[{"date_updated":"2024-01-10T12:45:25Z","year":"2023","citation":{"apa":"Harish, R. K., Gupta, M., Zöller, D., Hartmann, H., Gheisari, A., Machate, A., … Brand, M. (2023). Real-time monitoring of an endogenous Fgf8a gradient attests to its role as a morphogen during zebrafish gastrulation. <i>Development</i>. The Company of Biologists. <a href=\"https://doi.org/10.1242/dev.201559\">https://doi.org/10.1242/dev.201559</a>","ama":"Harish RK, Gupta M, Zöller D, et al. Real-time monitoring of an endogenous Fgf8a gradient attests to its role as a morphogen during zebrafish gastrulation. <i>Development</i>. 2023;150(19). doi:<a href=\"https://doi.org/10.1242/dev.201559\">10.1242/dev.201559</a>","chicago":"Harish, Rohit K, Mansi Gupta, Daniela Zöller, Hella Hartmann, Ali Gheisari, Anja Machate, Stefan Hans, and Michael Brand. “Real-Time Monitoring of an Endogenous Fgf8a Gradient Attests to Its Role as a Morphogen during Zebrafish Gastrulation.” <i>Development</i>. The Company of Biologists, 2023. <a href=\"https://doi.org/10.1242/dev.201559\">https://doi.org/10.1242/dev.201559</a>.","ieee":"R. K. Harish <i>et al.</i>, “Real-time monitoring of an endogenous Fgf8a gradient attests to its role as a morphogen during zebrafish gastrulation,” <i>Development</i>, vol. 150, no. 19. The Company of Biologists, 2023.","mla":"Harish, Rohit K., et al. “Real-Time Monitoring of an Endogenous Fgf8a Gradient Attests to Its Role as a Morphogen during Zebrafish Gastrulation.” <i>Development</i>, vol. 150, no. 19, dev201559, The Company of Biologists, 2023, doi:<a href=\"https://doi.org/10.1242/dev.201559\">10.1242/dev.201559</a>.","short":"R.K. Harish, M. Gupta, D. Zöller, H. Hartmann, A. Gheisari, A. Machate, S. Hans, M. Brand, Development 150 (2023).","ista":"Harish RK, Gupta M, Zöller D, Hartmann H, Gheisari A, Machate A, Hans S, Brand M. 2023. Real-time monitoring of an endogenous Fgf8a gradient attests to its role as a morphogen during zebrafish gastrulation. Development. 150(19), dev201559."},"isi":1,"external_id":{"isi":["001097449100002"],"pmid":["37665167"]},"doi":"10.1242/dev.201559","day":"01","abstract":[{"lang":"eng","text":"Morphogen gradients impart positional information to cells in a homogenous tissue field. Fgf8a, a highly conserved growth factor, has been proposed to act as a morphogen during zebrafish gastrulation. However, technical limitations have so far prevented direct visualization of the endogenous Fgf8a gradient and confirmation of its morphogenic activity. Here, we monitor Fgf8a propagation in the developing neural plate using a CRISPR/Cas9-mediated EGFP knock-in at the endogenous fgf8a locus. By combining sensitive imaging with single-molecule fluorescence correlation spectroscopy, we demonstrate that Fgf8a, which is produced at the embryonic margin, propagates by diffusion through the extracellular space and forms a graded distribution towards the animal pole. Overlaying the Fgf8a gradient curve with expression profiles of its downstream targets determines the precise input-output relationship of Fgf8a-mediated patterning. Manipulation of the extracellular Fgf8a levels alters the signaling outcome, thus establishing Fgf8a as a bona fide morphogen during zebrafish gastrulation. Furthermore, by hindering Fgf8a diffusion, we demonstrate that extracellular diffusion of the protein from the source is crucial for it to achieve its morphogenic potential."}],"volume":150,"acknowledgement":"We thank members of the Brand lab, as well as Justina Stark (Ivo Sbalzarini group, Max Planck Institute of Molecular Cell Biology and Genetics, Dresden, Germany) for project-related discussions; Darren Gilmour (University of Zurich), Karuna Sampath (University of Warwick) and Gokul Kesavan (Vowels Lifesciences Private Limited, Bangalore) for comments on the manuscript; personnel of the CMCB technology platform, TU Dresden for imaging and image analysis-related support; and Maurizio Abbate (Technical support, Arivis) for help with image analysis. We are also grateful to Stapornwongkul and Briscoe for commenting on a preprint version of our work (Stapornwongkul and Briscoe, 2022).\r\nThis work was supported by the Deutsche Forschungsgemeinschaft (BR 1746/6-2, BR 1746/11-1 and BR 1746/3 to M.B.), by a Cluster of Excellence ‘Physics of Life’ seed grant and by institutional funds from Technische Universitat Dresden (to M.B.). Open Access funding provided by Technische Universitat Dresden. Deposited in PMC for immediate release.","ddc":["570"],"_id":"14774","pmid":1,"author":[{"id":"1bae78aa-ee0e-11ec-9b76-bc42990f409d","first_name":"Rohit K","last_name":"Harish","full_name":"Harish, Rohit K"},{"last_name":"Gupta","first_name":"Mansi","full_name":"Gupta, Mansi"},{"full_name":"Zöller, Daniela","first_name":"Daniela","last_name":"Zöller"},{"full_name":"Hartmann, Hella","last_name":"Hartmann","first_name":"Hella"},{"last_name":"Gheisari","first_name":"Ali","full_name":"Gheisari, Ali"},{"full_name":"Machate, Anja","last_name":"Machate","first_name":"Anja"},{"full_name":"Hans, Stefan","first_name":"Stefan","last_name":"Hans"},{"last_name":"Brand","first_name":"Michael","full_name":"Brand, Michael"}],"issue":"19","publication_status":"published","article_processing_charge":"Yes (via OA deal)","date_created":"2024-01-10T09:18:54Z","department":[{"_id":"AnKi"}],"title":"Real-time monitoring of an endogenous Fgf8a gradient attests to its role as a morphogen during zebrafish gastrulation","intvolume":"       150","quality_controlled":"1","file_date_updated":"2024-01-10T12:41:13Z","publisher":"The Company of Biologists","article_type":"original","tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","short":"CC BY (4.0)","image":"/images/cc_by.png","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)"},"date_published":"2023-10-01T00:00:00Z","type":"journal_article","publication_identifier":{"issn":["0950-1991"],"eissn":["1477-9129"]},"oa":1,"file":[{"file_name":"2023_Development_Harish.pdf","content_type":"application/pdf","date_updated":"2024-01-10T12:41:13Z","checksum":"2d6f52dc33260a9b2352b8f28374ba5f","file_size":12836306,"date_created":"2024-01-10T12:41:13Z","creator":"dernst","file_id":"14790","relation":"main_file","success":1,"access_level":"open_access"}],"status":"public","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","publication":"Development","has_accepted_license":"1","oa_version":"Published Version","month":"10","article_number":"dev201559","language":[{"iso":"eng"}],"keyword":["Developmental Biology","Molecular Biology"]},{"language":[{"iso":"eng"}],"keyword":["Developmental Biology","Cell Biology","General Biochemistry","Genetics and Molecular Biology","Molecular Biology"],"month":"09","oa_version":"Preprint","publication":"Developmental Cell","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","status":"public","main_file_link":[{"open_access":"1","url":"https://www.biorxiv.org/content/10.1101/2023.07.09.548244"}],"oa":1,"publication_identifier":{"issn":["1534-5807"]},"date_published":"2023-09-11T00:00:00Z","type":"journal_article","article_type":"original","publisher":"Elsevier","page":"1578-1592.e5","quality_controlled":"1","title":"Spatial organization and function of RNA molecules within phase-separated condensates in zebrafish are controlled by Dnd1","intvolume":"        58","publication_status":"published","date_created":"2024-01-10T09:41:21Z","department":[{"_id":"Bio"}],"article_processing_charge":"No","author":[{"full_name":"Westerich, Kim Joana","last_name":"Westerich","first_name":"Kim Joana"},{"last_name":"Tarbashevich","first_name":"Katsiaryna","full_name":"Tarbashevich, Katsiaryna"},{"full_name":"Schick, Jan","first_name":"Jan","last_name":"Schick"},{"first_name":"Antra","last_name":"Gupta","full_name":"Gupta, Antra"},{"full_name":"Zhu, Mingzhao","first_name":"Mingzhao","last_name":"Zhu"},{"first_name":"Kenneth","last_name":"Hull","full_name":"Hull, Kenneth"},{"last_name":"Romo","first_name":"Daniel","full_name":"Romo, Daniel"},{"full_name":"Zeuschner, Dagmar","last_name":"Zeuschner","first_name":"Dagmar"},{"id":"3384113A-F248-11E8-B48F-1D18A9856A87","full_name":"Goudarzi, Mohammad","last_name":"Goudarzi","first_name":"Mohammad"},{"first_name":"Theresa","last_name":"Gross-Thebing","full_name":"Gross-Thebing, Theresa"},{"last_name":"Raz","first_name":"Erez","full_name":"Raz, Erez"}],"issue":"17","pmid":1,"_id":"14781","volume":58,"acknowledgement":"We thank Celeste Brennecka for editing and Michal Reichman-Fried for critical comments on the manuscript. We thank Ursula Jordan, Esther Messerschmidt, and Ines Sandbote for technical assistance. This work was supported by funding from the University of Münster (K.J.W., K.T., E.R., A.G., T.G.-T., J.S., and M.G.), the Max Planck Institute for Molecular Biomedicine (D.Z.), the German Research Foundation grant CRU 326 (P2) RA863/12-2 (E.R.), Baylor University (K.H. and D.R.), and the National Institutes of Health grant R35 GM 134910 (D.R.). We thank the referees for insightful comments that helped improve the manuscript.","abstract":[{"text":"Germ granules, condensates of phase-separated RNA and protein, are organelles that are essential for germline development in different organisms. The patterning of the granules and their relevance for germ cell fate are not fully understood. Combining three-dimensional in vivo structural and functional analyses, we study the dynamic spatial organization of molecules within zebrafish germ granules. We find that the localization of RNA molecules to the periphery of the granules, where ribosomes are localized, depends on translational activity at this location. In addition, we find that the vertebrate-specific Dead end (Dnd1) protein is essential for nanos3 RNA localization at the condensates’ periphery. Accordingly, in the absence of Dnd1, or when translation is inhibited, nanos3 RNA translocates into the granule interior, away from the ribosomes, a process that is correlated with the loss of germ cell fate. These findings highlight the relevance of sub-granule compartmentalization for post-transcriptional control and its importance for preserving germ cell totipotency.","lang":"eng"}],"doi":"10.1016/j.devcel.2023.06.009","day":"11","external_id":{"pmid":["37463577"]},"date_updated":"2024-01-16T08:56:36Z","year":"2023","citation":{"chicago":"Westerich, Kim Joana, Katsiaryna Tarbashevich, Jan Schick, Antra Gupta, Mingzhao Zhu, Kenneth Hull, Daniel Romo, et al. “Spatial Organization and Function of RNA Molecules within Phase-Separated Condensates in Zebrafish Are Controlled by Dnd1.” <i>Developmental Cell</i>. Elsevier, 2023. <a href=\"https://doi.org/10.1016/j.devcel.2023.06.009\">https://doi.org/10.1016/j.devcel.2023.06.009</a>.","ieee":"K. J. Westerich <i>et al.</i>, “Spatial organization and function of RNA molecules within phase-separated condensates in zebrafish are controlled by Dnd1,” <i>Developmental Cell</i>, vol. 58, no. 17. Elsevier, p. 1578–1592.e5, 2023.","apa":"Westerich, K. J., Tarbashevich, K., Schick, J., Gupta, A., Zhu, M., Hull, K., … Raz, E. (2023). Spatial organization and function of RNA molecules within phase-separated condensates in zebrafish are controlled by Dnd1. <i>Developmental Cell</i>. Elsevier. <a href=\"https://doi.org/10.1016/j.devcel.2023.06.009\">https://doi.org/10.1016/j.devcel.2023.06.009</a>","ama":"Westerich KJ, Tarbashevich K, Schick J, et al. Spatial organization and function of RNA molecules within phase-separated condensates in zebrafish are controlled by Dnd1. <i>Developmental Cell</i>. 2023;58(17):1578-1592.e5. doi:<a href=\"https://doi.org/10.1016/j.devcel.2023.06.009\">10.1016/j.devcel.2023.06.009</a>","ista":"Westerich KJ, Tarbashevich K, Schick J, Gupta A, Zhu M, Hull K, Romo D, Zeuschner D, Goudarzi M, Gross-Thebing T, Raz E. 2023. Spatial organization and function of RNA molecules within phase-separated condensates in zebrafish are controlled by Dnd1. Developmental Cell. 58(17), 1578–1592.e5.","short":"K.J. Westerich, K. Tarbashevich, J. Schick, A. Gupta, M. Zhu, K. Hull, D. Romo, D. Zeuschner, M. Goudarzi, T. Gross-Thebing, E. Raz, Developmental Cell 58 (2023) 1578–1592.e5.","mla":"Westerich, Kim Joana, et al. “Spatial Organization and Function of RNA Molecules within Phase-Separated Condensates in Zebrafish Are Controlled by Dnd1.” <i>Developmental Cell</i>, vol. 58, no. 17, Elsevier, 2023, p. 1578–1592.e5, doi:<a href=\"https://doi.org/10.1016/j.devcel.2023.06.009\">10.1016/j.devcel.2023.06.009</a>."}},{"publisher":"Elsevier","article_type":"review","quality_controlled":"1","ec_funded":1,"page":"58-65","file_date_updated":"2024-01-08T10:16:04Z","department":[{"_id":"EdHa"}],"date_created":"2023-01-12T12:09:47Z","article_processing_charge":"Yes (via OA deal)","publication_status":"published","title":"Modelling the dynamics of mammalian gut homeostasis","scopus_import":"1","_id":"12162","pmid":1,"author":[{"id":"43BE2298-F248-11E8-B48F-1D18A9856A87","last_name":"Corominas-Murtra","first_name":"Bernat","full_name":"Corominas-Murtra, Bernat","orcid":"0000-0001-9806-5643"},{"id":"3A9DB764-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0001-6005-1561","full_name":"Hannezo, Edouard B","first_name":"Edouard B","last_name":"Hannezo"}],"acknowledgement":"This work received funding from the ERC under the European Union’s Horizon 2020 research and innovation programme (grant agreement No. 851288 to E.H.).\r\nB. C-M wants to acknowledge the support of the field of excellence Complexity of Life, in Basic Research and Innovation of the University of Graz.","volume":"150-151","ddc":["570"],"day":"02","doi":"10.1016/j.semcdb.2022.11.005","abstract":[{"lang":"eng","text":"Homeostatic balance in the intestinal epithelium relies on a fast cellular turnover, which is coordinated by an intricate interplay between biochemical signalling, mechanical forces and organ geometry. We review recent modelling approaches that have been developed to understand different facets of this remarkable homeostatic equilibrium. Existing models offer different, albeit complementary, perspectives on the problem. First, biomechanical models aim to explain the local and global mechanical stresses driving cell renewal as well as tissue shape maintenance. Second, compartmental models provide insights into the conditions necessary to keep a constant flow of cells with well-defined ratios of cell types, and how perturbations can lead to an unbalance of relative compartment sizes. A third family of models address, at the cellular level, the nature and regulation of stem fate choices that are necessary to fuel cellular turnover. We also review how these different approaches are starting to be integrated together across scales, to provide quantitative predictions and new conceptual frameworks to think about the dynamics of cell renewal in complex tissues."}],"citation":{"short":"B. Corominas-Murtra, E.B. Hannezo, Seminars in Cell &#38; Developmental Biology 150–151 (2023) 58–65.","mla":"Corominas-Murtra, Bernat, and Edouard B. Hannezo. “Modelling the Dynamics of Mammalian Gut Homeostasis.” <i>Seminars in Cell &#38; Developmental Biology</i>, vol. 150–151, Elsevier, 2023, pp. 58–65, doi:<a href=\"https://doi.org/10.1016/j.semcdb.2022.11.005\">10.1016/j.semcdb.2022.11.005</a>.","ista":"Corominas-Murtra B, Hannezo EB. 2023. Modelling the dynamics of mammalian gut homeostasis. Seminars in Cell &#38; Developmental Biology. 150–151, 58–65.","apa":"Corominas-Murtra, B., &#38; Hannezo, E. B. (2023). Modelling the dynamics of mammalian gut homeostasis. <i>Seminars in Cell &#38; Developmental Biology</i>. Elsevier. <a href=\"https://doi.org/10.1016/j.semcdb.2022.11.005\">https://doi.org/10.1016/j.semcdb.2022.11.005</a>","ama":"Corominas-Murtra B, Hannezo EB. Modelling the dynamics of mammalian gut homeostasis. <i>Seminars in Cell &#38; Developmental Biology</i>. 2023;150-151:58-65. doi:<a href=\"https://doi.org/10.1016/j.semcdb.2022.11.005\">10.1016/j.semcdb.2022.11.005</a>","chicago":"Corominas-Murtra, Bernat, and Edouard B Hannezo. “Modelling the Dynamics of Mammalian Gut Homeostasis.” <i>Seminars in Cell &#38; Developmental Biology</i>. Elsevier, 2023. <a href=\"https://doi.org/10.1016/j.semcdb.2022.11.005\">https://doi.org/10.1016/j.semcdb.2022.11.005</a>.","ieee":"B. Corominas-Murtra and E. B. Hannezo, “Modelling the dynamics of mammalian gut homeostasis,” <i>Seminars in Cell &#38; Developmental Biology</i>, vol. 150–151. Elsevier, pp. 58–65, 2023."},"year":"2023","date_updated":"2024-01-16T13:22:32Z","external_id":{"isi":["001053522200001"],"pmid":["36470715"]},"isi":1,"keyword":["Cell Biology","Developmental Biology"],"language":[{"iso":"eng"}],"project":[{"name":"Design Principles of Branching Morphogenesis","grant_number":"851288","_id":"05943252-7A3F-11EA-A408-12923DDC885E","call_identifier":"H2020"}],"oa_version":"Published Version","month":"12","has_accepted_license":"1","publication":"Seminars in Cell & Developmental Biology","file":[{"file_id":"14741","creator":"dernst","success":1,"relation":"main_file","access_level":"open_access","date_updated":"2024-01-08T10:16:04Z","file_name":"2023_SeminarsCellDevBiology_CorominasMurtra.pdf","content_type":"application/pdf","date_created":"2024-01-08T10:16:04Z","file_size":1343750,"checksum":"c619887cf130f4649bf3035417186004"}],"user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","status":"public","publication_identifier":{"issn":["1084-9521"]},"oa":1,"tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","short":"CC BY (4.0)","image":"/images/cc_by.png","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)"},"type":"journal_article","date_published":"2023-12-02T00:00:00Z"},{"publication":"Molecular Autism","has_accepted_license":"1","month":"06","article_number":"27","oa_version":"Published Version","language":[{"iso":"eng"}],"keyword":["Psychiatry and Mental health","Developmental Biology","Developmental Neuroscience","Molecular Biology"],"date_published":"2022-06-22T00:00:00Z","type":"journal_article","tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","short":"CC BY (4.0)","image":"/images/cc_by.png","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)"},"oa":1,"publication_identifier":{"issn":["2040-2392"]},"status":"public","user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","related_material":{"link":[{"relation":"erratum","url":"https://doi.org/10.1186/s13229-023-00539-4"}]},"file":[{"file_id":"11461","creator":"dernst","success":1,"access_level":"open_access","relation":"main_file","date_updated":"2022-06-24T08:22:59Z","content_type":"application/pdf","file_name":"2022_MolecularAutism_Schaaf.pdf","date_created":"2022-06-24T08:22:59Z","file_size":7552298,"checksum":"525d2618e855139089bbfc3e3d49d1b2"}],"author":[{"full_name":"Schaaf, Zachary A.","first_name":"Zachary A.","last_name":"Schaaf"},{"last_name":"Tat","first_name":"Lyvin","full_name":"Tat, Lyvin"},{"full_name":"Cannizzaro, Noemi","first_name":"Noemi","last_name":"Cannizzaro"},{"last_name":"Green","first_name":"Ralph","full_name":"Green, Ralph"},{"first_name":"Thomas","last_name":"Rülicke","full_name":"Rülicke, Thomas"},{"id":"37B36620-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0003-2279-1061","full_name":"Hippenmeyer, Simon","first_name":"Simon","last_name":"Hippenmeyer"},{"first_name":"Konstantinos S.","last_name":"Zarbalis","full_name":"Zarbalis, Konstantinos S."}],"_id":"11460","title":"WDFY3 mutation alters laminar position and morphology of cortical neurons","intvolume":"        13","publication_status":"published","department":[{"_id":"SiHi"}],"date_created":"2022-06-23T14:28:55Z","article_processing_charge":"No","file_date_updated":"2022-06-24T08:22:59Z","quality_controlled":"1","article_type":"original","publisher":"Springer Nature","isi":1,"external_id":{"isi":["000814641400001"]},"date_updated":"2023-08-03T07:21:32Z","citation":{"ista":"Schaaf ZA, Tat L, Cannizzaro N, Green R, Rülicke T, Hippenmeyer S, Zarbalis KS. 2022. WDFY3 mutation alters laminar position and morphology of cortical neurons. Molecular Autism. 13, 27.","short":"Z.A. Schaaf, L. Tat, N. Cannizzaro, R. Green, T. Rülicke, S. Hippenmeyer, K.S. Zarbalis, Molecular Autism 13 (2022).","mla":"Schaaf, Zachary A., et al. “WDFY3 Mutation Alters Laminar Position and Morphology of Cortical Neurons.” <i>Molecular Autism</i>, vol. 13, 27, Springer Nature, 2022, doi:<a href=\"https://doi.org/10.1186/s13229-022-00508-3\">10.1186/s13229-022-00508-3</a>.","ieee":"Z. A. Schaaf <i>et al.</i>, “WDFY3 mutation alters laminar position and morphology of cortical neurons,” <i>Molecular Autism</i>, vol. 13. Springer Nature, 2022.","chicago":"Schaaf, Zachary A., Lyvin Tat, Noemi Cannizzaro, Ralph Green, Thomas Rülicke, Simon Hippenmeyer, and Konstantinos S. Zarbalis. “WDFY3 Mutation Alters Laminar Position and Morphology of Cortical Neurons.” <i>Molecular Autism</i>. Springer Nature, 2022. <a href=\"https://doi.org/10.1186/s13229-022-00508-3\">https://doi.org/10.1186/s13229-022-00508-3</a>.","apa":"Schaaf, Z. A., Tat, L., Cannizzaro, N., Green, R., Rülicke, T., Hippenmeyer, S., &#38; Zarbalis, K. S. (2022). WDFY3 mutation alters laminar position and morphology of cortical neurons. <i>Molecular Autism</i>. Springer Nature. <a href=\"https://doi.org/10.1186/s13229-022-00508-3\">https://doi.org/10.1186/s13229-022-00508-3</a>","ama":"Schaaf ZA, Tat L, Cannizzaro N, et al. WDFY3 mutation alters laminar position and morphology of cortical neurons. <i>Molecular Autism</i>. 2022;13. doi:<a href=\"https://doi.org/10.1186/s13229-022-00508-3\">10.1186/s13229-022-00508-3</a>"},"year":"2022","abstract":[{"lang":"eng","text":"Background: Proper cerebral cortical development depends on the tightly orchestrated migration of newly born neurons from the inner ventricular and subventricular zones to the outer cortical plate. Any disturbance in this process during prenatal stages may lead to neuronal migration disorders (NMDs), which can vary in extent from focal to global. Furthermore, NMDs show a substantial comorbidity with other neurodevelopmental disorders, notably autism spectrum disorders (ASDs). Our previous work demonstrated focal neuronal migration defects in mice carrying loss-of-function alleles of the recognized autism risk gene WDFY3. However, the cellular origins of these defects in Wdfy3 mutant mice remain elusive and uncovering it will provide critical insight into WDFY3-dependent disease pathology.\r\nMethods: Here, in an effort to untangle the origins of NMDs in Wdfy3lacZ mice, we employed mosaic analysis with double markers (MADM). MADM technology enabled us to genetically distinctly track and phenotypically analyze mutant and wild-type cells concomitantly in vivo using immunofluorescent techniques.\r\nResults: We revealed a cell autonomous requirement of WDFY3 for accurate laminar positioning of cortical projection neurons and elimination of mispositioned cells during early postnatal life. In addition, we identified significant deviations in dendritic arborization, as well as synaptic density and morphology between wild type, heterozygous, and homozygous Wdfy3 mutant neurons in Wdfy3-MADM reporter mice at postnatal stages.\r\nLimitations: While Wdfy3 mutant mice have provided valuable insight into prenatal aspects of ASD pathology that remain inaccessible to investigation in humans, like most animal models, they do not a perfectly replicate all aspects of human ASD biology. The lack of human data makes it indeterminate whether morphological deviations described here apply to ASD patients or some of the other neurodevelopmental conditions associated with WDFY3 mutation.\r\nConclusions: Our genetic approach revealed several cell autonomous requirements of WDFY3 in neuronal development that could underlie the pathogenic mechanisms of WDFY3-related neurodevelopmental conditions. The results are also consistent with findings in other ASD animal models and patients and suggest an important role for WDFY3 in regulating neuronal function and interconnectivity in postnatal life."}],"doi":"10.1186/s13229-022-00508-3","day":"22","ddc":["570"],"acknowledgement":"This study was funded by NIMH R21MH115347 to KSZ. KSZ is further supported by Shriners Hospitals for Children.\r\nWe would like to thank Angelo Harlan de Crescenzo for early contributions to this project.","volume":13},{"doi":"10.1016/j.devcel.2022.11.006","day":"05","abstract":[{"lang":"eng","text":"Plant root architecture flexibly adapts to changing nitrate (NO3−) availability in the soil; however, the underlying molecular mechanism of this adaptive development remains under-studied. To explore the regulation of NO3−-mediated root growth, we screened for low-nitrate-resistant mutant (lonr) and identified mutants that were defective in the NAC transcription factor NAC075 (lonr1) as being less sensitive to low NO3− in terms of primary root growth. We show that NAC075 is a mobile transcription factor relocating from the root stele tissues to the endodermis based on NO3− availability. Under low-NO3− availability, the kinase CBL-interacting protein kinase 1 (CIPK1) is activated, and it phosphorylates NAC075, restricting its movement from the stele, which leads to the transcriptional regulation of downstream target WRKY53, consequently leading to adapted root architecture. Our work thus identifies an adaptive mechanism involving translocation of transcription factor based on nutrient availability and leading to cell-specific reprogramming of plant root growth."}],"date_updated":"2023-10-04T08:23:20Z","citation":{"ista":"Xiao H, Hu Y, Wang Y, Cheng J, Wang J, Chen G, Li Q, Wang S, Wang Y, Wang S-S, Wang Y, Xuan W, Li Z, Guo Y, Gong Z, Friml J, Zhang J. 2022. Nitrate availability controls translocation of the transcription factor NAC075 for cell-type-specific reprogramming of root growth. Developmental Cell. 57(23), 2638–2651.e6.","short":"H. Xiao, Y. Hu, Y. Wang, J. Cheng, J. Wang, G. Chen, Q. Li, S. Wang, Y. Wang, S.-S. Wang, Y. Wang, W. Xuan, Z. Li, Y. Guo, Z. Gong, J. Friml, J. Zhang, Developmental Cell 57 (2022) 2638–2651.e6.","mla":"Xiao, Huixin, et al. “Nitrate Availability Controls Translocation of the Transcription Factor NAC075 for Cell-Type-Specific Reprogramming of Root Growth.” <i>Developmental Cell</i>, vol. 57, no. 23, Elsevier, 2022, p. 2638–2651.e6, doi:<a href=\"https://doi.org/10.1016/j.devcel.2022.11.006\">10.1016/j.devcel.2022.11.006</a>.","chicago":"Xiao, Huixin, Yumei Hu, Yaping Wang, Jinkui Cheng, Jinyi Wang, Guojingwei Chen, Qian Li, et al. “Nitrate Availability Controls Translocation of the Transcription Factor NAC075 for Cell-Type-Specific Reprogramming of Root Growth.” <i>Developmental Cell</i>. Elsevier, 2022. <a href=\"https://doi.org/10.1016/j.devcel.2022.11.006\">https://doi.org/10.1016/j.devcel.2022.11.006</a>.","ieee":"H. Xiao <i>et al.</i>, “Nitrate availability controls translocation of the transcription factor NAC075 for cell-type-specific reprogramming of root growth,” <i>Developmental Cell</i>, vol. 57, no. 23. Elsevier, p. 2638–2651.e6, 2022.","apa":"Xiao, H., Hu, Y., Wang, Y., Cheng, J., Wang, J., Chen, G., … Zhang, J. (2022). Nitrate availability controls translocation of the transcription factor NAC075 for cell-type-specific reprogramming of root growth. <i>Developmental Cell</i>. Elsevier. <a href=\"https://doi.org/10.1016/j.devcel.2022.11.006\">https://doi.org/10.1016/j.devcel.2022.11.006</a>","ama":"Xiao H, Hu Y, Wang Y, et al. Nitrate availability controls translocation of the transcription factor NAC075 for cell-type-specific reprogramming of root growth. <i>Developmental Cell</i>. 2022;57(23):2638-2651.e6. doi:<a href=\"https://doi.org/10.1016/j.devcel.2022.11.006\">10.1016/j.devcel.2022.11.006</a>"},"year":"2022","isi":1,"external_id":{"isi":["000919603800005"],"pmid":["36473460"]},"acknowledgement":"The authors are grateful to Jörg Kudla, Ying Miao, Yu Zheng, Gang Li, and Jun Zheng for providing published materials and to Wenkun Zhou and Caifu Jiang for helpful discussions. This work was supported by grants from the National Key Research and Development Program of China (2021YFF1000500), the National Natural Science Foundation of China (32170265 and 32022007), the Beijing Municipal Natural Science Foundation (5192011), and the Chinese Universities Scientific Fund (2022TC153).","volume":57,"publication_status":"published","article_processing_charge":"No","date_created":"2023-01-12T11:57:00Z","department":[{"_id":"JiFr"}],"title":"Nitrate availability controls translocation of the transcription factor NAC075 for cell-type-specific reprogramming of root growth","intvolume":"        57","pmid":1,"_id":"12120","scopus_import":"1","author":[{"full_name":"Xiao, Huixin","first_name":"Huixin","last_name":"Xiao"},{"first_name":"Yumei","last_name":"Hu","full_name":"Hu, Yumei"},{"first_name":"Yaping","last_name":"Wang","full_name":"Wang, Yaping"},{"first_name":"Jinkui","last_name":"Cheng","full_name":"Cheng, Jinkui"},{"full_name":"Wang, Jinyi","last_name":"Wang","first_name":"Jinyi"},{"last_name":"Chen","first_name":"Guojingwei","full_name":"Chen, Guojingwei"},{"full_name":"Li, Qian","last_name":"Li","first_name":"Qian"},{"full_name":"Wang, Shuwei","last_name":"Wang","first_name":"Shuwei"},{"first_name":"Yalu","last_name":"Wang","full_name":"Wang, Yalu"},{"full_name":"Wang, Shao-Shuai","first_name":"Shao-Shuai","last_name":"Wang"},{"full_name":"Wang, Yi","first_name":"Yi","last_name":"Wang"},{"first_name":"Wei","last_name":"Xuan","full_name":"Xuan, Wei"},{"last_name":"Li","first_name":"Zhen","full_name":"Li, Zhen"},{"last_name":"Guo","first_name":"Yan","full_name":"Guo, Yan"},{"full_name":"Gong, Zhizhong","first_name":"Zhizhong","last_name":"Gong"},{"first_name":"Jiří","last_name":"Friml","orcid":"0000-0002-8302-7596","full_name":"Friml, Jiří","id":"4159519E-F248-11E8-B48F-1D18A9856A87"},{"first_name":"Jing","last_name":"Zhang","full_name":"Zhang, Jing"}],"issue":"23","publisher":"Elsevier","article_type":"original","page":"2638-2651.e6","quality_controlled":"1","publication_identifier":{"issn":["1534-5807"]},"date_published":"2022-12-05T00:00:00Z","type":"journal_article","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","status":"public","oa_version":"None","month":"12","publication":"Developmental Cell","language":[{"iso":"eng"}],"keyword":["Developmental Biology","Cell Biology","General Biochemistry","Genetics and Molecular Biology","Molecular Biology"]},{"volume":149,"acknowledgement":"iona intestinalis adults were provided by Dr Yutaka Satou (Kyoto University) and Dr Manabu Yoshida (the University of Tokyo) with support from the National Bio-Resource Project of AMED, Japan. We thank Dr Hidehiko Hashimoto and Dr Yuji Mizotani for technical information about 1P-myosin antibody staining. We thank Dr Kaoru Imai and Dr Yutaka Satou for valuable discussion about Admp and for the DNA construct of Bmp2/4 under the Dlx.b upstream sequence. We thank Ms Maki Kogure for constructing the FUSION360 of the intercalating epidermal cell.\r\nThis work was supported by funding from the Japan Society for the Promotion of Science (JP16H01451, JP21H00440). Open Access funding provided by Keio University: Keio Gijuku Daigaku.","ddc":["570"],"year":"2022","citation":{"ista":"Kogure YS, Muraoka H, Koizumi WC, Gelin-alessi R, Godard BG, Oka K, Heisenberg C-PJ, Hotta K. 2022. Admp regulates tail bending by controlling ventral epidermal cell polarity via phosphorylated myosin localization in Ciona. Development. 149(21), dev200215.","short":"Y.S. Kogure, H. Muraoka, W.C. Koizumi, R. Gelin-alessi, B.G. Godard, K. Oka, C.-P.J. Heisenberg, K. Hotta, Development 149 (2022).","mla":"Kogure, Yuki S., et al. “Admp Regulates Tail Bending by Controlling Ventral Epidermal Cell Polarity via Phosphorylated Myosin Localization in Ciona.” <i>Development</i>, vol. 149, no. 21, dev200215, The Company of Biologists, 2022, doi:<a href=\"https://doi.org/10.1242/dev.200215\">10.1242/dev.200215</a>.","chicago":"Kogure, Yuki S., Hiromochi Muraoka, Wataru C. Koizumi, Raphaël Gelin-alessi, Benoit G Godard, Kotaro Oka, Carl-Philipp J Heisenberg, and Kohji Hotta. “Admp Regulates Tail Bending by Controlling Ventral Epidermal Cell Polarity via Phosphorylated Myosin Localization in Ciona.” <i>Development</i>. The Company of Biologists, 2022. <a href=\"https://doi.org/10.1242/dev.200215\">https://doi.org/10.1242/dev.200215</a>.","ieee":"Y. S. Kogure <i>et al.</i>, “Admp regulates tail bending by controlling ventral epidermal cell polarity via phosphorylated myosin localization in Ciona,” <i>Development</i>, vol. 149, no. 21. The Company of Biologists, 2022.","apa":"Kogure, Y. S., Muraoka, H., Koizumi, W. C., Gelin-alessi, R., Godard, B. G., Oka, K., … Hotta, K. (2022). Admp regulates tail bending by controlling ventral epidermal cell polarity via phosphorylated myosin localization in Ciona. <i>Development</i>. The Company of Biologists. <a href=\"https://doi.org/10.1242/dev.200215\">https://doi.org/10.1242/dev.200215</a>","ama":"Kogure YS, Muraoka H, Koizumi WC, et al. Admp regulates tail bending by controlling ventral epidermal cell polarity via phosphorylated myosin localization in Ciona. <i>Development</i>. 2022;149(21). doi:<a href=\"https://doi.org/10.1242/dev.200215\">10.1242/dev.200215</a>"},"date_updated":"2023-08-04T09:33:24Z","external_id":{"isi":["000903991700002"],"pmid":["36227591"]},"isi":1,"day":"01","doi":"10.1242/dev.200215","abstract":[{"lang":"eng","text":"Ventral tail bending, which is transient but pronounced, is found in many chordate embryos and constitutes an interesting model of how tissue interactions control embryo shape. Here, we identify one key upstream regulator of ventral tail bending in embryos of the ascidian Ciona. We show that during the early tailbud stages, ventral epidermal cells exhibit a boat-shaped morphology (boat cell) with a narrow apical surface where phosphorylated myosin light chain (pMLC) accumulates. We further show that interfering with the function of the BMP ligand Admp led to pMLC localizing to the basal instead of the apical side of ventral epidermal cells and a reduced number of boat cells. Finally, we show that cutting ventral epidermal midline cells at their apex using an ultraviolet laser relaxed ventral tail bending. Based on these results, we propose a previously unreported function for Admp in localizing pMLC to the apical side of ventral epidermal cells, which causes the tail to bend ventrally by resisting antero-posterior notochord extension at the ventral side of the tail."}],"quality_controlled":"1","file_date_updated":"2023-01-27T10:36:50Z","publisher":"The Company of Biologists","article_type":"original","scopus_import":"1","pmid":1,"_id":"12231","issue":"21","author":[{"first_name":"Yuki S.","last_name":"Kogure","full_name":"Kogure, Yuki S."},{"full_name":"Muraoka, Hiromochi","last_name":"Muraoka","first_name":"Hiromochi"},{"full_name":"Koizumi, Wataru C.","last_name":"Koizumi","first_name":"Wataru C."},{"last_name":"Gelin-alessi","first_name":"Raphaël","full_name":"Gelin-alessi, Raphaël"},{"full_name":"Godard, Benoit G","last_name":"Godard","first_name":"Benoit G","id":"3263621A-F248-11E8-B48F-1D18A9856A87"},{"full_name":"Oka, Kotaro","last_name":"Oka","first_name":"Kotaro"},{"id":"39427864-F248-11E8-B48F-1D18A9856A87","full_name":"Heisenberg, Carl-Philipp J","orcid":"0000-0002-0912-4566","last_name":"Heisenberg","first_name":"Carl-Philipp J"},{"full_name":"Hotta, Kohji","last_name":"Hotta","first_name":"Kohji"}],"date_created":"2023-01-16T09:50:12Z","department":[{"_id":"CaHe"}],"article_processing_charge":"No","publication_status":"published","intvolume":"       149","title":"Admp regulates tail bending by controlling ventral epidermal cell polarity via phosphorylated myosin localization in Ciona","file":[{"creator":"dernst","file_id":"12423","relation":"main_file","success":1,"access_level":"open_access","content_type":"application/pdf","file_name":"2022_Development_Kogure.pdf","date_updated":"2023-01-27T10:36:50Z","checksum":"871b9c58eb79b9e60752de25a46938d6","file_size":9160451,"date_created":"2023-01-27T10:36:50Z"}],"status":"public","user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","short":"CC BY (4.0)","image":"/images/cc_by.png","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)"},"type":"journal_article","date_published":"2022-11-01T00:00:00Z","publication_identifier":{"eissn":["1477-9129"],"issn":["0950-1991"]},"oa":1,"keyword":["Developmental Biology","Molecular Biology"],"language":[{"iso":"eng"}],"has_accepted_license":"1","publication":"Development","oa_version":"Published Version","article_number":"dev200215","month":"11"},{"citation":{"apa":"Hino, N., Matsuda, K., Jikko, Y., Maryu, G., Sakai, K., Imamura, R., … Matsuda, M. (2022). A feedback loop between lamellipodial extension and HGF-ERK signaling specifies leader cells during collective cell migration. <i>Developmental Cell</i>. Elsevier. <a href=\"https://doi.org/10.1016/j.devcel.2022.09.003\">https://doi.org/10.1016/j.devcel.2022.09.003</a>","ama":"Hino N, Matsuda K, Jikko Y, et al. A feedback loop between lamellipodial extension and HGF-ERK signaling specifies leader cells during collective cell migration. <i>Developmental Cell</i>. 2022;57(19):2290-2304.e7. doi:<a href=\"https://doi.org/10.1016/j.devcel.2022.09.003\">10.1016/j.devcel.2022.09.003</a>","ieee":"N. Hino <i>et al.</i>, “A feedback loop between lamellipodial extension and HGF-ERK signaling specifies leader cells during collective cell migration,” <i>Developmental Cell</i>, vol. 57, no. 19. Elsevier, p. 2290–2304.e7, 2022.","chicago":"Hino, Naoya, Kimiya Matsuda, Yuya Jikko, Gembu Maryu, Katsuya Sakai, Ryu Imamura, Shinya Tsukiji, et al. “A Feedback Loop between Lamellipodial Extension and HGF-ERK Signaling Specifies Leader Cells during Collective Cell Migration.” <i>Developmental Cell</i>. Elsevier, 2022. <a href=\"https://doi.org/10.1016/j.devcel.2022.09.003\">https://doi.org/10.1016/j.devcel.2022.09.003</a>.","mla":"Hino, Naoya, et al. “A Feedback Loop between Lamellipodial Extension and HGF-ERK Signaling Specifies Leader Cells during Collective Cell Migration.” <i>Developmental Cell</i>, vol. 57, no. 19, Elsevier, 2022, p. 2290–2304.e7, doi:<a href=\"https://doi.org/10.1016/j.devcel.2022.09.003\">10.1016/j.devcel.2022.09.003</a>.","short":"N. Hino, K. Matsuda, Y. Jikko, G. Maryu, K. Sakai, R. Imamura, S. Tsukiji, K. Aoki, K. Terai, T. Hirashima, X. Trepat, M. Matsuda, Developmental Cell 57 (2022) 2290–2304.e7.","ista":"Hino N, Matsuda K, Jikko Y, Maryu G, Sakai K, Imamura R, Tsukiji S, Aoki K, Terai K, Hirashima T, Trepat X, Matsuda M. 2022. A feedback loop between lamellipodial extension and HGF-ERK signaling specifies leader cells during collective cell migration. Developmental Cell. 57(19), 2290–2304.e7."},"year":"2022","date_updated":"2023-08-04T09:38:53Z","external_id":{"isi":["000898428700006"],"pmid":["36174555"]},"isi":1,"day":"01","doi":"10.1016/j.devcel.2022.09.003","abstract":[{"lang":"eng","text":"Upon the initiation of collective cell migration, the cells at the free edge are specified as leader cells; however, the mechanism underlying the leader cell specification remains elusive. Here, we show that lamellipodial extension after the release from mechanical confinement causes sustained extracellular signal-regulated kinase (ERK) activation and underlies the leader cell specification. Live-imaging of Madin-Darby canine kidney (MDCK) cells and mouse epidermis through the use of Förster resonance energy transfer (FRET)-based biosensors showed that leader cells exhibit sustained ERK activation in a hepatocyte growth factor (HGF)-dependent manner. Meanwhile, follower cells exhibit oscillatory ERK activation waves in an epidermal growth factor (EGF) signaling-dependent manner. Lamellipodial extension at the free edge increases the cellular sensitivity to HGF. The HGF-dependent ERK activation, in turn, promotes lamellipodial extension, thereby forming a positive feedback loop between cell extension and ERK activation and specifying the cells at the free edge as the leader cells. Our findings show that the integration of physical and biochemical cues underlies the leader cell specification during collective cell migration."}],"acknowledgement":"We thank the members of the Matsuda Laboratory for their helpful discussion and encouragement, and we thank K. Hirano and K. Takakura for their technical assistance. This work was supported by the Kyoto University Live Imaging Center. Financial support was provided in the form of JSPS KAKENHI grants (nos. 17J02107 and 20K22653 to N.H., and 20H05898 and 19H00993 to M.M.), a JST CREST grant (no. JPMJCR1654 to M.M.), a Moonshot R&D grant (no. JPMJPS2022-11 to M.M.), Generalitat de Catalunya and the CERCA Programme (no. SGR-2017-01602 to X.T.), MICCINN/FEDER (no. PGC2018-099645-B-I00 to X.T.), and European Research Council (no. Adv-883739 to X.T.). IBEC is a recipient of a Severo Ochoa Award of Excellence from the MINECO. This work was partly supported by an Extramural Collaborative Research Grant of Cancer Research Institute, Kanazawa University.","volume":57,"scopus_import":"1","pmid":1,"_id":"12238","issue":"19","author":[{"full_name":"Hino, Naoya","last_name":"Hino","first_name":"Naoya","id":"5299a9ce-7679-11eb-a7bc-d1e62b936307"},{"last_name":"Matsuda","first_name":"Kimiya","full_name":"Matsuda, Kimiya"},{"last_name":"Jikko","first_name":"Yuya","full_name":"Jikko, Yuya"},{"full_name":"Maryu, Gembu","first_name":"Gembu","last_name":"Maryu"},{"last_name":"Sakai","first_name":"Katsuya","full_name":"Sakai, Katsuya"},{"first_name":"Ryu","last_name":"Imamura","full_name":"Imamura, Ryu"},{"first_name":"Shinya","last_name":"Tsukiji","full_name":"Tsukiji, Shinya"},{"last_name":"Aoki","first_name":"Kazuhiro","full_name":"Aoki, Kazuhiro"},{"last_name":"Terai","first_name":"Kenta","full_name":"Terai, Kenta"},{"first_name":"Tsuyoshi","last_name":"Hirashima","full_name":"Hirashima, Tsuyoshi"},{"last_name":"Trepat","first_name":"Xavier","full_name":"Trepat, Xavier"},{"last_name":"Matsuda","first_name":"Michiyuki","full_name":"Matsuda, Michiyuki"}],"department":[{"_id":"CaHe"}],"article_processing_charge":"No","date_created":"2023-01-16T09:51:39Z","publication_status":"published","intvolume":"        57","title":"A feedback loop between lamellipodial extension and HGF-ERK signaling specifies leader cells during collective cell migration","quality_controlled":"1","page":"2290-2304.e7","publisher":"Elsevier","article_type":"original","type":"journal_article","date_published":"2022-10-01T00:00:00Z","publication_identifier":{"issn":["1534-5807"]},"user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","status":"public","publication":"Developmental Cell","oa_version":"None","month":"10","keyword":["Developmental Biology","Cell Biology","General Biochemistry","Genetics and Molecular Biology","Molecular Biology"],"language":[{"iso":"eng"}]},{"keyword":["Developmental Biology","Molecular Biology"],"language":[{"iso":"eng"}],"has_accepted_license":"1","publication":"Development","oa_version":"Published Version","article_number":"dev200474","month":"10","file":[{"date_updated":"2023-01-30T08:35:44Z","content_type":"application/pdf","file_name":"2022_Development_Soto.pdf","date_created":"2023-01-30T08:35:44Z","file_size":9348839,"checksum":"d7c29b74e9e4032308228cc704a30e88","file_id":"12438","creator":"dernst","access_level":"open_access","relation":"main_file","success":1}],"related_material":{"link":[{"url":" https://github.com/burtonjosh/StepwiseMir9","relation":"software"}]},"status":"public","user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","short":"CC BY (4.0)","image":"/images/cc_by.png","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)"},"type":"journal_article","date_published":"2022-10-01T00:00:00Z","publication_identifier":{"issn":["0950-1991"],"eissn":["1477-9129"]},"oa":1,"quality_controlled":"1","file_date_updated":"2023-01-30T08:35:44Z","publisher":"The Company of Biologists","article_type":"original","scopus_import":"1","pmid":1,"_id":"12245","issue":"19","author":[{"full_name":"Soto, Ximena","last_name":"Soto","first_name":"Ximena"},{"full_name":"Burton, Joshua","first_name":"Joshua","last_name":"Burton"},{"last_name":"Manning","first_name":"Cerys S.","full_name":"Manning, Cerys S."},{"id":"7d1648cb-19e9-11eb-8e7a-f8c037fb3e3f","first_name":"Thomas","last_name":"Minchington","full_name":"Minchington, Thomas"},{"last_name":"Lea","first_name":"Robert","full_name":"Lea, Robert"},{"first_name":"Jessica","last_name":"Lee","full_name":"Lee, Jessica"},{"full_name":"Kursawe, Jochen","last_name":"Kursawe","first_name":"Jochen"},{"last_name":"Rattray","first_name":"Magnus","full_name":"Rattray, Magnus"},{"full_name":"Papalopulu, Nancy","last_name":"Papalopulu","first_name":"Nancy"}],"date_created":"2023-01-16T09:53:17Z","department":[{"_id":"AnKi"}],"article_processing_charge":"No","publication_status":"published","intvolume":"       149","title":"Sequential and additive expression of miR-9 precursors control timing of neurogenesis","volume":149,"acknowledgement":"We are grateful to Dr Tom Pettini for the advice on smiFISH technique and Dr Laure Bally-Cuif for sharing plasmids. The authors also thank the Biological Services Facility, Bioimaging and Systems Microscopy Facilities of the University of Manchester for technical support.\r\nThis work was supported by a Wellcome Trust Senior Research Fellowship (090868/Z/09/Z) and a Wellcome Trust Investigator Award (224394/Z/21/Z) to N.P. and a Medical Research Council Career Development Award to C.S.M. (MR/V032534/1). J.B. was supported by a Wellcome Trust Four-Year PhD Studentship in Basic Science (219992/Z/19/Z). Open Access funding provided by The University of Manchester. Deposited in PMC for immediate release.","ddc":["570"],"citation":{"ieee":"X. Soto <i>et al.</i>, “Sequential and additive expression of miR-9 precursors control timing of neurogenesis,” <i>Development</i>, vol. 149, no. 19. The Company of Biologists, 2022.","chicago":"Soto, Ximena, Joshua Burton, Cerys S. Manning, Thomas Minchington, Robert Lea, Jessica Lee, Jochen Kursawe, Magnus Rattray, and Nancy Papalopulu. “Sequential and Additive Expression of MiR-9 Precursors Control Timing of Neurogenesis.” <i>Development</i>. The Company of Biologists, 2022. <a href=\"https://doi.org/10.1242/dev.200474\">https://doi.org/10.1242/dev.200474</a>.","apa":"Soto, X., Burton, J., Manning, C. S., Minchington, T., Lea, R., Lee, J., … Papalopulu, N. (2022). Sequential and additive expression of miR-9 precursors control timing of neurogenesis. <i>Development</i>. The Company of Biologists. <a href=\"https://doi.org/10.1242/dev.200474\">https://doi.org/10.1242/dev.200474</a>","ama":"Soto X, Burton J, Manning CS, et al. Sequential and additive expression of miR-9 precursors control timing of neurogenesis. <i>Development</i>. 2022;149(19). doi:<a href=\"https://doi.org/10.1242/dev.200474\">10.1242/dev.200474</a>","ista":"Soto X, Burton J, Manning CS, Minchington T, Lea R, Lee J, Kursawe J, Rattray M, Papalopulu N. 2022. Sequential and additive expression of miR-9 precursors control timing of neurogenesis. Development. 149(19), dev200474.","short":"X. Soto, J. Burton, C.S. Manning, T. Minchington, R. Lea, J. Lee, J. Kursawe, M. Rattray, N. Papalopulu, Development 149 (2022).","mla":"Soto, Ximena, et al. “Sequential and Additive Expression of MiR-9 Precursors Control Timing of Neurogenesis.” <i>Development</i>, vol. 149, no. 19, dev200474, The Company of Biologists, 2022, doi:<a href=\"https://doi.org/10.1242/dev.200474\">10.1242/dev.200474</a>."},"year":"2022","date_updated":"2023-08-04T09:41:08Z","external_id":{"pmid":["36189829"],"isi":["000918161000003"]},"isi":1,"day":"01","doi":"10.1242/dev.200474","abstract":[{"text":"MicroRNAs (miRs) have an important role in tuning dynamic gene expression. However, the mechanism by which they are quantitatively controlled is unknown. We show that the amount of mature miR-9, a key regulator of neuronal development, increases during zebrafish neurogenesis in a sharp stepwise manner. We characterize the spatiotemporal profile of seven distinct microRNA primary transcripts (pri-mir)-9s that produce the same mature miR-9 and show that they are sequentially expressed during hindbrain neurogenesis. Expression of late-onset pri-mir-9-1 is added on to, rather than replacing, the expression of early onset pri-mir-9-4 and -9-5 in single cells. CRISPR/Cas9 mutation of the late-onset pri-mir-9-1 prevents the developmental increase of mature miR-9, reduces late neuronal differentiation and fails to downregulate Her6 at late stages. Mathematical modelling shows that an adaptive network containing Her6 is insensitive to linear increases in miR-9 but responds to stepwise increases of miR-9. We suggest that a sharp stepwise increase of mature miR-9 is created by sequential and additive temporal activation of distinct loci. This may be a strategy to overcome adaptation and facilitate a transition of Her6 to a new dynamic regime or steady state.","lang":"eng"}]},{"month":"11","oa_version":"None","publication":"Developmental Cell","language":[{"iso":"eng"}],"keyword":["Developmental Biology","Cell Biology","General Biochemistry","Genetics and Molecular Biology","Molecular Biology"],"publication_identifier":{"issn":["1534-5807"]},"date_published":"2021-11-08T00:00:00Z","type":"journal_article","status":"public","user_id":"72615eeb-f1f3-11ec-aa25-d4573ddc34fd","title":"Identification of long-lived proteins in the mitochondria reveals increased stability of the electron transport chain","intvolume":"        56","publication_status":"published","date_created":"2022-04-07T07:43:14Z","article_processing_charge":"No","author":[{"full_name":"Krishna, Shefali","first_name":"Shefali","last_name":"Krishna"},{"full_name":"Arrojo e Drigo, Rafael","last_name":"Arrojo e Drigo","first_name":"Rafael"},{"last_name":"Capitanio","first_name":"Juliana S.","full_name":"Capitanio, Juliana S."},{"full_name":"Ramachandra, Ranjan","first_name":"Ranjan","last_name":"Ramachandra"},{"first_name":"Mark","last_name":"Ellisman","full_name":"Ellisman, Mark"},{"last_name":"HETZER","first_name":"Martin W","full_name":"HETZER, Martin W","orcid":"0000-0002-2111-992X","id":"86c0d31b-b4eb-11ec-ac5a-eae7b2e135ed"}],"issue":"21","pmid":1,"_id":"11052","scopus_import":"1","article_type":"original","publisher":"Elsevier","page":"P2952-2965.e9","quality_controlled":"1","abstract":[{"lang":"eng","text":"In order to combat molecular damage, most cellular proteins undergo rapid turnover. We have previously identified large nuclear protein assemblies that can persist for years in post-mitotic tissues and are subject to age-related decline. Here, we report that mitochondria can be long lived in the mouse brain and reveal that specific mitochondrial proteins have half-lives longer than the average proteome. These mitochondrial long-lived proteins (mitoLLPs) are core components of the electron transport chain (ETC) and display increased longevity in respiratory supercomplexes. We find that COX7C, a mitoLLP that forms a stable contact site between complexes I and IV, is required for complex IV and supercomplex assembly. Remarkably, even upon depletion of COX7C transcripts, ETC function is maintained for days, effectively uncoupling mitochondrial function from ongoing transcription of its mitoLLPs. Our results suggest that modulating protein longevity within the ETC is critical for mitochondrial proteome maintenance and the robustness of mitochondrial function."}],"doi":"10.1016/j.devcel.2021.10.008","day":"08","external_id":{"pmid":["34715012"]},"date_updated":"2022-07-18T08:26:38Z","year":"2021","citation":{"short":"S. Krishna, R. Arrojo e Drigo, J.S. Capitanio, R. Ramachandra, M. Ellisman, M. Hetzer, Developmental Cell 56 (2021) P2952–2965.e9.","mla":"Krishna, Shefali, et al. “Identification of Long-Lived Proteins in the Mitochondria Reveals Increased Stability of the Electron Transport Chain.” <i>Developmental Cell</i>, vol. 56, no. 21, Elsevier, 2021, p. P2952–2965.e9, doi:<a href=\"https://doi.org/10.1016/j.devcel.2021.10.008\">10.1016/j.devcel.2021.10.008</a>.","ista":"Krishna S, Arrojo e Drigo R, Capitanio JS, Ramachandra R, Ellisman M, Hetzer M. 2021. Identification of long-lived proteins in the mitochondria reveals increased stability of the electron transport chain. Developmental Cell. 56(21), P2952–2965.e9.","ama":"Krishna S, Arrojo e Drigo R, Capitanio JS, Ramachandra R, Ellisman M, Hetzer M. Identification of long-lived proteins in the mitochondria reveals increased stability of the electron transport chain. <i>Developmental Cell</i>. 2021;56(21):P2952-2965.e9. doi:<a href=\"https://doi.org/10.1016/j.devcel.2021.10.008\">10.1016/j.devcel.2021.10.008</a>","apa":"Krishna, S., Arrojo e Drigo, R., Capitanio, J. S., Ramachandra, R., Ellisman, M., &#38; Hetzer, M. (2021). Identification of long-lived proteins in the mitochondria reveals increased stability of the electron transport chain. <i>Developmental Cell</i>. Elsevier. <a href=\"https://doi.org/10.1016/j.devcel.2021.10.008\">https://doi.org/10.1016/j.devcel.2021.10.008</a>","chicago":"Krishna, Shefali, Rafael Arrojo e Drigo, Juliana S. Capitanio, Ranjan Ramachandra, Mark Ellisman, and Martin Hetzer. “Identification of Long-Lived Proteins in the Mitochondria Reveals Increased Stability of the Electron Transport Chain.” <i>Developmental Cell</i>. Elsevier, 2021. <a href=\"https://doi.org/10.1016/j.devcel.2021.10.008\">https://doi.org/10.1016/j.devcel.2021.10.008</a>.","ieee":"S. Krishna, R. Arrojo e Drigo, J. S. Capitanio, R. Ramachandra, M. Ellisman, and M. Hetzer, “Identification of long-lived proteins in the mitochondria reveals increased stability of the electron transport chain,” <i>Developmental Cell</i>, vol. 56, no. 21. Elsevier, p. P2952–2965.e9, 2021."},"extern":"1","volume":56},{"file_date_updated":"2021-08-11T10:28:06Z","page":"71-81","quality_controlled":"1","ec_funded":1,"article_type":"original","publisher":"Elsevier","author":[{"id":"30A536BA-F248-11E8-B48F-1D18A9856A87","first_name":"Alexandra","last_name":"Schauer","orcid":"0000-0001-7659-9142","full_name":"Schauer, Alexandra"},{"id":"39427864-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-0912-4566","full_name":"Heisenberg, Carl-Philipp J","first_name":"Carl-Philipp J","last_name":"Heisenberg"}],"_id":"8966","scopus_import":"1","title":"Reassembling gastrulation","intvolume":"       474","publication_status":"published","article_processing_charge":"Yes (via OA deal)","date_created":"2020-12-22T09:53:34Z","department":[{"_id":"CaHe"}],"ddc":["570"],"acknowledgement":"We thank Nicoletta Petridou, Diana Pinheiro, Cornelia Schwayer and Stefania Tavano for feedback on the manuscript. Research in the Heisenberg lab is supported by an ERC Advanced Grant (MECSPEC 742573) to C.-P.H. A.S. is a recipient of a DOC Fellowship of the Austrian Academy of Science.","volume":474,"isi":1,"external_id":{"isi":["000639461800008"]},"date_updated":"2023-08-07T13:30:01Z","year":"2021","citation":{"chicago":"Schauer, Alexandra, and Carl-Philipp J Heisenberg. “Reassembling Gastrulation.” <i>Developmental Biology</i>. Elsevier, 2021. <a href=\"https://doi.org/10.1016/j.ydbio.2020.12.014\">https://doi.org/10.1016/j.ydbio.2020.12.014</a>.","ieee":"A. Schauer and C.-P. J. Heisenberg, “Reassembling gastrulation,” <i>Developmental Biology</i>, vol. 474. Elsevier, pp. 71–81, 2021.","apa":"Schauer, A., &#38; Heisenberg, C.-P. J. (2021). Reassembling gastrulation. <i>Developmental Biology</i>. Elsevier. <a href=\"https://doi.org/10.1016/j.ydbio.2020.12.014\">https://doi.org/10.1016/j.ydbio.2020.12.014</a>","ama":"Schauer A, Heisenberg C-PJ. Reassembling gastrulation. <i>Developmental Biology</i>. 2021;474:71-81. doi:<a href=\"https://doi.org/10.1016/j.ydbio.2020.12.014\">10.1016/j.ydbio.2020.12.014</a>","ista":"Schauer A, Heisenberg C-PJ. 2021. Reassembling gastrulation. Developmental Biology. 474, 71–81.","short":"A. Schauer, C.-P.J. Heisenberg, Developmental Biology 474 (2021) 71–81.","mla":"Schauer, Alexandra, and Carl-Philipp J. Heisenberg. “Reassembling Gastrulation.” <i>Developmental Biology</i>, vol. 474, Elsevier, 2021, pp. 71–81, doi:<a href=\"https://doi.org/10.1016/j.ydbio.2020.12.014\">10.1016/j.ydbio.2020.12.014</a>."},"abstract":[{"text":"During development, a single cell is transformed into a highly complex organism through progressive cell division, specification and rearrangement. An important prerequisite for the emergence of patterns within the developing organism is to establish asymmetries at various scales, ranging from individual cells to the entire embryo, eventually giving rise to the different body structures. This becomes especially apparent during gastrulation, when the earliest major lineage restriction events lead to the formation of the different germ layers. Traditionally, the unfolding of the developmental program from symmetry breaking to germ layer formation has been studied by dissecting the contributions of different signaling pathways and cellular rearrangements in the in vivo context of intact embryos. Recent efforts, using the intrinsic capacity of embryonic stem cells to self-assemble and generate embryo-like structures de novo, have opened new avenues for understanding the many ways by which an embryo can be built and the influence of extrinsic factors therein. Here, we discuss and compare divergent and conserved strategies leading to germ layer formation in embryos as compared to in vitro systems, their upstream molecular cascades and the role of extrinsic factors in this process.","lang":"eng"}],"doi":"10.1016/j.ydbio.2020.12.014","day":"01","language":[{"iso":"eng"}],"keyword":["Developmental Biology","Cell Biology","Molecular Biology"],"publication":"Developmental Biology","has_accepted_license":"1","month":"06","oa_version":"Published Version","project":[{"call_identifier":"H2020","_id":"260F1432-B435-11E9-9278-68D0E5697425","name":"Interaction and feedback between cell mechanics and fate specification in vertebrate gastrulation","grant_number":"742573"},{"name":"Mesendoderm specification in zebrafish: The role of extraembryonic tissues","grant_number":"25239","_id":"26B1E39C-B435-11E9-9278-68D0E5697425"}],"related_material":{"record":[{"status":"public","relation":"dissertation_contains","id":"12891"}]},"user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","status":"public","file":[{"date_updated":"2021-08-11T10:28:06Z","file_name":"2021_DevBiology_Schauer.pdf","content_type":"application/pdf","date_created":"2021-08-11T10:28:06Z","file_size":1440321,"checksum":"fa2a5731fd16ab171b029f32f031c440","file_id":"9880","creator":"kschuh","success":1,"relation":"main_file","access_level":"open_access"}],"date_published":"2021-06-01T00:00:00Z","type":"journal_article","tmp":{"legal_code_url":"https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode","short":"CC BY-NC-ND (4.0)","name":"Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0)","image":"/images/cc_by_nc_nd.png"},"oa":1,"publication_identifier":{"issn":["0012-1606"]}},{"author":[{"full_name":"Kang, Hyeseon","first_name":"Hyeseon","last_name":"Kang"},{"first_name":"Maxim N.","last_name":"Shokhirev","full_name":"Shokhirev, Maxim N."},{"full_name":"Xu, Zhichao","first_name":"Zhichao","last_name":"Xu"},{"full_name":"Chandran, Sahaana","first_name":"Sahaana","last_name":"Chandran"},{"first_name":"Jesse R.","last_name":"Dixon","full_name":"Dixon, Jesse R."},{"first_name":"Martin W","last_name":"HETZER","orcid":"0000-0002-2111-992X","full_name":"HETZER, Martin W","id":"86c0d31b-b4eb-11ec-ac5a-eae7b2e135ed"}],"issue":"13-14","pmid":1,"_id":"11057","scopus_import":"1","title":"Dynamic regulation of histone modifications and long-range chromosomal interactions during postmitotic transcriptional reactivation","intvolume":"        34","publication_status":"published","date_created":"2022-04-07T07:44:09Z","article_processing_charge":"No","file_date_updated":"2022-04-08T07:12:33Z","page":"913-930","quality_controlled":"1","article_type":"original","publisher":"Cold Spring Harbor Laboratory Press","external_id":{"pmid":["32499403"]},"date_updated":"2022-07-18T08:31:08Z","citation":{"chicago":"Kang, Hyeseon, Maxim N. Shokhirev, Zhichao Xu, Sahaana Chandran, Jesse R. Dixon, and Martin Hetzer. “Dynamic Regulation of Histone Modifications and Long-Range Chromosomal Interactions during Postmitotic Transcriptional Reactivation.” <i>Genes &#38; Development</i>. Cold Spring Harbor Laboratory Press, 2020. <a href=\"https://doi.org/10.1101/gad.335794.119\">https://doi.org/10.1101/gad.335794.119</a>.","ieee":"H. Kang, M. N. Shokhirev, Z. Xu, S. Chandran, J. R. Dixon, and M. Hetzer, “Dynamic regulation of histone modifications and long-range chromosomal interactions during postmitotic transcriptional reactivation,” <i>Genes &#38; Development</i>, vol. 34, no. 13–14. Cold Spring Harbor Laboratory Press, pp. 913–930, 2020.","apa":"Kang, H., Shokhirev, M. N., Xu, Z., Chandran, S., Dixon, J. R., &#38; Hetzer, M. (2020). Dynamic regulation of histone modifications and long-range chromosomal interactions during postmitotic transcriptional reactivation. <i>Genes &#38; Development</i>. Cold Spring Harbor Laboratory Press. <a href=\"https://doi.org/10.1101/gad.335794.119\">https://doi.org/10.1101/gad.335794.119</a>","ama":"Kang H, Shokhirev MN, Xu Z, Chandran S, Dixon JR, Hetzer M. Dynamic regulation of histone modifications and long-range chromosomal interactions during postmitotic transcriptional reactivation. <i>Genes &#38; Development</i>. 2020;34(13-14):913-930. doi:<a href=\"https://doi.org/10.1101/gad.335794.119\">10.1101/gad.335794.119</a>","ista":"Kang H, Shokhirev MN, Xu Z, Chandran S, Dixon JR, Hetzer M. 2020. Dynamic regulation of histone modifications and long-range chromosomal interactions during postmitotic transcriptional reactivation. Genes &#38; Development. 34(13–14), 913–930.","short":"H. Kang, M.N. Shokhirev, Z. Xu, S. Chandran, J.R. Dixon, M. Hetzer, Genes &#38; Development 34 (2020) 913–930.","mla":"Kang, Hyeseon, et al. “Dynamic Regulation of Histone Modifications and Long-Range Chromosomal Interactions during Postmitotic Transcriptional Reactivation.” <i>Genes &#38; Development</i>, vol. 34, no. 13–14, Cold Spring Harbor Laboratory Press, 2020, pp. 913–30, doi:<a href=\"https://doi.org/10.1101/gad.335794.119\">10.1101/gad.335794.119</a>."},"year":"2020","abstract":[{"text":"During mitosis, transcription of genomic DNA is dramatically reduced, before it is reactivated during nuclear reformation in anaphase/telophase. Many aspects of the underlying principles that mediate transcriptional memory and reactivation in the daughter cells remain unclear. Here, we used ChIP-seq on synchronized cells at different stages after mitosis to generate genome-wide maps of histone modifications. Combined with EU-RNA-seq and Hi-C analyses, we found that during prometaphase, promoters, enhancers, and insulators retain H3K4me3 and H3K4me1, while losing H3K27ac. Enhancers globally retaining mitotic H3K4me1 or locally retaining mitotic H3K27ac are associated with cell type-specific genes and their transcription factors for rapid transcriptional activation. As cells exit mitosis, promoters regain H3K27ac, which correlates with transcriptional reactivation. Insulators also gain H3K27ac and CCCTC-binding factor (CTCF) in anaphase/telophase. This increase of H3K27ac in anaphase/telophase is required for posttranscriptional activation and may play a role in the establishment of topologically associating domains (TADs). Together, our results suggest that the genome is reorganized in a sequential order, in which histone methylations occur first in prometaphase, histone acetylation, and CTCF in anaphase/telophase, transcription in cytokinesis, and long-range chromatin interactions in early G1. We thus provide insights into the histone modification landscape that allows faithful reestablishment of the transcriptional program and TADs during cell division.","lang":"eng"}],"doi":"10.1101/gad.335794.119","day":"28","extern":"1","ddc":["570"],"volume":34,"publication":"Genes & Development","has_accepted_license":"1","month":"04","oa_version":"Published Version","language":[{"iso":"eng"}],"keyword":["Developmental Biology","Genetics"],"date_published":"2020-04-28T00:00:00Z","type":"journal_article","tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","short":"CC BY (4.0)","image":"/images/cc_by.png","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)"},"oa":1,"publication_identifier":{"issn":["0890-9369","1549-5477"]},"status":"public","user_id":"72615eeb-f1f3-11ec-aa25-d4573ddc34fd","file":[{"relation":"main_file","access_level":"open_access","success":1,"creator":"dernst","file_id":"11136","checksum":"84e92d40e67936c739628315c238daf9","file_size":4406772,"date_created":"2022-04-08T07:12:33Z","content_type":"application/pdf","file_name":"2020_GenesDevelopment_Kang.pdf","date_updated":"2022-04-08T07:12:33Z"}]},{"language":[{"iso":"eng"}],"keyword":["Biotechnology","Plant Science","General Biochemistry","Genetics and Molecular Biology","Developmental Biology","Cell Biology","Physiology","Ecology","Evolution","Behavior and Systematics","Structural Biology","General Agricultural and Biological Sciences"],"oa_version":"Published Version","month":"01","article_number":"2","publication":"BMC Biology","main_file_link":[{"open_access":"1","url":"https://doi.org/10.1186/s12915-019-0733-6"}],"status":"public","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","publication_identifier":{"issn":["1741-7007"]},"oa":1,"date_published":"2020-01-06T00:00:00Z","type":"journal_article","publisher":"Springer Nature","article_type":"original","quality_controlled":"1","publication_status":"published","article_processing_charge":"No","date_created":"2020-09-17T10:26:53Z","title":"The mitochondrial carrier pathway transports non-canonical substrates with an odd number of transmembrane segments","intvolume":"        18","pmid":1,"_id":"8402","author":[{"full_name":"Rampelt, Heike","first_name":"Heike","last_name":"Rampelt"},{"last_name":"Sucec","first_name":"Iva","full_name":"Sucec, Iva"},{"first_name":"Beate","last_name":"Bersch","full_name":"Bersch, Beate"},{"full_name":"Horten, Patrick","first_name":"Patrick","last_name":"Horten"},{"full_name":"Perschil, Inge","last_name":"Perschil","first_name":"Inge"},{"full_name":"Martinou, Jean-Claude","last_name":"Martinou","first_name":"Jean-Claude"},{"full_name":"van der Laan, Martin","last_name":"van der Laan","first_name":"Martin"},{"full_name":"Wiedemann, Nils","first_name":"Nils","last_name":"Wiedemann"},{"orcid":"0000-0002-9350-7606","full_name":"Schanda, Paul","first_name":"Paul","last_name":"Schanda","id":"7B541462-FAF6-11E9-A490-E8DFE5697425"},{"last_name":"Pfanner","first_name":"Nikolaus","full_name":"Pfanner, Nikolaus"}],"volume":18,"extern":"1","doi":"10.1186/s12915-019-0733-6","day":"06","abstract":[{"lang":"eng","text":"Background: The mitochondrial pyruvate carrier (MPC) plays a central role in energy metabolism by transporting pyruvate across the inner mitochondrial membrane. Its heterodimeric composition and homology to SWEET and semiSWEET transporters set the MPC apart from the canonical mitochondrial carrier family (named MCF or SLC25). The import of the canonical carriers is mediated by the carrier translocase of the inner membrane (TIM22) pathway and is dependent on their structure, which features an even number of transmembrane segments and both termini in the intermembrane space. The import pathway of MPC proteins has not been elucidated. The odd number of transmembrane segments and positioning of the N-terminus in the matrix argues against an import via the TIM22 carrier pathway but favors an import via the flexible presequence pathway.\r\nResults: Here, we systematically analyzed the import pathways of Mpc2 and Mpc3 and report that, contrary to an expected import via the flexible presequence pathway, yeast MPC proteins with an odd number of transmembrane segments and matrix-exposed N-terminus are imported by the carrier pathway, using the receptor Tom70, small TIM chaperones, and the TIM22 complex. The TIM9·10 complex chaperones MPC proteins through the mitochondrial intermembrane space using conserved hydrophobic motifs that are also required for the interaction with canonical carrier proteins.\r\nConclusions: The carrier pathway can import paired and non-paired transmembrane helices and translocate N-termini to either side of the mitochondrial inner membrane, revealing an unexpected versatility of the mitochondrial import pathway for non-cleavable inner membrane proteins."}],"date_updated":"2021-01-12T08:19:02Z","citation":{"chicago":"Rampelt, Heike, Iva Sucec, Beate Bersch, Patrick Horten, Inge Perschil, Jean-Claude Martinou, Martin van der Laan, Nils Wiedemann, Paul Schanda, and Nikolaus Pfanner. “The Mitochondrial Carrier Pathway Transports Non-Canonical Substrates with an Odd Number of Transmembrane Segments.” <i>BMC Biology</i>. Springer Nature, 2020. <a href=\"https://doi.org/10.1186/s12915-019-0733-6\">https://doi.org/10.1186/s12915-019-0733-6</a>.","ieee":"H. Rampelt <i>et al.</i>, “The mitochondrial carrier pathway transports non-canonical substrates with an odd number of transmembrane segments,” <i>BMC Biology</i>, vol. 18. Springer Nature, 2020.","ama":"Rampelt H, Sucec I, Bersch B, et al. The mitochondrial carrier pathway transports non-canonical substrates with an odd number of transmembrane segments. <i>BMC Biology</i>. 2020;18. doi:<a href=\"https://doi.org/10.1186/s12915-019-0733-6\">10.1186/s12915-019-0733-6</a>","apa":"Rampelt, H., Sucec, I., Bersch, B., Horten, P., Perschil, I., Martinou, J.-C., … Pfanner, N. (2020). The mitochondrial carrier pathway transports non-canonical substrates with an odd number of transmembrane segments. <i>BMC Biology</i>. Springer Nature. <a href=\"https://doi.org/10.1186/s12915-019-0733-6\">https://doi.org/10.1186/s12915-019-0733-6</a>","ista":"Rampelt H, Sucec I, Bersch B, Horten P, Perschil I, Martinou J-C, van der Laan M, Wiedemann N, Schanda P, Pfanner N. 2020. The mitochondrial carrier pathway transports non-canonical substrates with an odd number of transmembrane segments. BMC Biology. 18, 2.","short":"H. Rampelt, I. Sucec, B. Bersch, P. Horten, I. Perschil, J.-C. Martinou, M. van der Laan, N. Wiedemann, P. Schanda, N. Pfanner, BMC Biology 18 (2020).","mla":"Rampelt, Heike, et al. “The Mitochondrial Carrier Pathway Transports Non-Canonical Substrates with an Odd Number of Transmembrane Segments.” <i>BMC Biology</i>, vol. 18, 2, Springer Nature, 2020, doi:<a href=\"https://doi.org/10.1186/s12915-019-0733-6\">10.1186/s12915-019-0733-6</a>."},"year":"2020","external_id":{"pmid":["31907035"]}},{"volume":32,"extern":"1","doi":"10.1101/gad.315523.118","day":"18","abstract":[{"text":"The total number of nuclear pore complexes (NPCs) per nucleus varies greatly between different cell types and is known to change during cell differentiation and cell transformation. However, the underlying mechanisms that control how many nuclear transport channels are assembled into a given nuclear envelope remain unclear. Here, we report that depletion of the NPC basket protein Tpr, but not Nup153, dramatically increases the total NPC number in various cell types. This negative regulation of Tpr occurs via a phosphorylation cascade of extracellular signal-regulated kinase (ERK), the central kinase of the mitogen-activated protein kinase (MAPK) pathway. Tpr serves as a scaffold for ERK to phosphorylate the nucleoporin (Nup) Nup153, which is critical for early stages of NPC biogenesis. Our results reveal a critical role of the Nup Tpr in coordinating signal transduction pathways during cell proliferation and the dynamic organization of the nucleus.","lang":"eng"}],"date_updated":"2022-07-18T08:32:32Z","year":"2018","citation":{"chicago":"McCloskey, Asako, Arkaitz Ibarra, and Martin Hetzer. “Tpr Regulates the Total Number of Nuclear Pore Complexes per Cell Nucleus.” <i>Genes &#38; Development</i>. Cold Spring Harbor Laboratory, 2018. <a href=\"https://doi.org/10.1101/gad.315523.118\">https://doi.org/10.1101/gad.315523.118</a>.","ieee":"A. McCloskey, A. Ibarra, and M. Hetzer, “Tpr regulates the total number of nuclear pore complexes per cell nucleus,” <i>Genes &#38; Development</i>, vol. 32, no. 19–20. Cold Spring Harbor Laboratory, pp. 1321–1331, 2018.","apa":"McCloskey, A., Ibarra, A., &#38; Hetzer, M. (2018). Tpr regulates the total number of nuclear pore complexes per cell nucleus. <i>Genes &#38; Development</i>. Cold Spring Harbor Laboratory. <a href=\"https://doi.org/10.1101/gad.315523.118\">https://doi.org/10.1101/gad.315523.118</a>","ama":"McCloskey A, Ibarra A, Hetzer M. Tpr regulates the total number of nuclear pore complexes per cell nucleus. <i>Genes &#38; Development</i>. 2018;32(19-20):1321-1331. doi:<a href=\"https://doi.org/10.1101/gad.315523.118\">10.1101/gad.315523.118</a>","ista":"McCloskey A, Ibarra A, Hetzer M. 2018. Tpr regulates the total number of nuclear pore complexes per cell nucleus. Genes &#38; Development. 32(19–20), 1321–1331.","short":"A. McCloskey, A. Ibarra, M. Hetzer, Genes &#38; Development 32 (2018) 1321–1331.","mla":"McCloskey, Asako, et al. “Tpr Regulates the Total Number of Nuclear Pore Complexes per Cell Nucleus.” <i>Genes &#38; Development</i>, vol. 32, no. 19–20, Cold Spring Harbor Laboratory, 2018, pp. 1321–31, doi:<a href=\"https://doi.org/10.1101/gad.315523.118\">10.1101/gad.315523.118</a>."},"external_id":{"pmid":["30228202"]},"publisher":"Cold Spring Harbor Laboratory","article_type":"original","page":"1321-1331","quality_controlled":"1","publication_status":"published","date_created":"2022-04-07T07:45:30Z","article_processing_charge":"No","title":"Tpr regulates the total number of nuclear pore complexes per cell nucleus","intvolume":"        32","pmid":1,"_id":"11063","scopus_import":"1","author":[{"full_name":"McCloskey, Asako","last_name":"McCloskey","first_name":"Asako"},{"first_name":"Arkaitz","last_name":"Ibarra","full_name":"Ibarra, Arkaitz"},{"id":"86c0d31b-b4eb-11ec-ac5a-eae7b2e135ed","orcid":"0000-0002-2111-992X","full_name":"HETZER, Martin W","first_name":"Martin W","last_name":"HETZER"}],"issue":"19-20","main_file_link":[{"url":"https://doi.org/10.1101/gad.315523.118","open_access":"1"}],"user_id":"72615eeb-f1f3-11ec-aa25-d4573ddc34fd","status":"public","publication_identifier":{"issn":["0890-9369","1549-5477"]},"oa":1,"date_published":"2018-09-18T00:00:00Z","type":"journal_article","language":[{"iso":"eng"}],"keyword":["Developmental Biology","Genetics"],"oa_version":"Published Version","month":"09","publication":"Genes & Development"},{"scopus_import":"1","_id":"11066","pmid":1,"issue":"22","author":[{"last_name":"Franks","first_name":"Tobias M.","full_name":"Franks, Tobias M."},{"full_name":"McCloskey, Asako","first_name":"Asako","last_name":"McCloskey"},{"full_name":"Shokhirev, Maxim Nikolaievich","last_name":"Shokhirev","first_name":"Maxim Nikolaievich"},{"full_name":"Benner, Chris","first_name":"Chris","last_name":"Benner"},{"full_name":"Rathore, Annie","last_name":"Rathore","first_name":"Annie"},{"orcid":"0000-0002-2111-992X","full_name":"HETZER, Martin W","first_name":"Martin W","last_name":"HETZER","id":"86c0d31b-b4eb-11ec-ac5a-eae7b2e135ed"}],"date_created":"2022-04-07T07:45:59Z","article_processing_charge":"No","publication_status":"published","intvolume":"        31","title":"Nup98 recruits the Wdr82–Set1A/COMPASS complex to promoters to regulate H3K4 trimethylation in hematopoietic progenitor cells","quality_controlled":"1","page":"2222-2234","publisher":"Cold Spring Harbor Laboratory","article_type":"original","year":"2017","citation":{"chicago":"Franks, Tobias M., Asako McCloskey, Maxim Nikolaievich Shokhirev, Chris Benner, Annie Rathore, and Martin Hetzer. “Nup98 Recruits the Wdr82–Set1A/COMPASS Complex to Promoters to Regulate H3K4 Trimethylation in Hematopoietic Progenitor Cells.” <i>Genes &#38; Development</i>. Cold Spring Harbor Laboratory, 2017. <a href=\"https://doi.org/10.1101/gad.306753.117\">https://doi.org/10.1101/gad.306753.117</a>.","ieee":"T. M. Franks, A. McCloskey, M. N. Shokhirev, C. Benner, A. Rathore, and M. Hetzer, “Nup98 recruits the Wdr82–Set1A/COMPASS complex to promoters to regulate H3K4 trimethylation in hematopoietic progenitor cells,” <i>Genes &#38; Development</i>, vol. 31, no. 22. Cold Spring Harbor Laboratory, pp. 2222–2234, 2017.","ama":"Franks TM, McCloskey A, Shokhirev MN, Benner C, Rathore A, Hetzer M. Nup98 recruits the Wdr82–Set1A/COMPASS complex to promoters to regulate H3K4 trimethylation in hematopoietic progenitor cells. <i>Genes &#38; Development</i>. 2017;31(22):2222-2234. doi:<a href=\"https://doi.org/10.1101/gad.306753.117\">10.1101/gad.306753.117</a>","apa":"Franks, T. M., McCloskey, A., Shokhirev, M. N., Benner, C., Rathore, A., &#38; Hetzer, M. (2017). Nup98 recruits the Wdr82–Set1A/COMPASS complex to promoters to regulate H3K4 trimethylation in hematopoietic progenitor cells. <i>Genes &#38; Development</i>. Cold Spring Harbor Laboratory. <a href=\"https://doi.org/10.1101/gad.306753.117\">https://doi.org/10.1101/gad.306753.117</a>","ista":"Franks TM, McCloskey A, Shokhirev MN, Benner C, Rathore A, Hetzer M. 2017. Nup98 recruits the Wdr82–Set1A/COMPASS complex to promoters to regulate H3K4 trimethylation in hematopoietic progenitor cells. Genes &#38; Development. 31(22), 2222–2234.","mla":"Franks, Tobias M., et al. “Nup98 Recruits the Wdr82–Set1A/COMPASS Complex to Promoters to Regulate H3K4 Trimethylation in Hematopoietic Progenitor Cells.” <i>Genes &#38; Development</i>, vol. 31, no. 22, Cold Spring Harbor Laboratory, 2017, pp. 2222–34, doi:<a href=\"https://doi.org/10.1101/gad.306753.117\">10.1101/gad.306753.117</a>.","short":"T.M. Franks, A. McCloskey, M.N. Shokhirev, C. Benner, A. Rathore, M. Hetzer, Genes &#38; Development 31 (2017) 2222–2234."},"date_updated":"2022-07-18T08:33:05Z","external_id":{"pmid":["29269482"]},"day":"21","doi":"10.1101/gad.306753.117","abstract":[{"lang":"eng","text":"Recent studies have shown that a subset of nucleoporins (Nups) can detach from the nuclear pore complex and move into the nuclear interior to regulate transcription. One such dynamic Nup, called Nup98, has been implicated in gene activation in healthy cells and has been shown to drive leukemogenesis when mutated in patients with acute myeloid leukemia (AML). Here we show that in hematopoietic cells, Nup98 binds predominantly to transcription start sites to recruit the Wdr82–Set1A/COMPASS (complex of proteins associated with Set1) complex, which is required for deposition of the histone 3 Lys4 trimethyl (H3K4me3)-activating mark. Depletion of Nup98 or Wdr82 abolishes Set1A recruitment to chromatin and subsequently ablates H3K4me3 at adjacent promoters. Furthermore, expression of a Nup98 fusion protein implicated in aggressive AML causes mislocalization of H3K4me3 at abnormal regions and up-regulation of associated genes. Our findings establish a function of Nup98 in hematopoietic gene activation and provide mechanistic insight into which Nup98 leukemic fusion proteins promote AML."}],"volume":31,"extern":"1","publication":"Genes & Development","oa_version":"Published Version","month":"12","keyword":["Developmental Biology","Genetics"],"language":[{"iso":"eng"}],"type":"journal_article","date_published":"2017-12-21T00:00:00Z","publication_identifier":{"issn":["0890-9369","1549-5477"]},"oa":1,"main_file_link":[{"open_access":"1","url":"https://doi.org/10.1101/gad.306753.117"}],"status":"public","user_id":"72615eeb-f1f3-11ec-aa25-d4573ddc34fd"},{"extern":"1","volume":30,"abstract":[{"lang":"eng","text":"The organization of the genome in the three-dimensional space of the nucleus is coupled with cell type-specific gene expression. However, how nuclear architecture influences transcription that governs cell identity remains unknown. Here, we show that nuclear pore complex (NPC) components Nup93 and Nup153 bind superenhancers (SE), regulatory structures that drive the expression of key genes that specify cell identity. We found that nucleoporin-associated SEs localize preferentially to the nuclear periphery, and absence of Nup153 and Nup93 results in dramatic transcriptional changes of SE-associated genes. Our results reveal a crucial role of NPC components in the regulation of cell type-specifying genes and highlight nuclear architecture as a regulatory layer of genome functions in cell fate."}],"doi":"10.1101/gad.287417.116","day":"02","external_id":{"pmid":["27807035"]},"date_updated":"2022-07-18T08:33:49Z","citation":{"apa":"Ibarra, A., Benner, C., Tyagi, S., Cool, J., &#38; Hetzer, M. (2016). Nucleoporin-mediated regulation of cell identity genes. <i>Genes &#38; Development</i>. Cold Spring Harbor Laboratory. <a href=\"https://doi.org/10.1101/gad.287417.116\">https://doi.org/10.1101/gad.287417.116</a>","ama":"Ibarra A, Benner C, Tyagi S, Cool J, Hetzer M. Nucleoporin-mediated regulation of cell identity genes. <i>Genes &#38; Development</i>. 2016;30(20):2253-2258. doi:<a href=\"https://doi.org/10.1101/gad.287417.116\">10.1101/gad.287417.116</a>","chicago":"Ibarra, Arkaitz, Chris Benner, Swati Tyagi, Jonah Cool, and Martin Hetzer. “Nucleoporin-Mediated Regulation of Cell Identity Genes.” <i>Genes &#38; Development</i>. Cold Spring Harbor Laboratory, 2016. <a href=\"https://doi.org/10.1101/gad.287417.116\">https://doi.org/10.1101/gad.287417.116</a>.","ieee":"A. Ibarra, C. Benner, S. Tyagi, J. Cool, and M. Hetzer, “Nucleoporin-mediated regulation of cell identity genes,” <i>Genes &#38; Development</i>, vol. 30, no. 20. Cold Spring Harbor Laboratory, pp. 2253–2258, 2016.","mla":"Ibarra, Arkaitz, et al. “Nucleoporin-Mediated Regulation of Cell Identity Genes.” <i>Genes &#38; Development</i>, vol. 30, no. 20, Cold Spring Harbor Laboratory, 2016, pp. 2253–58, doi:<a href=\"https://doi.org/10.1101/gad.287417.116\">10.1101/gad.287417.116</a>.","short":"A. Ibarra, C. Benner, S. Tyagi, J. Cool, M. Hetzer, Genes &#38; Development 30 (2016) 2253–2258.","ista":"Ibarra A, Benner C, Tyagi S, Cool J, Hetzer M. 2016. Nucleoporin-mediated regulation of cell identity genes. Genes &#38; Development. 30(20), 2253–2258."},"year":"2016","article_type":"original","publisher":"Cold Spring Harbor Laboratory","page":"2253-2258","quality_controlled":"1","title":"Nucleoporin-mediated regulation of cell identity genes","intvolume":"        30","publication_status":"published","article_processing_charge":"No","date_created":"2022-04-07T07:48:08Z","author":[{"full_name":"Ibarra, Arkaitz","last_name":"Ibarra","first_name":"Arkaitz"},{"full_name":"Benner, Chris","last_name":"Benner","first_name":"Chris"},{"full_name":"Tyagi, Swati","first_name":"Swati","last_name":"Tyagi"},{"first_name":"Jonah","last_name":"Cool","full_name":"Cool, Jonah"},{"id":"86c0d31b-b4eb-11ec-ac5a-eae7b2e135ed","first_name":"Martin W","last_name":"HETZER","orcid":"0000-0002-2111-992X","full_name":"HETZER, Martin W"}],"issue":"20","_id":"11070","pmid":1,"scopus_import":"1","status":"public","user_id":"72615eeb-f1f3-11ec-aa25-d4573ddc34fd","main_file_link":[{"open_access":"1","url":"https://doi.org/10.1101/gad.287417.116"}],"oa":1,"publication_identifier":{"issn":["0890-9369"],"eissn":["1549-5477"]},"date_published":"2016-11-02T00:00:00Z","type":"journal_article","language":[{"iso":"eng"}],"keyword":["Developmental Biology","Genetics"],"month":"11","oa_version":"Published Version","publication":"Genes & Development"},{"keyword":["Developmental Biology","Genetics"],"language":[{"iso":"eng"}],"publication":"Genes & Development","oa_version":"Published Version","month":"05","main_file_link":[{"open_access":"1","url":"https://doi.org/10.1101/gad.280941.116"}],"user_id":"72615eeb-f1f3-11ec-aa25-d4573ddc34fd","status":"public","type":"journal_article","date_published":"2016-05-19T00:00:00Z","publication_identifier":{"issn":["0890-9369"],"eissn":["1549-5477"]},"oa":1,"quality_controlled":"1","page":"1155-1171","publisher":"Cold Spring Harbor Laboratory","article_type":"original","scopus_import":"1","_id":"11071","pmid":1,"issue":"10","author":[{"last_name":"Franks","first_name":"Tobias M.","full_name":"Franks, Tobias M."},{"first_name":"Chris","last_name":"Benner","full_name":"Benner, Chris"},{"first_name":"Iñigo","last_name":"Narvaiza","full_name":"Narvaiza, Iñigo"},{"last_name":"Marchetto","first_name":"Maria C.N.","full_name":"Marchetto, Maria C.N."},{"full_name":"Young, Janet M.","first_name":"Janet M.","last_name":"Young"},{"full_name":"Malik, Harmit S.","last_name":"Malik","first_name":"Harmit S."},{"full_name":"Gage, Fred H.","last_name":"Gage","first_name":"Fred H."},{"first_name":"Martin W","last_name":"HETZER","orcid":"0000-0002-2111-992X","full_name":"HETZER, Martin W","id":"86c0d31b-b4eb-11ec-ac5a-eae7b2e135ed"}],"article_processing_charge":"No","date_created":"2022-04-07T07:48:20Z","publication_status":"published","intvolume":"        30","title":"Evolution of a transcriptional regulator from a transmembrane nucleoporin","volume":30,"extern":"1","year":"2016","citation":{"ieee":"T. M. Franks <i>et al.</i>, “Evolution of a transcriptional regulator from a transmembrane nucleoporin,” <i>Genes &#38; Development</i>, vol. 30, no. 10. Cold Spring Harbor Laboratory, pp. 1155–1171, 2016.","chicago":"Franks, Tobias M., Chris Benner, Iñigo Narvaiza, Maria C.N. Marchetto, Janet M. Young, Harmit S. Malik, Fred H. Gage, and Martin Hetzer. “Evolution of a Transcriptional Regulator from a Transmembrane Nucleoporin.” <i>Genes &#38; Development</i>. Cold Spring Harbor Laboratory, 2016. <a href=\"https://doi.org/10.1101/gad.280941.116\">https://doi.org/10.1101/gad.280941.116</a>.","apa":"Franks, T. M., Benner, C., Narvaiza, I., Marchetto, M. C. N., Young, J. M., Malik, H. S., … Hetzer, M. (2016). Evolution of a transcriptional regulator from a transmembrane nucleoporin. <i>Genes &#38; Development</i>. Cold Spring Harbor Laboratory. <a href=\"https://doi.org/10.1101/gad.280941.116\">https://doi.org/10.1101/gad.280941.116</a>","ama":"Franks TM, Benner C, Narvaiza I, et al. Evolution of a transcriptional regulator from a transmembrane nucleoporin. <i>Genes &#38; Development</i>. 2016;30(10):1155-1171. doi:<a href=\"https://doi.org/10.1101/gad.280941.116\">10.1101/gad.280941.116</a>","ista":"Franks TM, Benner C, Narvaiza I, Marchetto MCN, Young JM, Malik HS, Gage FH, Hetzer M. 2016. Evolution of a transcriptional regulator from a transmembrane nucleoporin. Genes &#38; Development. 30(10), 1155–1171.","short":"T.M. Franks, C. Benner, I. Narvaiza, M.C.N. Marchetto, J.M. Young, H.S. Malik, F.H. Gage, M. Hetzer, Genes &#38; Development 30 (2016) 1155–1171.","mla":"Franks, Tobias M., et al. “Evolution of a Transcriptional Regulator from a Transmembrane Nucleoporin.” <i>Genes &#38; Development</i>, vol. 30, no. 10, Cold Spring Harbor Laboratory, 2016, pp. 1155–71, doi:<a href=\"https://doi.org/10.1101/gad.280941.116\">10.1101/gad.280941.116</a>."},"date_updated":"2022-07-18T08:33:50Z","external_id":{"pmid":["27198230"]},"day":"19","doi":"10.1101/gad.280941.116","abstract":[{"text":"Nuclear pore complexes (NPCs) emerged as nuclear transport channels in eukaryotic cells ∼1.5 billion years ago. While the primary role of NPCs is to regulate nucleo–cytoplasmic transport, recent research suggests that certain NPC proteins have additionally acquired the role of affecting gene expression at the nuclear periphery and in the nucleoplasm in metazoans. Here we identify a widely expressed variant of the transmembrane nucleoporin (Nup) Pom121 (named sPom121, for “soluble Pom121”) that arose by genomic rearrangement before the divergence of hominoids. sPom121 lacks the nuclear membrane-anchoring domain and thus does not localize to the NPC. Instead, sPom121 colocalizes and interacts with nucleoplasmic Nup98, a previously identified transcriptional regulator, at gene promoters to control transcription of its target genes in human cells. Interestingly, sPom121 transcripts appear independently in several mammalian species, suggesting convergent innovation of Nup-mediated transcription regulation during mammalian evolution. Our findings implicate alternate transcription initiation as a mechanism to increase the functional diversity of NPC components.","lang":"eng"}]},{"month":"02","oa_version":"Published Version","publication":"Genes & Development","language":[{"iso":"eng"}],"keyword":["Developmental Biology","Genetics"],"oa":1,"publication_identifier":{"issn":["0890-9369"],"eissn":["1549-5477"]},"date_published":"2015-02-01T00:00:00Z","type":"journal_article","user_id":"72615eeb-f1f3-11ec-aa25-d4573ddc34fd","status":"public","main_file_link":[{"url":"https://doi.org/10.1101/gad.256495.114","open_access":"1"}],"title":"Nuclear pore proteins and the control of genome functions","intvolume":"        29","publication_status":"published","date_created":"2022-04-07T07:49:21Z","article_processing_charge":"No","author":[{"first_name":"Arkaitz","last_name":"Ibarra","full_name":"Ibarra, Arkaitz"},{"id":"86c0d31b-b4eb-11ec-ac5a-eae7b2e135ed","full_name":"HETZER, Martin W","orcid":"0000-0002-2111-992X","last_name":"HETZER","first_name":"Martin W"}],"issue":"4","pmid":1,"_id":"11076","scopus_import":"1","article_type":"original","publisher":"Cold Spring Harbor Laboratory","page":"337-349","quality_controlled":"1","abstract":[{"text":"Nuclear pore complexes (NPCs) are composed of several copies of ∼30 different proteins called nucleoporins (Nups). NPCs penetrate the nuclear envelope (NE) and regulate the nucleocytoplasmic trafficking of macromolecules. Beyond this vital role, NPC components influence genome functions in a transport-independent manner. Nups play an evolutionarily conserved role in gene expression regulation that, in metazoans, extends into the nuclear interior. Additionally, in proliferative cells, Nups play a crucial role in genome integrity maintenance and mitotic progression. Here we discuss genome-related functions of Nups and their impact on essential DNA metabolism processes such as transcription, chromosome duplication, and segregation.","lang":"eng"}],"doi":"10.1101/gad.256495.114","day":"01","external_id":{"pmid":["25691464"]},"date_updated":"2022-07-18T08:43:20Z","citation":{"ama":"Ibarra A, Hetzer M. Nuclear pore proteins and the control of genome functions. <i>Genes &#38; Development</i>. 2015;29(4):337-349. doi:<a href=\"https://doi.org/10.1101/gad.256495.114\">10.1101/gad.256495.114</a>","apa":"Ibarra, A., &#38; Hetzer, M. (2015). Nuclear pore proteins and the control of genome functions. <i>Genes &#38; Development</i>. Cold Spring Harbor Laboratory. <a href=\"https://doi.org/10.1101/gad.256495.114\">https://doi.org/10.1101/gad.256495.114</a>","ieee":"A. Ibarra and M. Hetzer, “Nuclear pore proteins and the control of genome functions,” <i>Genes &#38; Development</i>, vol. 29, no. 4. Cold Spring Harbor Laboratory, pp. 337–349, 2015.","chicago":"Ibarra, Arkaitz, and Martin Hetzer. “Nuclear Pore Proteins and the Control of Genome Functions.” <i>Genes &#38; Development</i>. Cold Spring Harbor Laboratory, 2015. <a href=\"https://doi.org/10.1101/gad.256495.114\">https://doi.org/10.1101/gad.256495.114</a>.","short":"A. Ibarra, M. Hetzer, Genes &#38; Development 29 (2015) 337–349.","mla":"Ibarra, Arkaitz, and Martin Hetzer. “Nuclear Pore Proteins and the Control of Genome Functions.” <i>Genes &#38; Development</i>, vol. 29, no. 4, Cold Spring Harbor Laboratory, 2015, pp. 337–49, doi:<a href=\"https://doi.org/10.1101/gad.256495.114\">10.1101/gad.256495.114</a>.","ista":"Ibarra A, Hetzer M. 2015. Nuclear pore proteins and the control of genome functions. Genes &#38; Development. 29(4), 337–349."},"year":"2015","extern":"1","volume":29},{"type":"journal_article","date_published":"2015-06-16T00:00:00Z","publication_identifier":{"eissn":["1549-5477"],"issn":["0890-9369"]},"oa":1,"main_file_link":[{"open_access":"1","url":"https://doi.org/10.1101/gad.260919.115"}],"status":"public","user_id":"72615eeb-f1f3-11ec-aa25-d4573ddc34fd","publication":"Genes & Development","oa_version":"Published Version","month":"06","keyword":["Developmental Biology","Genetics"],"language":[{"iso":"eng"}],"citation":{"short":"F.V. Jacinto, C. Benner, M. Hetzer, Genes &#38; Development 29 (2015) 1224–1238.","mla":"Jacinto, Filipe V., et al. “The Nucleoporin Nup153 Regulates Embryonic Stem Cell Pluripotency through Gene Silencing.” <i>Genes &#38; Development</i>, vol. 29, no. 12, Cold Spring Harbor Laboratory, 2015, pp. 1224–38, doi:<a href=\"https://doi.org/10.1101/gad.260919.115\">10.1101/gad.260919.115</a>.","ista":"Jacinto FV, Benner C, Hetzer M. 2015. The nucleoporin Nup153 regulates embryonic stem cell pluripotency through gene silencing. Genes &#38; Development. 29(12), 1224–1238.","ama":"Jacinto FV, Benner C, Hetzer M. The nucleoporin Nup153 regulates embryonic stem cell pluripotency through gene silencing. <i>Genes &#38; Development</i>. 2015;29(12):1224-1238. doi:<a href=\"https://doi.org/10.1101/gad.260919.115\">10.1101/gad.260919.115</a>","apa":"Jacinto, F. V., Benner, C., &#38; Hetzer, M. (2015). The nucleoporin Nup153 regulates embryonic stem cell pluripotency through gene silencing. <i>Genes &#38; Development</i>. Cold Spring Harbor Laboratory. <a href=\"https://doi.org/10.1101/gad.260919.115\">https://doi.org/10.1101/gad.260919.115</a>","chicago":"Jacinto, Filipe V., Chris Benner, and Martin Hetzer. “The Nucleoporin Nup153 Regulates Embryonic Stem Cell Pluripotency through Gene Silencing.” <i>Genes &#38; Development</i>. Cold Spring Harbor Laboratory, 2015. <a href=\"https://doi.org/10.1101/gad.260919.115\">https://doi.org/10.1101/gad.260919.115</a>.","ieee":"F. V. Jacinto, C. Benner, and M. Hetzer, “The nucleoporin Nup153 regulates embryonic stem cell pluripotency through gene silencing,” <i>Genes &#38; Development</i>, vol. 29, no. 12. Cold Spring Harbor Laboratory, pp. 1224–1238, 2015."},"year":"2015","date_updated":"2022-07-18T08:43:51Z","external_id":{"pmid":["26080816"]},"day":"16","doi":"10.1101/gad.260919.115","abstract":[{"text":"Nucleoporins (Nups) are a family of proteins best known as the constituent building blocks of nuclear pore complexes (NPCs), membrane-embedded channels that mediate nuclear transport across the nuclear envelope. Recent evidence suggests that several Nups have additional roles in controlling the activation and silencing of developmental genes; however, the mechanistic details of these functions remain poorly understood. Here, we show that depletion of Nup153 in mouse embryonic stem cells (mESCs) causes the derepression of developmental genes and induction of early differentiation. This loss of stem cell identity is not associated with defects in the nuclear import of key pluripotency factors. Rather, Nup153 binds around the transcriptional start site (TSS) of developmental genes and mediates the recruitment of the polycomb-repressive complex 1 (PRC1) to a subset of its target loci. Our results demonstrate a chromatin-associated role of Nup153 in maintaining stem cell pluripotency by functioning in mammalian epigenetic gene silencing.","lang":"eng"}],"volume":29,"extern":"1","scopus_import":"1","_id":"11077","pmid":1,"issue":"12","author":[{"first_name":"Filipe V.","last_name":"Jacinto","full_name":"Jacinto, Filipe V."},{"last_name":"Benner","first_name":"Chris","full_name":"Benner, Chris"},{"id":"86c0d31b-b4eb-11ec-ac5a-eae7b2e135ed","last_name":"HETZER","first_name":"Martin W","full_name":"HETZER, Martin W","orcid":"0000-0002-2111-992X"}],"article_processing_charge":"No","date_created":"2022-04-07T07:49:31Z","publication_status":"published","intvolume":"        29","title":"The nucleoporin Nup153 regulates embryonic stem cell pluripotency through gene silencing","quality_controlled":"1","page":"1224-1238","publisher":"Cold Spring Harbor Laboratory","article_type":"original"},{"volume":54,"acknowledgement":"The authors thank all the members of the Division of Morphogenesis, National Institute for Basic Biology, for their contributions to the research, their encouragement, and helpful discussions, particularly Dr M. Suzuki for his critical reading of the manuscript. We also thank the Model Animal Research and Spectrography and Bioimaging Facilities, NIBB Core Research Facilities, for technical support. M.H. was supported by a research fellowship from the Japan Society for the Promotion of Science (JSPS). Our work introduced in this review was supported by a Grant-in-Aid for Scientific Research on Innovative Areas from the Ministry of Education, Culture, Sports, Science, and Technology (MEXT), Japan, to N.U.","abstract":[{"text":"In the last several decades, developmental biology has clarified the molecular mechanisms of embryogenesis and organogenesis. In particular, it has demonstrated that the “tool-kit genes” essential for regulating developmental processes are not only highly conserved among species, but are also used as systems at various times and places in an organism to control distinct developmental events. Therefore, mutations in many of these tool-kit genes may cause congenital diseases involving morphological abnormalities. This link between genes and abnormal morphological phenotypes underscores the importance of understanding how cells behave and contribute to morphogenesis as a result of gene function. Recent improvements in live imaging and in quantitative analyses of cellular dynamics will advance our understanding of the cellular pathogenesis of congenital diseases associated with aberrant morphologies. In these studies, it is critical to select an appropriate model organism for the particular phenomenon of interest.","lang":"eng"}],"day":"01","doi":"10.1111/cga.12039","external_id":{"pmid":["24666178"]},"year":"2014","citation":{"ista":"Hashimoto M, Morita H, Ueno N. 2014. Molecular and cellular mechanisms of development underlying congenital diseases. Congenital Anomalies. 54(1), 1–7.","mla":"Hashimoto, Masakazu, et al. “Molecular and Cellular Mechanisms of Development Underlying Congenital Diseases.” <i>Congenital Anomalies</i>, vol. 54, no. 1, Wiley, 2014, pp. 1–7, doi:<a href=\"https://doi.org/10.1111/cga.12039\">10.1111/cga.12039</a>.","short":"M. Hashimoto, H. Morita, N. Ueno, Congenital Anomalies 54 (2014) 1–7.","chicago":"Hashimoto, Masakazu, Hitoshi Morita, and Naoto Ueno. “Molecular and Cellular Mechanisms of Development Underlying Congenital Diseases.” <i>Congenital Anomalies</i>. Wiley, 2014. <a href=\"https://doi.org/10.1111/cga.12039\">https://doi.org/10.1111/cga.12039</a>.","ieee":"M. Hashimoto, H. Morita, and N. Ueno, “Molecular and cellular mechanisms of development underlying congenital diseases,” <i>Congenital Anomalies</i>, vol. 54, no. 1. Wiley, pp. 1–7, 2014.","apa":"Hashimoto, M., Morita, H., &#38; Ueno, N. (2014). Molecular and cellular mechanisms of development underlying congenital diseases. <i>Congenital Anomalies</i>. Wiley. <a href=\"https://doi.org/10.1111/cga.12039\">https://doi.org/10.1111/cga.12039</a>","ama":"Hashimoto M, Morita H, Ueno N. Molecular and cellular mechanisms of development underlying congenital diseases. <i>Congenital Anomalies</i>. 2014;54(1):1-7. doi:<a href=\"https://doi.org/10.1111/cga.12039\">10.1111/cga.12039</a>"},"date_updated":"2022-03-04T08:26:05Z","article_type":"original","publisher":"Wiley","quality_controlled":"1","page":"1-7","intvolume":"        54","title":"Molecular and cellular mechanisms of development underlying congenital diseases","department":[{"_id":"CaHe"}],"date_created":"2022-03-04T08:17:25Z","article_processing_charge":"No","publication_status":"published","issue":"1","author":[{"full_name":"Hashimoto, Masakazu","first_name":"Masakazu","last_name":"Hashimoto"},{"full_name":"Morita, Hitoshi","last_name":"Morita","first_name":"Hitoshi","id":"4C6E54C6-F248-11E8-B48F-1D18A9856A87"},{"full_name":"Ueno, Naoto","first_name":"Naoto","last_name":"Ueno"}],"scopus_import":"1","pmid":1,"_id":"10815","status":"public","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","main_file_link":[{"url":"https://doi.org/10.1111/cga.12039","open_access":"1"}],"oa":1,"publication_identifier":{"issn":["0914-3505"]},"type":"journal_article","date_published":"2014-02-01T00:00:00Z","keyword":["Developmental Biology","Embryology","General Medicine","Pediatrics","Perinatology","and Child Health"],"language":[{"iso":"eng"}],"month":"02","oa_version":"None","publication":"Congenital Anomalies"},{"article_type":"original","publisher":"Elsevier","quality_controlled":"1","page":"446-458","intvolume":"        22","title":"A change in nuclear pore complex composition regulates cell differentiation","article_processing_charge":"No","date_created":"2022-04-07T07:52:10Z","publication_status":"published","issue":"2","author":[{"full_name":"D'Angelo, Maximiliano A.","last_name":"D'Angelo","first_name":"Maximiliano A."},{"last_name":"Gomez-Cavazos","first_name":"J. Sebastian","full_name":"Gomez-Cavazos, J. Sebastian"},{"full_name":"Mei, Arianna","last_name":"Mei","first_name":"Arianna"},{"last_name":"Lackner","first_name":"Daniel H.","full_name":"Lackner, Daniel H."},{"id":"86c0d31b-b4eb-11ec-ac5a-eae7b2e135ed","orcid":"0000-0002-2111-992X","full_name":"HETZER, Martin W","first_name":"Martin W","last_name":"HETZER"}],"scopus_import":"1","_id":"11093","pmid":1,"extern":"1","volume":22,"abstract":[{"text":"Nuclear pore complexes (NPCs) are built from ∼30 different proteins called nucleoporins or Nups. Previous studies have shown that several Nups exhibit cell-type-specific expression and that mutations in NPC components result in tissue-specific diseases. Here we show that a specific change in NPC composition is required for both myogenic and neuronal differentiation. The transmembrane nucleoporin Nup210 is absent in proliferating myoblasts and embryonic stem cells (ESCs) but becomes expressed and incorporated into NPCs during cell differentiation. Preventing Nup210 production by RNAi blocks myogenesis and the differentiation of ESCs into neuroprogenitors. We found that the addition of Nup210 to NPCs does not affect nuclear transport but is required for the induction of genes that are essential for cell differentiation. Our results identify a single change in NPC composition as an essential step in cell differentiation and establish a role for Nup210 in gene expression regulation and cell fate determination.","lang":"eng"}],"day":"19","doi":"10.1016/j.devcel.2011.11.021","external_id":{"pmid":["22264802"]},"citation":{"short":"M.A. D’Angelo, J.S. Gomez-Cavazos, A. Mei, D.H. Lackner, M. Hetzer, Developmental Cell 22 (2012) 446–458.","mla":"D’Angelo, Maximiliano A., et al. “A Change in Nuclear Pore Complex Composition Regulates Cell Differentiation.” <i>Developmental Cell</i>, vol. 22, no. 2, Elsevier, 2012, pp. 446–58, doi:<a href=\"https://doi.org/10.1016/j.devcel.2011.11.021\">10.1016/j.devcel.2011.11.021</a>.","ista":"D’Angelo MA, Gomez-Cavazos JS, Mei A, Lackner DH, Hetzer M. 2012. A change in nuclear pore complex composition regulates cell differentiation. Developmental Cell. 22(2), 446–458.","apa":"D’Angelo, M. A., Gomez-Cavazos, J. S., Mei, A., Lackner, D. H., &#38; Hetzer, M. (2012). A change in nuclear pore complex composition regulates cell differentiation. <i>Developmental Cell</i>. Elsevier. <a href=\"https://doi.org/10.1016/j.devcel.2011.11.021\">https://doi.org/10.1016/j.devcel.2011.11.021</a>","ama":"D’Angelo MA, Gomez-Cavazos JS, Mei A, Lackner DH, Hetzer M. A change in nuclear pore complex composition regulates cell differentiation. <i>Developmental Cell</i>. 2012;22(2):446-458. doi:<a href=\"https://doi.org/10.1016/j.devcel.2011.11.021\">10.1016/j.devcel.2011.11.021</a>","chicago":"D’Angelo, Maximiliano A., J. Sebastian Gomez-Cavazos, Arianna Mei, Daniel H. Lackner, and Martin Hetzer. “A Change in Nuclear Pore Complex Composition Regulates Cell Differentiation.” <i>Developmental Cell</i>. Elsevier, 2012. <a href=\"https://doi.org/10.1016/j.devcel.2011.11.021\">https://doi.org/10.1016/j.devcel.2011.11.021</a>.","ieee":"M. A. D’Angelo, J. S. Gomez-Cavazos, A. Mei, D. H. Lackner, and M. Hetzer, “A change in nuclear pore complex composition regulates cell differentiation,” <i>Developmental Cell</i>, vol. 22, no. 2. Elsevier, pp. 446–458, 2012."},"year":"2012","date_updated":"2022-07-18T08:53:16Z","keyword":["Developmental Biology","Cell Biology","General Biochemistry","Genetics and Molecular Biology","Molecular Biology"],"language":[{"iso":"eng"}],"month":"01","oa_version":"Published Version","publication":"Developmental Cell","status":"public","user_id":"72615eeb-f1f3-11ec-aa25-d4573ddc34fd","main_file_link":[{"url":"https://doi.org/10.1016/j.devcel.2011.11.021","open_access":"1"}],"oa":1,"publication_identifier":{"issn":["1534-5807"]},"type":"journal_article","date_published":"2012-01-19T00:00:00Z"}]