyo Foundation. the Yamanouchi Founda-tion. the Biomolecular Engineering Research Institute, CREST and the International Resource Program of the National Cancer Institute. \r\n" article_processing_charge: No article_type: original author: - first_name: Dai full_name: Watanabe, Dai last_name: Watanabe - first_name: Hitoshi full_name: Inokawa, Hitoshi last_name: Inokawa - first_name: Kouichi full_name: Hashimoto, Kouichi last_name: Hashimoto - first_name: Noboru full_name: Suzuki, Noboru last_name: Suzuki - first_name: Masanobu full_name: Kano, Masanobu last_name: Kano - first_name: Ryuichi full_name: Shigemoto, Ryuichi id: 499F3ABC-F248-11E8-B48F-1D18A9856A87 last_name: Shigemoto orcid: 0000-0001-8761-9444 - first_name: Tomoo full_name: Hirano, Tomoo last_name: Hirano - first_name: Keisuke full_name: Toyama, Keisuke last_name: Toyama - first_name: Satoshi full_name: Kaneko, Satoshi last_name: Kaneko - first_name: Mineto full_name: Yokoi, Mineto last_name: Yokoi - first_name: Koki full_name: Moriyoshi, Koki last_name: Moriyoshi - first_name: Misao full_name: Suzuki, Misao last_name: Suzuki - first_name: Kazuto full_name: Kobayashi, Kazuto last_name: Kobayashi - first_name: Toshiharu full_name: Nagatsu, Toshiharu last_name: Nagatsu - first_name: Robert full_name: Kreitman, Robert last_name: Kreitman - first_name: Ira full_name: Pastan, Ira last_name: Pastan - first_name: Shigetada full_name: Nakanishi, Shigetada last_name: Nakanishi citation: ama: Watanabe D, Inokawa H, Hashimoto K, et al. Ablation of cerebellar Golgi cells disrupts synaptic integration involving GABA inhibition and NMDA receptor activation in motor coordination. Cell. 1998;95(1):17-27. doi:10.1016/S0092-8674(00)81779-1 apa: Watanabe, D., Inokawa, H., Hashimoto, K., Suzuki, N., Kano, M., Shigemoto, R., … Nakanishi, S. (1998). Ablation of cerebellar Golgi cells disrupts synaptic integration involving GABA inhibition and NMDA receptor activation in motor coordination. Cell. Cell Press. https://doi.org/10.1016/S0092-8674(00)81779-1 chicago: Watanabe, Dai, Hitoshi Inokawa, Kouichi Hashimoto, Noboru Suzuki, Masanobu Kano, Ryuichi Shigemoto, Tomoo Hirano, et al. “Ablation of Cerebellar Golgi Cells Disrupts Synaptic Integration Involving GABA Inhibition and NMDA Receptor Activation in Motor Coordination.” Cell. Cell Press, 1998. https://doi.org/10.1016/S0092-8674(00)81779-1. ieee: D. Watanabe et al., “Ablation of cerebellar Golgi cells disrupts synaptic integration involving GABA inhibition and NMDA receptor activation in motor coordination,” Cell, vol. 95, no. 1. Cell Press, pp. 17–27, 1998. ista: Watanabe D, Inokawa H, Hashimoto K, Suzuki N, Kano M, Shigemoto R, Hirano T, Toyama K, Kaneko S, Yokoi M, Moriyoshi K, Suzuki M, Kobayashi K, Nagatsu T, Kreitman R, Pastan I, Nakanishi S. 1998. Ablation of cerebellar Golgi cells disrupts synaptic integration involving GABA inhibition and NMDA receptor activation in motor coordination. Cell. 95(1), 17–27. mla: Watanabe, Dai, et al. “Ablation of Cerebellar Golgi Cells Disrupts Synaptic Integration Involving GABA Inhibition and NMDA Receptor Activation in Motor Coordination.” Cell, vol. 95, no. 1, Cell Press, 1998, pp. 17–27, doi:10.1016/S0092-8674(00)81779-1. short: D. Watanabe, H. Inokawa, K. Hashimoto, N. Suzuki, M. Kano, R. Shigemoto, T. Hirano, K. Toyama, S. Kaneko, M. Yokoi, K. Moriyoshi, M. Suzuki, K. Kobayashi, T. Nagatsu, R. Kreitman, I. Pastan, S. Nakanishi, Cell 95 (1998) 17–27. date_created: 2018-12-11T11:58:32Z date_published: 1998-10-02T00:00:00Z date_updated: 2022-08-31T13:46:20Z day: '02' doi: 10.1016/S0092-8674(00)81779-1 extern: '1' external_id: pmid: - '9778244 ' intvolume: ' 95' issue: '1' language: - iso: eng month: '10' oa_version: None page: 17 - 27 pmid: 1 publication: Cell publication_identifier: issn: - 0092-8674 publication_status: published publisher: Cell Press publist_id: '4312' quality_controlled: '1' scopus_import: '1' status: public title: Ablation of cerebellar Golgi cells disrupts synaptic integration involving GABA inhibition and NMDA receptor activation in motor coordination type: journal_article user_id: ea97e931-d5af-11eb-85d4-e6957dddbf17 volume: 95 year: '1998' ... --- _id: '6160' abstract: - lang: eng text: Natural isolates of C. elegans exhibit either solitary or social feeding behavior. Solitary foragers move slowly on a bacterial lawn and disperse across it, while social foragers move rapidly on bacteria and aggregate together. A loss-of-function mutation in the npr-1 gene, which encodes a predicted G protein–coupled receptor similar to neuropeptide Y receptors, causes a solitary strain to take on social behavior. Two isoforms of NPR-1 that differ at a single residue occur in the wild. One isoform, NPR-1 215F, is found exclusively in social strains, while the other isoform, NPR-1 215V, is found exclusively in solitary strains. An NPR-1 215V transgene can induce solitary feeding behavior in a wild social strain. Thus, isoforms of a putative neuropeptide receptor generate natural variation in C. elegans feeding behavior. author: - first_name: Mario full_name: de Bono, Mario id: 4E3FF80E-F248-11E8-B48F-1D18A9856A87 last_name: de Bono orcid: 0000-0001-8347-0443 - first_name: Cornelia I full_name: Bargmann, Cornelia I last_name: Bargmann citation: ama: de Bono M, Bargmann CI. Natural variation in a neuropeptide Y receptor homolog modifies social behavior and food response in C. elegans. Cell. 1998;94(5):679-689. doi:10.1016/s0092-8674(00)81609-8 apa: de Bono, M., & Bargmann, C. I. (1998). Natural variation in a neuropeptide Y receptor homolog modifies social behavior and food response in C. elegans. Cell. Elsevier. https://doi.org/10.1016/s0092-8674(00)81609-8 chicago: Bono, Mario de, and Cornelia I Bargmann. “Natural Variation in a Neuropeptide Y Receptor Homolog Modifies Social Behavior and Food Response in C. Elegans.” Cell. Elsevier, 1998. https://doi.org/10.1016/s0092-8674(00)81609-8. ieee: M. de Bono and C. I. Bargmann, “Natural variation in a neuropeptide Y receptor homolog modifies social behavior and food response in C. elegans,” Cell, vol. 94, no. 5. Elsevier, pp. 679–689, 1998. ista: de Bono M, Bargmann CI. 1998. Natural variation in a neuropeptide Y receptor homolog modifies social behavior and food response in C. elegans. Cell. 94(5), 679–689. mla: de Bono, Mario, and Cornelia I. Bargmann. “Natural Variation in a Neuropeptide Y Receptor Homolog Modifies Social Behavior and Food Response in C. Elegans.” Cell, vol. 94, no. 5, Elsevier, 1998, pp. 679–89, doi:10.1016/s0092-8674(00)81609-8. short: M. de Bono, C.I. Bargmann, Cell 94 (1998) 679–689. date_created: 2019-03-21T10:32:06Z date_published: 1998-09-04T00:00:00Z date_updated: 2021-01-12T08:06:28Z day: '04' doi: 10.1016/s0092-8674(00)81609-8 extern: '1' external_id: pmid: - '9741632' intvolume: ' 94' issue: '5' language: - iso: eng month: '09' oa_version: None page: 679-689 pmid: 1 publication: Cell publication_identifier: issn: - 0092-8674 publication_status: published publisher: Elsevier quality_controlled: '1' status: public title: Natural variation in a neuropeptide Y receptor homolog modifies social behavior and food response in C. elegans type: journal_article user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87 volume: 94 year: '1998' ... --- _id: '2559' abstract: - lang: eng text: Taking advantage of the restricted expression of metabotropic glutamate receptor subtype 6 (mGIuR6) in retinal ON bipolar cells, we generated knockout mice lacking mGIuR6 expression. The homozygous mutant mice showed a loss of ON responses but unchanged OFF responses to light. The mutant mice displayed no obvious changes in retinal cell organization nor in the projection of optic fibers to the brain. Furthermore, the mGIuR6-deficient mice showed visual behavioral responses to light stimulation as examined by shuttle box avoidance behavior experiments using light exposure as a conditioned stimulus. The results demonstrate that mGIuR6 is essential in synaptic transmission to the ON bipolar cell and that the OFF response provides an important means for transmitting visual information. acknowledgement: We thank Drs. N. Mizuno, M. Iso, M. Tachibana, A. Kaneko, M. Tessier-Lavigne, and T. Hensch for useful advice and A. Uesugi for photographic assistance. This work is supported by grants in aid for specially promoted research, for scientific research on priority areas, and for scientific research (A) from the Ministry of Education, Science, and Culture in Japan and by grants from the Ministry of Health and Welfare of Japan, the Sankyo Foundation, and the Senri Life Science Foundation. article_processing_charge: No article_type: original author: - first_name: Masayuki full_name: Masu, Masayuki last_name: Masu - first_name: Hideki full_name: Iwakabe, Hideki last_name: Iwakabe - first_name: Yoshiaki full_name: Tagawa, Yoshiaki last_name: Tagawa - first_name: Tomomitsu full_name: Miyoshi, Tomomitsu last_name: Miyoshi - first_name: Masayuki full_name: Yamashita, Masayuki last_name: Yamashita - first_name: Yutaka full_name: Fukuda, Yutaka last_name: Fukuda - first_name: Hitoshi full_name: Sasaki, Hitoshi last_name: Sasaki - first_name: Kano full_name: Hiroi, Kano last_name: Hiroi - first_name: Yasuhisa full_name: Nakamura, Yasuhisa last_name: Nakamura - first_name: Ryuichi full_name: Shigemoto, Ryuichi id: 499F3ABC-F248-11E8-B48F-1D18A9856A87 last_name: Shigemoto orcid: 0000-0001-8761-9444 - first_name: Masahiko full_name: Takada, Masahiko last_name: Takada - first_name: Kenji full_name: Nakamura, Kenji last_name: Nakamura - first_name: Kazuki full_name: Nakao, Kazuki last_name: Nakao - first_name: Motoya full_name: Katsuki, Motoya last_name: Katsuki - first_name: Shigetada full_name: Nakanishi, Shigetada last_name: Nakanishi citation: ama: Masu M, Iwakabe H, Tagawa Y, et al. Specific deficit of the ON response in visual transmission by targeted disruption of the mGIuR6 gene. Cell. 1995;80(5):757-765. doi:10.1016/0092-8674(95)90354-2 apa: Masu, M., Iwakabe, H., Tagawa, Y., Miyoshi, T., Yamashita, M., Fukuda, Y., … Nakanishi, S. (1995). Specific deficit of the ON response in visual transmission by targeted disruption of the mGIuR6 gene. Cell. Cell Press. https://doi.org/10.1016/0092-8674(95)90354-2 chicago: Masu, Masayuki, Hideki Iwakabe, Yoshiaki Tagawa, Tomomitsu Miyoshi, Masayuki Yamashita, Yutaka Fukuda, Hitoshi Sasaki, et al. “Specific Deficit of the ON Response in Visual Transmission by Targeted Disruption of the MGIuR6 Gene.” Cell. Cell Press, 1995. https://doi.org/10.1016/0092-8674(95)90354-2. ieee: M. Masu et al., “Specific deficit of the ON response in visual transmission by targeted disruption of the mGIuR6 gene,” Cell, vol. 80, no. 5. Cell Press, pp. 757–765, 1995. ista: Masu M, Iwakabe H, Tagawa Y, Miyoshi T, Yamashita M, Fukuda Y, Sasaki H, Hiroi K, Nakamura Y, Shigemoto R, Takada M, Nakamura K, Nakao K, Katsuki M, Nakanishi S. 1995. Specific deficit of the ON response in visual transmission by targeted disruption of the mGIuR6 gene. Cell. 80(5), 757–765. mla: Masu, Masayuki, et al. “Specific Deficit of the ON Response in Visual Transmission by Targeted Disruption of the MGIuR6 Gene.” Cell, vol. 80, no. 5, Cell Press, 1995, pp. 757–65, doi:10.1016/0092-8674(95)90354-2. short: M. Masu, H. Iwakabe, Y. Tagawa, T. Miyoshi, M. Yamashita, Y. Fukuda, H. Sasaki, K. Hiroi, Y. Nakamura, R. Shigemoto, M. Takada, K. Nakamura, K. Nakao, M. Katsuki, S. Nakanishi, Cell 80 (1995) 757–765. date_created: 2018-12-11T11:58:23Z date_published: 1995-02-10T00:00:00Z date_updated: 2022-06-28T13:27:50Z day: '10' doi: 10.1016/0092-8674(95)90354-2 extern: '1' external_id: pmid: - '7889569' intvolume: ' 80' issue: '5' language: - iso: eng main_file_link: - open_access: '1' url: https://www.sciencedirect.com/science/article/pii/0092867495903542 month: '02' oa: 1 oa_version: Published Version page: 757 - 765 pmid: 1 publication: Cell publication_identifier: issn: - 0092-8674 publication_status: published publisher: Cell Press publist_id: '4339' quality_controlled: '1' status: public title: Specific deficit of the ON response in visual transmission by targeted disruption of the mGIuR6 gene type: journal_article user_id: ea97e931-d5af-11eb-85d4-e6957dddbf17 volume: 80 year: '1995' ... --- _id: '2554' abstract: - lang: eng text: 'The retinal bipolar cell receiving glutamate transmission from photoreceptors mediates a key process in segregating visual signals into ON center and OFF center pathways. This transmission involves a G protein- coupled metabotropic glutamate receptor (mGluR). Immunocytochemical and immunoelectron microscopic studies indicate the restricted localization of a specific mGluR subtype, mGluR6, at the postsynaptic site of the rat rod bipolar cell. This specialization is developmentally regulated: mGluR6 is initially distributed in both the soma and dendrites and is finally concentrated on the postsynaptic site. The mGluR6 localization is reversed when photoreceptors degenerate in the mutant rat with retinal dystrophy. Evidence is thus presented indicating specialized, developmentally regulated receptor distribution in the central nervous system and the crucial role of mGluR6 in photoreceptor-bipolar cell synaptic transmission.' acknowledgement: "We thank M. Tachibana for technical advice concerning dissociated bipolar cell preparation, Y. Honda for advice \r\nconcerning RCS rat experiments, and A. Uesugi for photographic assistance. This work is partly supported by research grants from the Ministry of Education, Science, and Culture of Japan and from the Ministry of Health and Welfare of\r\nJapan. " article_processing_charge: No article_type: original author: - first_name: Akinori full_name: Nomura, Akinori last_name: Nomura - first_name: Ryuichi full_name: Shigemoto, Ryuichi id: 499F3ABC-F248-11E8-B48F-1D18A9856A87 last_name: Shigemoto orcid: 0000-0001-8761-9444 - first_name: Yasuhisa full_name: Nakamura, Yasuhisa last_name: Nakamura - first_name: Naoyuki full_name: Okamoto, Naoyuki last_name: Okamoto - first_name: Noboru full_name: Mizuno, Noboru last_name: Mizuno - first_name: Shigetada full_name: Nakanishi, Shigetada last_name: Nakanishi citation: ama: Nomura A, Shigemoto R, Nakamura Y, Okamoto N, Mizuno N, Nakanishi S. Developmentally regulated postsynaptic localization of a metabotropic glutamate receptor in rat rod bipolar cells. Cell. 1994;77(3):361-369. doi:10.1016/0092-8674(94)90151-1 apa: Nomura, A., Shigemoto, R., Nakamura, Y., Okamoto, N., Mizuno, N., & Nakanishi, S. (1994). Developmentally regulated postsynaptic localization of a metabotropic glutamate receptor in rat rod bipolar cells. Cell. Cell Press. https://doi.org/10.1016/0092-8674(94)90151-1 chicago: Nomura, Akinori, Ryuichi Shigemoto, Yasuhisa Nakamura, Naoyuki Okamoto, Noboru Mizuno, and Shigetada Nakanishi. “Developmentally Regulated Postsynaptic Localization of a Metabotropic Glutamate Receptor in Rat Rod Bipolar Cells.” Cell. Cell Press, 1994. https://doi.org/10.1016/0092-8674(94)90151-1. ieee: A. Nomura, R. Shigemoto, Y. Nakamura, N. Okamoto, N. Mizuno, and S. Nakanishi, “Developmentally regulated postsynaptic localization of a metabotropic glutamate receptor in rat rod bipolar cells,” Cell, vol. 77, no. 3. Cell Press, pp. 361–369, 1994. ista: Nomura A, Shigemoto R, Nakamura Y, Okamoto N, Mizuno N, Nakanishi S. 1994. Developmentally regulated postsynaptic localization of a metabotropic glutamate receptor in rat rod bipolar cells. Cell. 77(3), 361–369. mla: Nomura, Akinori, et al. “Developmentally Regulated Postsynaptic Localization of a Metabotropic Glutamate Receptor in Rat Rod Bipolar Cells.” Cell, vol. 77, no. 3, Cell Press, 1994, pp. 361–69, doi:10.1016/0092-8674(94)90151-1. short: A. Nomura, R. Shigemoto, Y. Nakamura, N. Okamoto, N. Mizuno, S. Nakanishi, Cell 77 (1994) 361–369. date_created: 2018-12-11T11:58:21Z date_published: 1994-05-06T00:00:00Z date_updated: 2022-06-07T14:28:33Z day: '06' doi: 10.1016/0092-8674(94)90151-1 extern: '1' external_id: pmid: - '8181056' intvolume: ' 77' issue: '3' language: - iso: eng main_file_link: - url: https://www.sciencedirect.com/science/article/pii/0092867494901511?via%3Dihub month: '05' oa_version: None page: 361 - 369 pmid: 1 publication: Cell publication_identifier: issn: - 0092-8674 publication_status: published publisher: Cell Press publist_id: '4344' quality_controlled: '1' scopus_import: '1' status: public title: Developmentally regulated postsynaptic localization of a metabotropic glutamate receptor in rat rod bipolar cells type: journal_article user_id: ea97e931-d5af-11eb-85d4-e6957dddbf17 volume: 77 year: '1994' ...