[{"type":"journal_article","article_processing_charge":"No","citation":{"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>.","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>","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.","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>","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.","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>.","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."},"publisher":"Elsevier","date_updated":"2023-10-04T08:23:20Z","oa_version":"None","isi":1,"month":"12","status":"public","scopus_import":"1","publication_status":"published","date_created":"2023-01-12T11:57:00Z","external_id":{"isi":["000919603800005"],"pmid":["36473460"]},"abstract":[{"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.","lang":"eng"}],"issue":"23","quality_controlled":"1","_id":"12120","intvolume":"        57","date_published":"2022-12-05T00:00:00Z","author":[{"last_name":"Xiao","full_name":"Xiao, Huixin","first_name":"Huixin"},{"first_name":"Yumei","full_name":"Hu, Yumei","last_name":"Hu"},{"full_name":"Wang, Yaping","first_name":"Yaping","last_name":"Wang"},{"first_name":"Jinkui","full_name":"Cheng, Jinkui","last_name":"Cheng"},{"full_name":"Wang, Jinyi","first_name":"Jinyi","last_name":"Wang"},{"last_name":"Chen","full_name":"Chen, Guojingwei","first_name":"Guojingwei"},{"full_name":"Li, Qian","first_name":"Qian","last_name":"Li"},{"first_name":"Shuwei","full_name":"Wang, Shuwei","last_name":"Wang"},{"first_name":"Yalu","full_name":"Wang, Yalu","last_name":"Wang"},{"full_name":"Wang, Shao-Shuai","first_name":"Shao-Shuai","last_name":"Wang"},{"first_name":"Yi","full_name":"Wang, Yi","last_name":"Wang"},{"last_name":"Xuan","full_name":"Xuan, Wei","first_name":"Wei"},{"first_name":"Zhen","full_name":"Li, Zhen","last_name":"Li"},{"last_name":"Guo","full_name":"Guo, Yan","first_name":"Yan"},{"last_name":"Gong","full_name":"Gong, Zhizhong","first_name":"Zhizhong"},{"last_name":"Friml","full_name":"Friml, Jiří","id":"4159519E-F248-11E8-B48F-1D18A9856A87","first_name":"Jiří","orcid":"0000-0002-8302-7596"},{"last_name":"Zhang","full_name":"Zhang, Jing","first_name":"Jing"}],"page":"2638-2651.e6","volume":57,"article_type":"original","keyword":["Developmental Biology","Cell Biology","General Biochemistry","Genetics and Molecular Biology","Molecular Biology"],"language":[{"iso":"eng"}],"publication_identifier":{"issn":["1534-5807"]},"doi":"10.1016/j.devcel.2022.11.006","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","publication":"Developmental Cell","day":"05","title":"Nitrate availability controls translocation of the transcription factor NAC075 for cell-type-specific reprogramming of root growth","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).","year":"2022","department":[{"_id":"JiFr"}],"pmid":1},{"publication":"Journal of Cell Biology","day":"01","user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","doi":"10.1083/jcb.202203139","language":[{"iso":"eng"}],"publication_identifier":{"eissn":["1540-8140"],"issn":["0021-9525"]},"keyword":["Cell Biology"],"oa":1,"article_type":"original","article_number":"e202203139","pmid":1,"year":"2022","department":[{"_id":"JiFr"}],"acknowledgement":"We thank Suayip Ustün, Karin Schumacher, Erika Isono, Gerd Juergens, Takashi Ueda, Daniel Hofius, and Liwen Jiang for sharing published materials.\r\nWe acknowledge funding from Austrian Academy of Sciences, Austrian Science Fund (FWF, P 32355, P 34944), Austrian Science Fund (FWF-SFB F79), Vienna Science and Technology\r\nFund (WWTF, LS17-047) to Y. Dagdas; Austrian Academy of Sciences DOC Fellowship to J. Zhao, Marie Curie VIP2 Fellowship to J.C. De La Concepcion and M. Clavel; Hong Kong Research Grant Council (GRF14121019, 14113921, AoE/M-05/12, C4002-17G) to B.-H. Kang. We thank Vienna Biocenter Core Facilities (VBCF) Protein Chemistry, Biooptics, Plant Sciences, Molecular Biology, and Protein Technologies. We thank J. Matthew Watson\r\nand members of the Dagdas lab for the critical reading and editing of the manuscript.","title":"Plant autophagosomes mature into amphisomes prior to their delivery to the central vacuole","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)"},"file":[{"file_id":"12342","checksum":"050b5cc4b25e6b94fe3e3cbfe0f5c06b","creator":"dernst","date_created":"2023-01-23T10:30:11Z","access_level":"open_access","file_name":"2022_JCB_Zhao.pdf","success":1,"file_size":10365777,"content_type":"application/pdf","date_updated":"2023-01-23T10:30:11Z","relation":"main_file"}],"isi":1,"ddc":["580"],"month":"12","status":"public","date_updated":"2023-08-03T14:20:15Z","oa_version":"Published Version","citation":{"chicago":"Zhao, Jierui, Mai Thu Bui, Juncai Ma, Fabian Künzl, Lorenzo Picchianti, Juan Carlos De La Concepcion, Yixuan Chen, et al. “Plant Autophagosomes Mature into Amphisomes Prior to Their Delivery to the Central Vacuole.” <i>Journal of Cell Biology</i>. Rockefeller University Press, 2022. <a href=\"https://doi.org/10.1083/jcb.202203139\">https://doi.org/10.1083/jcb.202203139</a>.","apa":"Zhao, J., Bui, M. T., Ma, J., Künzl, F., Picchianti, L., De La Concepcion, J. C., … Dagdas, Y. (2022). Plant autophagosomes mature into amphisomes prior to their delivery to the central vacuole. <i>Journal of Cell Biology</i>. Rockefeller University Press. <a href=\"https://doi.org/10.1083/jcb.202203139\">https://doi.org/10.1083/jcb.202203139</a>","ieee":"J. Zhao <i>et al.</i>, “Plant autophagosomes mature into amphisomes prior to their delivery to the central vacuole,” <i>Journal of Cell Biology</i>, vol. 221, no. 12. Rockefeller University Press, 2022.","ista":"Zhao J, Bui MT, Ma J, Künzl F, Picchianti L, De La Concepcion JC, Chen Y, Petsangouraki S, Mohseni A, García-Leon M, Gomez MS, Giannini C, Gwennogan D, Kobylinska R, Clavel M, Schellmann S, Jaillais Y, Friml J, Kang B-H, Dagdas Y. 2022. Plant autophagosomes mature into amphisomes prior to their delivery to the central vacuole. Journal of Cell Biology. 221(12), e202203139.","ama":"Zhao J, Bui MT, Ma J, et al. Plant autophagosomes mature into amphisomes prior to their delivery to the central vacuole. <i>Journal of Cell Biology</i>. 2022;221(12). doi:<a href=\"https://doi.org/10.1083/jcb.202203139\">10.1083/jcb.202203139</a>","mla":"Zhao, Jierui, et al. “Plant Autophagosomes Mature into Amphisomes Prior to Their Delivery to the Central Vacuole.” <i>Journal of Cell Biology</i>, vol. 221, no. 12, e202203139, Rockefeller University Press, 2022, doi:<a href=\"https://doi.org/10.1083/jcb.202203139\">10.1083/jcb.202203139</a>.","short":"J. Zhao, M.T. Bui, J. Ma, F. Künzl, L. Picchianti, J.C. De La Concepcion, Y. Chen, S. Petsangouraki, A. Mohseni, M. García-Leon, M.S. Gomez, C. Giannini, D. Gwennogan, R. Kobylinska, M. Clavel, S. Schellmann, Y. Jaillais, J. Friml, B.-H. Kang, Y. Dagdas, Journal of Cell Biology 221 (2022)."},"has_accepted_license":"1","publisher":"Rockefeller University Press","article_processing_charge":"No","type":"journal_article","date_published":"2022-12-01T00:00:00Z","intvolume":"       221","volume":221,"author":[{"last_name":"Zhao","full_name":"Zhao, Jierui","first_name":"Jierui"},{"last_name":"Bui","first_name":"Mai Thu","full_name":"Bui, Mai Thu"},{"last_name":"Ma","full_name":"Ma, Juncai","first_name":"Juncai"},{"full_name":"Künzl, Fabian","first_name":"Fabian","last_name":"Künzl"},{"last_name":"Picchianti","full_name":"Picchianti, Lorenzo","first_name":"Lorenzo"},{"last_name":"De La Concepcion","first_name":"Juan Carlos","full_name":"De La Concepcion, Juan Carlos"},{"last_name":"Chen","first_name":"Yixuan","full_name":"Chen, Yixuan"},{"last_name":"Petsangouraki","full_name":"Petsangouraki, Sofia","first_name":"Sofia"},{"full_name":"Mohseni, Azadeh","first_name":"Azadeh","last_name":"Mohseni"},{"last_name":"García-Leon","first_name":"Marta","full_name":"García-Leon, Marta"},{"last_name":"Gomez","full_name":"Gomez, Marta Salas","first_name":"Marta Salas"},{"full_name":"Giannini, Caterina","first_name":"Caterina","id":"e3fdddd5-f6e0-11ea-865d-ca99ee6367f4","last_name":"Giannini"},{"first_name":"Dubois","full_name":"Gwennogan, Dubois","last_name":"Gwennogan"},{"last_name":"Kobylinska","full_name":"Kobylinska, Roksolana","first_name":"Roksolana"},{"last_name":"Clavel","full_name":"Clavel, Marion","first_name":"Marion"},{"full_name":"Schellmann, Swen","first_name":"Swen","last_name":"Schellmann"},{"full_name":"Jaillais, Yvon","first_name":"Yvon","last_name":"Jaillais"},{"last_name":"Friml","id":"4159519E-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-8302-7596","full_name":"Friml, Jiří","first_name":"Jiří"},{"first_name":"Byung-Ho","full_name":"Kang, Byung-Ho","last_name":"Kang"},{"first_name":"Yasin","full_name":"Dagdas, Yasin","last_name":"Dagdas"}],"_id":"12121","issue":"12","quality_controlled":"1","abstract":[{"text":"Autophagosomes are double-membraned vesicles that traffic harmful or unwanted cellular macromolecules to the vacuole for recycling. Although autophagosome biogenesis has been extensively studied, autophagosome maturation, i.e., delivery and fusion with the vacuole, remains largely unknown in plants. Here, we have identified an autophagy adaptor, CFS1, that directly interacts with the autophagosome marker ATG8 and localizes on both membranes of the autophagosome. Autophagosomes form normally in Arabidopsis thaliana cfs1 mutants, but their delivery to the vacuole is disrupted. CFS1’s function is evolutionarily conserved in plants, as it also localizes to the autophagosomes and plays a role in autophagic flux in the liverwort Marchantia polymorpha. CFS1 regulates autophagic flux by bridging autophagosomes with the multivesicular body-localized ESCRT-I component VPS23A, leading to the formation of amphisomes. Similar to CFS1-ATG8 interaction, disrupting the CFS1-VPS23A interaction blocks autophagic flux and renders plants sensitive to nitrogen starvation. Altogether, our results reveal a conserved vacuolar sorting hub that regulates autophagic flux in plants.","lang":"eng"}],"file_date_updated":"2023-01-23T10:30:11Z","external_id":{"isi":["000932958800001"],"pmid":["36260289"]},"date_created":"2023-01-12T11:57:10Z","publication_status":"published","scopus_import":"1"},{"article_number":"e202107134","article_type":"original","keyword":["Cell Biology"],"oa":1,"language":[{"iso":"eng"}],"publication_identifier":{"issn":["0021-9525"],"eissn":["1540-8140"]},"doi":"10.1083/jcb.202107134","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","publication":"Journal of Cell Biology","day":"05","title":"Multiple centrosomes enhance migration and immune cell effector functions of mature dendritic cells","project":[{"_id":"c08e9ad1-5a5b-11eb-8a69-9d1cf3b07473","name":"Tools for automation and feedback microscopy","grant_number":"CZI01"}],"acknowledgement":"We thank Markéta Dalecká and Irena Krejzová for their support with FIB-SEM imaging, the Imaging Methods Core Facility at BIOCEV supported by the Ministry of Education, Youth and Sports Czech Republic (Large RI Project LM2018129 Czech-BioImaging), and European Regional Development Fund (project No. CZ.02.1.01/0.0/0.0/18_046/0016045) for their support with obtaining imaging data presented in this paper. The authors further thank Andreas Villunger, Florian Gärtner, Frank Bradke, and Sarah Förster for helpful discussions; Andy Zielinski for help with statistics; and Björn Weiershausen for assisting with figure illustration.\r\n\r\nThis work was funded by a fellowship of the Ministry of Innovation, Science and Research of North-Rhine-Westphalia (AZ: 421-8.03.03.02-137069) to E. Kiermaier and the Deutsche Forschungsgemeinschaft (German Research Foundation) under Germany’s Excellence Strategy – EXC 2151 – 390873048. R. Hauschild was funded by grant number 2020-225401 from the Chan Zuckerberg Initiative Donor-Advised Fund, an advised fund of Silicon Valley Community Foundation. M. Hons is supported by Czech Science Foundation GACR 20-24603Y and Charles University PRIMUS/20/MED/013.","year":"2022","department":[{"_id":"Bio"}],"pmid":1,"type":"journal_article","article_processing_charge":"No","citation":{"apa":"Weier, A.-K., Homrich, M., Ebbinghaus, S., Juda, P., Miková, E., Hauschild, R., … Kiermaier, E. (2022). Multiple centrosomes enhance migration and immune cell effector functions of mature dendritic cells. <i>Journal of Cell Biology</i>. Rockefeller University Press. <a href=\"https://doi.org/10.1083/jcb.202107134\">https://doi.org/10.1083/jcb.202107134</a>","ieee":"A.-K. Weier <i>et al.</i>, “Multiple centrosomes enhance migration and immune cell effector functions of mature dendritic cells,” <i>Journal of Cell Biology</i>, vol. 221, no. 12. Rockefeller University Press, 2022.","chicago":"Weier, Ann-Kathrin, Mirka Homrich, Stephanie Ebbinghaus, Pavel Juda, Eliška Miková, Robert Hauschild, Lili Zhang, et al. “Multiple Centrosomes Enhance Migration and Immune Cell Effector Functions of Mature Dendritic Cells.” <i>Journal of Cell Biology</i>. Rockefeller University Press, 2022. <a href=\"https://doi.org/10.1083/jcb.202107134\">https://doi.org/10.1083/jcb.202107134</a>.","mla":"Weier, Ann-Kathrin, et al. “Multiple Centrosomes Enhance Migration and Immune Cell Effector Functions of Mature Dendritic Cells.” <i>Journal of Cell Biology</i>, vol. 221, no. 12, e202107134, Rockefeller University Press, 2022, doi:<a href=\"https://doi.org/10.1083/jcb.202107134\">10.1083/jcb.202107134</a>.","short":"A.-K. Weier, M. Homrich, S. Ebbinghaus, P. Juda, E. Miková, R. Hauschild, L. Zhang, T. Quast, E. Mass, A. Schlitzer, W. Kolanus, S. Burgdorf, O.J. Gruß, M. Hons, S. Wieser, E. Kiermaier, Journal of Cell Biology 221 (2022).","ama":"Weier A-K, Homrich M, Ebbinghaus S, et al. Multiple centrosomes enhance migration and immune cell effector functions of mature dendritic cells. <i>Journal of Cell Biology</i>. 2022;221(12). doi:<a href=\"https://doi.org/10.1083/jcb.202107134\">10.1083/jcb.202107134</a>","ista":"Weier A-K, Homrich M, Ebbinghaus S, Juda P, Miková E, Hauschild R, Zhang L, Quast T, Mass E, Schlitzer A, Kolanus W, Burgdorf S, Gruß OJ, Hons M, Wieser S, Kiermaier E. 2022. Multiple centrosomes enhance migration and immune cell effector functions of mature dendritic cells. Journal of Cell Biology. 221(12), e202107134."},"publisher":"Rockefeller University Press","has_accepted_license":"1","date_updated":"2023-08-16T11:29:12Z","oa_version":"Published Version","ddc":["570"],"isi":1,"month":"12","status":"public","tmp":{"legal_code_url":"https://creativecommons.org/licenses/by-nc-sa/4.0/legalcode","short":"CC BY-NC-SA (4.0)","name":"Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC BY-NC-SA 4.0)","image":"/images/cc_by_nc_sa.png"},"file":[{"relation":"main_file","file_size":11090179,"success":1,"date_updated":"2023-08-16T11:24:53Z","content_type":"application/pdf","file_name":"2023_JCB_Weier.pdf","date_created":"2023-08-16T11:24:53Z","access_level":"open_access","creator":"dernst","checksum":"0c9af38f82af30c6ce528f2caece4246","file_id":"14065"}],"scopus_import":"1","external_id":{"pmid":["36214847 "],"isi":["000932941400001"]},"date_created":"2023-01-12T12:01:09Z","publication_status":"published","abstract":[{"text":"Centrosomes play a crucial role during immune cell interactions and initiation of the immune response. In proliferating cells, centrosome numbers are tightly controlled and generally limited to one in G1 and two prior to mitosis. Defects in regulating centrosome numbers have been associated with cell transformation and tumorigenesis. Here, we report the emergence of extra centrosomes in leukocytes during immune activation. Upon antigen encounter, dendritic cells pass through incomplete mitosis and arrest in the subsequent G1 phase leading to tetraploid cells with accumulated centrosomes. In addition, cell stimulation increases expression of polo-like kinase 2, resulting in diploid cells with two centrosomes in G1-arrested cells. During cell migration, centrosomes tightly cluster and act as functional microtubule-organizing centers allowing for increased persistent locomotion along gradients of chemotactic cues. Moreover, dendritic cells with extra centrosomes display enhanced secretion of inflammatory cytokines and optimized T cell responses. Together, these results demonstrate a previously unappreciated role of extra centrosomes for regular cell and tissue homeostasis.","lang":"eng"}],"file_date_updated":"2023-08-16T11:24:53Z","issue":"12","quality_controlled":"1","_id":"12122","intvolume":"       221","date_published":"2022-12-05T00:00:00Z","volume":221,"author":[{"full_name":"Weier, Ann-Kathrin","first_name":"Ann-Kathrin","last_name":"Weier"},{"last_name":"Homrich","full_name":"Homrich, Mirka","first_name":"Mirka"},{"full_name":"Ebbinghaus, Stephanie","first_name":"Stephanie","last_name":"Ebbinghaus"},{"first_name":"Pavel","full_name":"Juda, Pavel","last_name":"Juda"},{"first_name":"Eliška","full_name":"Miková, Eliška","last_name":"Miková"},{"last_name":"Hauschild","first_name":"Robert","full_name":"Hauschild, Robert","id":"4E01D6B4-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0001-9843-3522"},{"last_name":"Zhang","first_name":"Lili","full_name":"Zhang, Lili"},{"last_name":"Quast","full_name":"Quast, Thomas","first_name":"Thomas"},{"full_name":"Mass, Elvira","first_name":"Elvira","last_name":"Mass"},{"full_name":"Schlitzer, Andreas","first_name":"Andreas","last_name":"Schlitzer"},{"last_name":"Kolanus","full_name":"Kolanus, Waldemar","first_name":"Waldemar"},{"full_name":"Burgdorf, Sven","first_name":"Sven","last_name":"Burgdorf"},{"last_name":"Gruß","first_name":"Oliver J.","full_name":"Gruß, Oliver J."},{"last_name":"Hons","first_name":"Miroslav","full_name":"Hons, Miroslav"},{"last_name":"Wieser","first_name":"Stefan","full_name":"Wieser, Stefan"},{"last_name":"Kiermaier","first_name":"Eva","full_name":"Kiermaier, Eva"}]},{"acknowledgement":"We thank A. Cheung,W. Lukowitz, V.Walbot, D.Weijers, and R. Yadegari for critically reading the manuscript; E. Xiong and G. Zhang for preparing some experiments, T. Schuck, J. Gonnering, and P. Engevold for plant care, the Arabidopsis Biological Resource Center (ABRC) for ARF10,ARF16, ARF17, EMS1,MIR160a BAC clones and cDNAs, the SALK_090804 seed, T. Nakagawa for pGBW vectors, Y. Zhao for the YUC1 cDNA, Q. Chen for the pHEE401E vector, R. Yadegari for pAT5G01860::n1GFP, pAT5G45980:n1GFP, pAT5G50490::n1GFP, pAT5G56200:n1GFP vectors, and D.Weijers for the pGreenII KAN SV40-3×GFP and R2D2 vectors, W. Yang for the splmutant, Y. Qin for the pKNU::KNU-VENUS vector and seed, G. Tang for the STTM160/160-48 vector, and L. Colombo for pPIN1::PIN1-GFP spl and pin1-5 seeds. This work was supported by the US National Science Foundation (NSF)-Israel Binational Science Foundation (BSF) research grant to D.Z. (IOS-1322796) and T.A. (2012756). D.Z. also\r\ngratefully acknowledges supports of the Shaw Scientist Award from the Greater Milwaukee Foundation, USDA National Institute of Food and Agriculture (NIFA, 2022-67013-36294), the UWM Discovery and Innovation Grant, the Bradley Catalyst Award from the UWM Research\r\nFoundation, and WiSys and UW System Applied Research Funding Programs.","department":[{"_id":"JiFr"}],"year":"2022","pmid":1,"title":"Specification of female germline by microRNA orchestrated auxin signaling in Arabidopsis","doi":"10.1038/s41467-022-34723-6","user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","day":"15","publication":"Nature Communications","article_number":"6960","article_type":"original","oa":1,"keyword":["General Physics and Astronomy","General Biochemistry","Genetics and Molecular Biology","General Chemistry","Multidisciplinary"],"language":[{"iso":"eng"}],"publication_identifier":{"issn":["2041-1723"]},"quality_controlled":"1","_id":"12130","volume":13,"author":[{"last_name":"Huang","full_name":"Huang, Jian","first_name":"Jian"},{"full_name":"Zhao, Lei","first_name":"Lei","last_name":"Zhao"},{"first_name":"Shikha","full_name":"Malik, Shikha","last_name":"Malik"},{"last_name":"Gentile","first_name":"Benjamin R.","full_name":"Gentile, Benjamin R."},{"full_name":"Xiong, Va","first_name":"Va","last_name":"Xiong"},{"last_name":"Arazi","first_name":"Tzahi","full_name":"Arazi, Tzahi"},{"full_name":"Owen, Heather A.","first_name":"Heather A.","last_name":"Owen"},{"last_name":"Friml","full_name":"Friml, Jiří","first_name":"Jiří","id":"4159519E-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-8302-7596"},{"last_name":"Zhao","first_name":"Dazhong","full_name":"Zhao, Dazhong"}],"intvolume":"        13","date_published":"2022-11-15T00:00:00Z","scopus_import":"1","publication_status":"published","external_id":{"pmid":["36379956"],"isi":["000884426700001"]},"date_created":"2023-01-12T12:02:41Z","abstract":[{"lang":"eng","text":"Germline determination is essential for species survival and evolution in multicellular organisms. In most flowering plants, formation of the female germline is initiated with specification of one megaspore mother cell (MMC) in each ovule; however, the molecular mechanism underlying this key event remains unclear. Here we report that spatially restricted auxin signaling promotes MMC fate in Arabidopsis. Our results show that the microRNA160 (miR160) targeted gene ARF17 (AUXIN RESPONSE FACTOR17) is required for promoting MMC specification by genetically interacting with the SPL/NZZ (SPOROCYTELESS/NOZZLE) gene. Alterations of auxin signaling cause formation of supernumerary MMCs in an ARF17- and SPL/NZZ-dependent manner. Furthermore, miR160 and ARF17 are indispensable for attaining a normal auxin maximum at the ovule apex via modulating the expression domain of PIN1 (PIN-FORMED1) auxin transporter. Our findings elucidate the mechanism by which auxin signaling promotes the acquisition of female germline cell fate in plants."}],"file_date_updated":"2023-01-23T11:17:33Z","oa_version":"Published Version","date_updated":"2023-08-04T08:52:01Z","month":"11","status":"public","ddc":["580"],"isi":1,"file":[{"file_name":"2022_NatureCommunications_Huang.pdf","date_updated":"2023-01-23T11:17:33Z","content_type":"application/pdf","file_size":3375249,"success":1,"relation":"main_file","file_id":"12346","checksum":"233922a7b9507d9d48591e6799e4526e","creator":"dernst","access_level":"open_access","date_created":"2023-01-23T11:17:33Z"}],"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","article_processing_charge":"No","has_accepted_license":"1","publisher":"Springer Nature","citation":{"short":"J. Huang, L. Zhao, S. Malik, B.R. Gentile, V. Xiong, T. Arazi, H.A. Owen, J. Friml, D. Zhao, Nature Communications 13 (2022).","mla":"Huang, Jian, et al. “Specification of Female Germline by MicroRNA Orchestrated Auxin Signaling in Arabidopsis.” <i>Nature Communications</i>, vol. 13, 6960, Springer Nature, 2022, doi:<a href=\"https://doi.org/10.1038/s41467-022-34723-6\">10.1038/s41467-022-34723-6</a>.","ama":"Huang J, Zhao L, Malik S, et al. Specification of female germline by microRNA orchestrated auxin signaling in Arabidopsis. <i>Nature Communications</i>. 2022;13. doi:<a href=\"https://doi.org/10.1038/s41467-022-34723-6\">10.1038/s41467-022-34723-6</a>","ista":"Huang J, Zhao L, Malik S, Gentile BR, Xiong V, Arazi T, Owen HA, Friml J, Zhao D. 2022. Specification of female germline by microRNA orchestrated auxin signaling in Arabidopsis. Nature Communications. 13, 6960.","apa":"Huang, J., Zhao, L., Malik, S., Gentile, B. R., Xiong, V., Arazi, T., … Zhao, D. (2022). Specification of female germline by microRNA orchestrated auxin signaling in Arabidopsis. <i>Nature Communications</i>. Springer Nature. <a href=\"https://doi.org/10.1038/s41467-022-34723-6\">https://doi.org/10.1038/s41467-022-34723-6</a>","ieee":"J. Huang <i>et al.</i>, “Specification of female germline by microRNA orchestrated auxin signaling in Arabidopsis,” <i>Nature Communications</i>, vol. 13. Springer Nature, 2022.","chicago":"Huang, Jian, Lei Zhao, Shikha Malik, Benjamin R. Gentile, Va Xiong, Tzahi Arazi, Heather A. Owen, Jiří Friml, and Dazhong Zhao. “Specification of Female Germline by MicroRNA Orchestrated Auxin Signaling in Arabidopsis.” <i>Nature Communications</i>. Springer Nature, 2022. <a href=\"https://doi.org/10.1038/s41467-022-34723-6\">https://doi.org/10.1038/s41467-022-34723-6</a>."}},{"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)"},"file":[{"relation":"main_file","file_name":"2022_MolecularCell_Zapletal.pdf","content_type":"application/pdf","date_updated":"2023-01-24T09:29:02Z","file_size":7368534,"success":1,"creator":"dernst","checksum":"999e443b54e4fdaa2542ca5a97619731","access_level":"open_access","date_created":"2023-01-24T09:29:02Z","file_id":"12354"}],"ddc":["570"],"isi":1,"status":"public","month":"11","date_updated":"2023-08-04T08:57:17Z","oa_version":"Published Version","citation":{"short":"D. Zapletal, E. Taborska, J. Pasulka, R. Malik, K. Kubicek, M. Zanova, C. Much, M. Sebesta, V. Buccheri, F. Horvat, I. Jenickova, M. Prochazkova, J. Prochazka, M. Pinkas, J. Novacek, D.F. Joseph, R. Sedlacek, C. Bernecky, D. O’Carroll, R. Stefl, P. Svoboda, Molecular Cell 82 (2022) 4064–4079.e13.","mla":"Zapletal, David, et al. “Structural and Functional Basis of Mammalian MicroRNA Biogenesis by Dicer.” <i>Molecular Cell</i>, vol. 82, no. 21, Elsevier, 2022, p. 4064–4079.e13, doi:<a href=\"https://doi.org/10.1016/j.molcel.2022.10.010\">10.1016/j.molcel.2022.10.010</a>.","ama":"Zapletal D, Taborska E, Pasulka J, et al. Structural and functional basis of mammalian microRNA biogenesis by Dicer. <i>Molecular Cell</i>. 2022;82(21):4064-4079.e13. doi:<a href=\"https://doi.org/10.1016/j.molcel.2022.10.010\">10.1016/j.molcel.2022.10.010</a>","ista":"Zapletal D, Taborska E, Pasulka J, Malik R, Kubicek K, Zanova M, Much C, Sebesta M, Buccheri V, Horvat F, Jenickova I, Prochazkova M, Prochazka J, Pinkas M, Novacek J, Joseph DF, Sedlacek R, Bernecky C, O’Carroll D, Stefl R, Svoboda P. 2022. Structural and functional basis of mammalian microRNA biogenesis by Dicer. Molecular Cell. 82(21), 4064–4079.e13.","apa":"Zapletal, D., Taborska, E., Pasulka, J., Malik, R., Kubicek, K., Zanova, M., … Svoboda, P. (2022). Structural and functional basis of mammalian microRNA biogenesis by Dicer. <i>Molecular Cell</i>. Elsevier. <a href=\"https://doi.org/10.1016/j.molcel.2022.10.010\">https://doi.org/10.1016/j.molcel.2022.10.010</a>","ieee":"D. Zapletal <i>et al.</i>, “Structural and functional basis of mammalian microRNA biogenesis by Dicer,” <i>Molecular Cell</i>, vol. 82, no. 21. Elsevier, p. 4064–4079.e13, 2022.","chicago":"Zapletal, David, Eliska Taborska, Josef Pasulka, Radek Malik, Karel Kubicek, Martina Zanova, Christian Much, et al. “Structural and Functional Basis of Mammalian MicroRNA Biogenesis by Dicer.” <i>Molecular Cell</i>. Elsevier, 2022. <a href=\"https://doi.org/10.1016/j.molcel.2022.10.010\">https://doi.org/10.1016/j.molcel.2022.10.010</a>."},"has_accepted_license":"1","publisher":"Elsevier","article_processing_charge":"No","type":"journal_article","date_published":"2022-11-03T00:00:00Z","intvolume":"        82","volume":82,"author":[{"last_name":"Zapletal","full_name":"Zapletal, David","first_name":"David"},{"last_name":"Taborska","full_name":"Taborska, Eliska","first_name":"Eliska"},{"first_name":"Josef","full_name":"Pasulka, Josef","last_name":"Pasulka"},{"full_name":"Malik, Radek","first_name":"Radek","last_name":"Malik"},{"full_name":"Kubicek, Karel","first_name":"Karel","last_name":"Kubicek"},{"last_name":"Zanova","first_name":"Martina","full_name":"Zanova, Martina"},{"full_name":"Much, Christian","first_name":"Christian","last_name":"Much"},{"first_name":"Marek","full_name":"Sebesta, Marek","last_name":"Sebesta"},{"full_name":"Buccheri, Valeria","first_name":"Valeria","last_name":"Buccheri"},{"full_name":"Horvat, Filip","first_name":"Filip","last_name":"Horvat"},{"last_name":"Jenickova","full_name":"Jenickova, Irena","first_name":"Irena"},{"first_name":"Michaela","full_name":"Prochazkova, Michaela","last_name":"Prochazkova"},{"last_name":"Prochazka","full_name":"Prochazka, Jan","first_name":"Jan"},{"first_name":"Matyas","full_name":"Pinkas, Matyas","last_name":"Pinkas"},{"full_name":"Novacek, Jiri","first_name":"Jiri","last_name":"Novacek"},{"full_name":"Joseph, Diego F.","first_name":"Diego F.","last_name":"Joseph"},{"last_name":"Sedlacek","first_name":"Radislav","full_name":"Sedlacek, Radislav"},{"last_name":"Bernecky","full_name":"Bernecky, Carrie A","first_name":"Carrie A","id":"2CB9DFE2-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0003-0893-7036"},{"full_name":"O’Carroll, Dónal","first_name":"Dónal","last_name":"O’Carroll"},{"last_name":"Stefl","first_name":"Richard","full_name":"Stefl, Richard"},{"full_name":"Svoboda, Petr","first_name":"Petr","last_name":"Svoboda"}],"page":"4064-4079.e13","_id":"12143","quality_controlled":"1","issue":"21","file_date_updated":"2023-01-24T09:29:02Z","abstract":[{"lang":"eng","text":"MicroRNA (miRNA) and RNA interference (RNAi) pathways rely on small RNAs produced by Dicer endonucleases. Mammalian Dicer primarily supports the essential gene-regulating miRNA pathway, but how it is specifically adapted to miRNA biogenesis is unknown. We show that the adaptation entails a unique structural role of Dicer’s DExD/H helicase domain. Although mice tolerate loss of its putative ATPase function, the complete absence of the domain is lethal because it assures high-fidelity miRNA biogenesis. Structures of murine Dicer⋅miRNA precursor complexes revealed that the DExD/H domain has a helicase-unrelated structural function. It locks Dicer in a closed state, which facilitates miRNA precursor selection. Transition to a cleavage-competent open state is stimulated by Dicer-binding protein TARBP2. Absence of the DExD/H domain or its mutations unlocks the closed state, reduces substrate selectivity, and activates RNAi. Thus, the DExD/H domain structurally contributes to mammalian miRNA biogenesis and underlies mechanistical partitioning of miRNA and RNAi pathways."}],"external_id":{"pmid":["36332606"],"isi":["000898565300011"]},"publication_status":"published","date_created":"2023-01-12T12:05:36Z","scopus_import":"1","publication":"Molecular Cell","day":"03","user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","doi":"10.1016/j.molcel.2022.10.010","language":[{"iso":"eng"}],"publication_identifier":{"issn":["1097-2765"]},"oa":1,"keyword":["Cell Biology","Molecular Biology"],"article_type":"original","acknowledged_ssus":[{"_id":"EM-Fac"}],"pmid":1,"year":"2022","department":[{"_id":"CaBe"}],"acknowledgement":"We thank Kristian Vlahovicek (University of Zagreb) for support of bioinformatics analyses and Vladimir Benes (EMBL Sequencing Facility) and Genomics and Bioinformatics Core Facility at the Institute of Molecular Genetics for help with RNA sequencing. The main funding was provided by the Czech Science Foundation (EXPRO grant 20-03950X to P.S. and 22-19896S to R. Stefl). Early stages of the work were supported by European Research Council grants under the European Union’s Horizon 2020 Research and Innovation Programme (grants 647403 to P.S. and 649030 to R. Stefl). V.B., D.F.J., and F.H. were in part supported by PhD student fellowships from the Charles University; this work will be in part fulfilling requirements for a PhD degree as “school work.” Funding of D.Z. included the OP RDE project “Internal Grant Agency of Masaryk University” no. CZ.02.2.69/0.0/0.0/19_073/0016943. The Ministry of Education, Youth, and Sports of the Czech Republic (MEYS CR) provided institutional support for CEITEC 2020 project LQ1601. For technical support, we acknowledge EMBL Monterotondo’s genome engineering and transgenic core facilities, the Czech Centre for Phenogenomics at the Institute of Molecular Genetics (supported by RVO 68378050 from the Czech Academy of Sciences and LM2018126 and CZ.02.1.01/0.0/0.0/18_046/0015861 CCP Infrastructure Upgrade II from MEYS CR), the Cryo-EM and Proteomics Core Facilities (CEITEC, Masaryk University) supported by the CIISB research infrastructure (LM2018127 from MEYS CR), and support from the Scientific Service Units of ISTA through resources from the Electron Microscopy Facility. Computational resources included e-Infrastruktura CZ (LM2018140) and ELIXIR-CZ (LM2018131) projects by MEYS CR and the Croatian National Centres of Research Excellence in Personalized Healthcare (#KK.01.1.1.01.0010) and Data Science and Advanced Cooperative Systems (#KK.01.1.1.01.0009) projects funded by the European Structural and Investment Funds grants.","title":"Structural and functional basis of mammalian microRNA biogenesis by Dicer"},{"doi":"10.1038/s41467-021-23073-4","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","publication":"Nature Communications","day":"17","article_number":"2868","article_type":"original","keyword":["General Physics and Astronomy","General Biochemistry","Genetics and Molecular Biology","General Chemistry","Multidisciplinary"],"oa":1,"language":[{"iso":"eng"}],"publication_identifier":{"issn":["2041-1723"]},"year":"2021","extern":"1","main_file_link":[{"url":"https://doi.org/10.1038/s41467-021-23073-4","open_access":"1"}],"title":"Health and sustainability of glaciers in High Mountain Asia","date_updated":"2023-02-28T13:21:51Z","oa_version":"Published Version","status":"public","month":"05","type":"journal_article","article_processing_charge":"No","citation":{"ieee":"E. Miles, M. McCarthy, A. Dehecq, M. Kneib, S. Fugger, and F. Pellicciotti, “Health and sustainability of glaciers in High Mountain Asia,” <i>Nature Communications</i>, vol. 12. Springer Nature, 2021.","apa":"Miles, E., McCarthy, M., Dehecq, A., Kneib, M., Fugger, S., &#38; Pellicciotti, F. (2021). Health and sustainability of glaciers in High Mountain Asia. <i>Nature Communications</i>. Springer Nature. <a href=\"https://doi.org/10.1038/s41467-021-23073-4\">https://doi.org/10.1038/s41467-021-23073-4</a>","chicago":"Miles, Evan, Michael McCarthy, Amaury Dehecq, Marin Kneib, Stefan Fugger, and Francesca Pellicciotti. “Health and Sustainability of Glaciers in High Mountain Asia.” <i>Nature Communications</i>. Springer Nature, 2021. <a href=\"https://doi.org/10.1038/s41467-021-23073-4\">https://doi.org/10.1038/s41467-021-23073-4</a>.","short":"E. Miles, M. McCarthy, A. Dehecq, M. Kneib, S. Fugger, F. Pellicciotti, Nature Communications 12 (2021).","mla":"Miles, Evan, et al. “Health and Sustainability of Glaciers in High Mountain Asia.” <i>Nature Communications</i>, vol. 12, 2868, Springer Nature, 2021, doi:<a href=\"https://doi.org/10.1038/s41467-021-23073-4\">10.1038/s41467-021-23073-4</a>.","ama":"Miles E, McCarthy M, Dehecq A, Kneib M, Fugger S, Pellicciotti F. Health and sustainability of glaciers in High Mountain Asia. <i>Nature Communications</i>. 2021;12. doi:<a href=\"https://doi.org/10.1038/s41467-021-23073-4\">10.1038/s41467-021-23073-4</a>","ista":"Miles E, McCarthy M, Dehecq A, Kneib M, Fugger S, Pellicciotti F. 2021. Health and sustainability of glaciers in High Mountain Asia. Nature Communications. 12, 2868."},"publisher":"Springer Nature","quality_controlled":"1","_id":"12585","intvolume":"        12","date_published":"2021-05-17T00:00:00Z","author":[{"last_name":"Miles","first_name":"Evan","full_name":"Miles, Evan"},{"last_name":"McCarthy","full_name":"McCarthy, Michael","first_name":"Michael"},{"last_name":"Dehecq","first_name":"Amaury","full_name":"Dehecq, Amaury"},{"last_name":"Kneib","full_name":"Kneib, Marin","first_name":"Marin"},{"last_name":"Fugger","full_name":"Fugger, Stefan","first_name":"Stefan"},{"first_name":"Francesca","full_name":"Pellicciotti, Francesca","id":"b28f055a-81ea-11ed-b70c-a9fe7f7b0e70","last_name":"Pellicciotti"}],"volume":12,"scopus_import":"1","publication_status":"published","date_created":"2023-02-20T08:11:29Z","abstract":[{"lang":"eng","text":"Glaciers in High Mountain Asia generate meltwater that supports the water needs of 250 million people, but current knowledge of annual accumulation and ablation is limited to sparse field measurements biased in location and glacier size. Here, we present altitudinally-resolved specific mass balances (surface, internal, and basal combined) for 5527 glaciers in High Mountain Asia for 2000–2016, derived by correcting observed glacier thinning patterns for mass redistribution due to ice flow. We find that 41% of glaciers accumulated mass over less than 20% of their area, and only 60% ± 10% of regional annual ablation was compensated by accumulation. Even without 21st century warming, 21% ± 1% of ice volume will be lost by 2100 due to current climatic-geometric imbalance, representing a reduction in glacier ablation into rivers of 28% ± 1%. The ablation of glaciers in the Himalayas and Tien Shan was mostly unsustainable and ice volume in these regions will reduce by at least 30% by 2100. The most important and vulnerable glacier-fed river basins (Amu Darya, Indus, Syr Darya, Tarim Interior) were supplied with >50% sustainable glacier ablation but will see long-term reductions in ice mass and glacier meltwater supply regardless of the Karakoram Anomaly."}]},{"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.","project":[{"grant_number":"742573","_id":"260F1432-B435-11E9-9278-68D0E5697425","name":"Interaction and feedback between cell mechanics and fate specification in vertebrate gastrulation","call_identifier":"H2020"},{"name":"Mesendoderm specification in zebrafish: The role of extraembryonic tissues","_id":"26B1E39C-B435-11E9-9278-68D0E5697425","grant_number":"25239"}],"department":[{"_id":"CaHe"}],"year":"2021","title":"Reassembling gastrulation","doi":"10.1016/j.ydbio.2020.12.014","user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","day":"01","publication":"Developmental Biology","article_type":"original","ec_funded":1,"keyword":["Developmental Biology","Cell Biology","Molecular Biology"],"oa":1,"language":[{"iso":"eng"}],"publication_identifier":{"issn":["0012-1606"]},"quality_controlled":"1","_id":"8966","page":"71-81","volume":474,"author":[{"last_name":"Schauer","first_name":"Alexandra","full_name":"Schauer, Alexandra","orcid":"0000-0001-7659-9142","id":"30A536BA-F248-11E8-B48F-1D18A9856A87"},{"last_name":"Heisenberg","orcid":"0000-0002-0912-4566","full_name":"Heisenberg, Carl-Philipp J","id":"39427864-F248-11E8-B48F-1D18A9856A87","first_name":"Carl-Philipp J"}],"date_published":"2021-06-01T00:00:00Z","intvolume":"       474","scopus_import":"1","date_created":"2020-12-22T09:53:34Z","external_id":{"isi":["000639461800008"]},"publication_status":"published","abstract":[{"lang":"eng","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."}],"file_date_updated":"2021-08-11T10:28:06Z","oa_version":"Published Version","date_updated":"2023-08-07T13:30:01Z","status":"public","month":"06","ddc":["570"],"isi":1,"file":[{"relation":"main_file","file_size":1440321,"success":1,"date_updated":"2021-08-11T10:28:06Z","content_type":"application/pdf","file_name":"2021_DevBiology_Schauer.pdf","date_created":"2021-08-11T10:28:06Z","access_level":"open_access","checksum":"fa2a5731fd16ab171b029f32f031c440","creator":"kschuh","file_id":"9880"}],"related_material":{"record":[{"status":"public","id":"12891","relation":"dissertation_contains"}]},"tmp":{"image":"/images/cc_by_nc_nd.png","name":"Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0)","short":"CC BY-NC-ND (4.0)","legal_code_url":"https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode"},"type":"journal_article","article_processing_charge":"Yes (via OA deal)","publisher":"Elsevier","has_accepted_license":"1","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>","ista":"Schauer A, Heisenberg C-PJ. 2021. Reassembling gastrulation. Developmental Biology. 474, 71–81.","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>","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>."}},{"article_number":"e1008529","article_type":"original","oa":1,"keyword":["Modelling and Simulation","Genetics","Molecular Biology","Antibiotics","Drug interactions"],"publication_identifier":{"issn":["1553-7358"]},"language":[{"iso":"eng"}],"doi":"10.1371/journal.pcbi.1008529","user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","publication":"PLOS Computational Biology","day":"07","title":"Minimal biophysical model of combined antibiotic action","project":[{"call_identifier":"FWF","_id":"25E9AF9E-B435-11E9-9278-68D0E5697425","name":"Revealing the mechanisms underlying drug interactions","grant_number":"P27201-B22"},{"call_identifier":"FWF","grant_number":"P28844-B27","name":"Biophysics of information processing in gene regulation","_id":"254E9036-B435-11E9-9278-68D0E5697425"}],"acknowledgement":"This work was supported in part by Tum stipend of Knafelj foundation (to B.K.), Austrian Science Fund (FWF) standalone grants P 27201-B22 (to T.B.) and P 28844(to G.T.), HFSP program Grant RGP0042/2013 (to T.B.), German Research Foundation (DFG) individual grant BO 3502/2-1 (to T.B.), and German Research Foundation (DFG) Collaborative Research Centre (SFB) 1310 (to T.B.). ","year":"2021","department":[{"_id":"GaTk"}],"type":"journal_article","article_processing_charge":"Yes","citation":{"ama":"Kavcic B, Tkačik G, Bollenbach MT. Minimal biophysical model of combined antibiotic action. <i>PLOS Computational Biology</i>. 2021;17. doi:<a href=\"https://doi.org/10.1371/journal.pcbi.1008529\">10.1371/journal.pcbi.1008529</a>","ista":"Kavcic B, Tkačik G, Bollenbach MT. 2021. Minimal biophysical model of combined antibiotic action. PLOS Computational Biology. 17, e1008529.","mla":"Kavcic, Bor, et al. “Minimal Biophysical Model of Combined Antibiotic Action.” <i>PLOS Computational Biology</i>, vol. 17, e1008529, Public Library of Science, 2021, doi:<a href=\"https://doi.org/10.1371/journal.pcbi.1008529\">10.1371/journal.pcbi.1008529</a>.","short":"B. Kavcic, G. Tkačik, M.T. Bollenbach, PLOS Computational Biology 17 (2021).","chicago":"Kavcic, Bor, Gašper Tkačik, and Mark Tobias Bollenbach. “Minimal Biophysical Model of Combined Antibiotic Action.” <i>PLOS Computational Biology</i>. Public Library of Science, 2021. <a href=\"https://doi.org/10.1371/journal.pcbi.1008529\">https://doi.org/10.1371/journal.pcbi.1008529</a>.","apa":"Kavcic, B., Tkačik, G., &#38; Bollenbach, M. T. (2021). Minimal biophysical model of combined antibiotic action. <i>PLOS Computational Biology</i>. Public Library of Science. <a href=\"https://doi.org/10.1371/journal.pcbi.1008529\">https://doi.org/10.1371/journal.pcbi.1008529</a>","ieee":"B. Kavcic, G. Tkačik, and M. T. Bollenbach, “Minimal biophysical model of combined antibiotic action,” <i>PLOS Computational Biology</i>, vol. 17. Public Library of Science, 2021."},"publisher":"Public Library of Science","has_accepted_license":"1","date_updated":"2024-02-21T12:41:41Z","oa_version":"Published Version","isi":1,"ddc":["570"],"status":"public","month":"01","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)"},"related_material":{"record":[{"id":"7673","relation":"earlier_version","status":"public"},{"relation":"research_data","id":"8930","status":"public"}]},"file":[{"relation":"main_file","file_name":"2021_PlosComBio_Kavcic.pdf","date_updated":"2021-02-04T12:30:48Z","content_type":"application/pdf","file_size":3690053,"success":1,"checksum":"e29f2b42651bef8e034781de8781ffac","creator":"dernst","access_level":"open_access","date_created":"2021-02-04T12:30:48Z","file_id":"9092"}],"publication_status":"published","external_id":{"isi":["000608045000010"]},"date_created":"2021-01-08T07:16:18Z","file_date_updated":"2021-02-04T12:30:48Z","abstract":[{"text":"Phenomenological relations such as Ohm’s or Fourier’s law have a venerable history in physics but are still scarce in biology. This situation restrains predictive theory. Here, we build on bacterial “growth laws,” which capture physiological feedback between translation and cell growth, to construct a minimal biophysical model for the combined action of ribosome-targeting antibiotics. Our model predicts drug interactions like antagonism or synergy solely from responses to individual drugs. We provide analytical results for limiting cases, which agree well with numerical results. We systematically refine the model by including direct physical interactions of different antibiotics on the ribosome. In a limiting case, our model provides a mechanistic underpinning for recent predictions of higher-order interactions that were derived using entropy maximization. We further refine the model to include the effects of antibiotics that mimic starvation and the presence of resistance genes. We describe the impact of a starvation-mimicking antibiotic on drug interactions analytically and verify it experimentally. Our extended model suggests a change in the type of drug interaction that depends on the strength of resistance, which challenges established rescaling paradigms. We experimentally show that the presence of unregulated resistance genes can lead to altered drug interaction, which agrees with the prediction of the model. While minimal, the model is readily adaptable and opens the door to predicting interactions of second and higher-order in a broad range of biological systems.","lang":"eng"}],"quality_controlled":"1","_id":"8997","intvolume":"        17","date_published":"2021-01-07T00:00:00Z","author":[{"orcid":"0000-0001-6041-254X","id":"350F91D2-F248-11E8-B48F-1D18A9856A87","full_name":"Kavcic, Bor","first_name":"Bor","last_name":"Kavcic"},{"last_name":"Tkačik","first_name":"Gašper","id":"3D494DCA-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-6699-1455","full_name":"Tkačik, Gašper"},{"first_name":"Tobias","full_name":"Bollenbach, Tobias","id":"3E6DB97A-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0003-4398-476X","last_name":"Bollenbach"}],"volume":17},{"day":"01","publication":"Neurochemistry International","user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","doi":"10.1016/j.neuint.2021.104986","language":[{"iso":"eng"}],"publication_identifier":{"issn":["0197-0186"]},"keyword":["Cell Biology","Cellular and Molecular Neuroscience"],"oa":1,"ec_funded":1,"article_type":"original","article_number":"104986","pmid":1,"department":[{"_id":"SiHi"}],"year":"2021","acknowledgement":"We thank Melissa Stouffer for critically reading the manuscript. This work was supported by IST Austria institutional funds; NÖ Forschung und Bildung n[f + b] life science call grant (C13-002) to S.H. and the European Research Council (ERC) under the European Union's Horizon 2020 research and innovation program (grant agreement 725780 LinPro) to S.H.","project":[{"name":"Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development","_id":"260018B0-B435-11E9-9278-68D0E5697425","grant_number":"725780","call_identifier":"H2020"},{"_id":"25D92700-B435-11E9-9278-68D0E5697425","name":"Mapping Cell-Type Specificity of the Genomic Imprintome in the Brain","grant_number":"LS13-002"}],"title":"Inducible uniparental chromosome disomy to probe genomic imprinting at single-cell level in brain and beyond","file":[{"access_level":"open_access","date_created":"2021-08-11T12:30:38Z","creator":"kschuh","checksum":"c6d7a40089cd29e289f9b22e75768304","file_id":"9883","relation":"main_file","date_updated":"2021-08-11T12:30:38Z","content_type":"application/pdf","file_size":7083499,"success":1,"file_name":"2021_NCI_Pauler.pdf"}],"tmp":{"image":"/images/cc_by_nc_nd.png","name":"Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0)","short":"CC BY-NC-ND (4.0)","legal_code_url":"https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode"},"month":"05","status":"public","isi":1,"ddc":["570"],"oa_version":"Published Version","date_updated":"2023-08-07T13:48:26Z","publisher":"Elsevier","has_accepted_license":"1","citation":{"short":"F. Pauler, Q. Hudson, S. Laukoter, S. Hippenmeyer, Neurochemistry International 145 (2021).","mla":"Pauler, Florian, et al. “Inducible Uniparental Chromosome Disomy to Probe Genomic Imprinting at Single-Cell Level in Brain and Beyond.” <i>Neurochemistry International</i>, vol. 145, no. 5, 104986, Elsevier, 2021, doi:<a href=\"https://doi.org/10.1016/j.neuint.2021.104986\">10.1016/j.neuint.2021.104986</a>.","ama":"Pauler F, Hudson Q, Laukoter S, Hippenmeyer S. Inducible uniparental chromosome disomy to probe genomic imprinting at single-cell level in brain and beyond. <i>Neurochemistry International</i>. 2021;145(5). doi:<a href=\"https://doi.org/10.1016/j.neuint.2021.104986\">10.1016/j.neuint.2021.104986</a>","ista":"Pauler F, Hudson Q, Laukoter S, Hippenmeyer S. 2021. Inducible uniparental chromosome disomy to probe genomic imprinting at single-cell level in brain and beyond. Neurochemistry International. 145(5), 104986.","ieee":"F. Pauler, Q. Hudson, S. Laukoter, and S. Hippenmeyer, “Inducible uniparental chromosome disomy to probe genomic imprinting at single-cell level in brain and beyond,” <i>Neurochemistry International</i>, vol. 145, no. 5. Elsevier, 2021.","apa":"Pauler, F., Hudson, Q., Laukoter, S., &#38; Hippenmeyer, S. (2021). Inducible uniparental chromosome disomy to probe genomic imprinting at single-cell level in brain and beyond. <i>Neurochemistry International</i>. Elsevier. <a href=\"https://doi.org/10.1016/j.neuint.2021.104986\">https://doi.org/10.1016/j.neuint.2021.104986</a>","chicago":"Pauler, Florian, Quanah Hudson, Susanne Laukoter, and Simon Hippenmeyer. “Inducible Uniparental Chromosome Disomy to Probe Genomic Imprinting at Single-Cell Level in Brain and Beyond.” <i>Neurochemistry International</i>. Elsevier, 2021. <a href=\"https://doi.org/10.1016/j.neuint.2021.104986\">https://doi.org/10.1016/j.neuint.2021.104986</a>."},"article_processing_charge":"Yes (via OA deal)","type":"journal_article","volume":145,"author":[{"full_name":"Pauler, Florian","id":"48EA0138-F248-11E8-B48F-1D18A9856A87","first_name":"Florian","last_name":"Pauler"},{"first_name":"Quanah","full_name":"Hudson, Quanah","last_name":"Hudson"},{"first_name":"Susanne","id":"2D6B7A9A-F248-11E8-B48F-1D18A9856A87","full_name":"Laukoter, Susanne","last_name":"Laukoter"},{"orcid":"0000-0003-2279-1061","full_name":"Hippenmeyer, Simon","first_name":"Simon","id":"37B36620-F248-11E8-B48F-1D18A9856A87","last_name":"Hippenmeyer"}],"date_published":"2021-05-01T00:00:00Z","intvolume":"       145","_id":"9188","quality_controlled":"1","issue":"5","file_date_updated":"2021-08-11T12:30:38Z","abstract":[{"text":"Genomic imprinting is an epigenetic mechanism that results in parental allele-specific expression of ~1% of all genes in mouse and human. Imprinted genes are key developmental regulators and play pivotal roles in many biological processes such as nutrient transfer from the mother to offspring and neuronal development. Imprinted genes are also involved in human disease, including neurodevelopmental disorders, and often occur in clusters that are regulated by a common imprint control region (ICR). In extra-embryonic tissues ICRs can act over large distances, with the largest surrounding Igf2r spanning over 10 million base-pairs. Besides classical imprinted expression that shows near exclusive maternal or paternal expression, widespread biased imprinted expression has been identified mainly in brain. In this review we discuss recent developments mapping cell type specific imprinted expression in extra-embryonic tissues and neocortex in the mouse. We highlight the advantages of using an inducible uniparental chromosome disomy (UPD) system to generate cells carrying either two maternal or two paternal copies of a specific chromosome to analyze the functional consequences of genomic imprinting. Mosaic Analysis with Double Markers (MADM) allows fluorescent labeling and concomitant induction of UPD sparsely in specific cell types, and thus to over-express or suppress all imprinted genes on that chromosome. To illustrate the utility of this technique, we explain how MADM-induced UPD revealed new insights about the function of the well-studied Cdkn1c imprinted gene, and how MADM-induced UPDs led to identification of highly cell type specific phenotypes related to perturbed imprinted expression in the mouse neocortex. Finally, we give an outlook on how MADM could be used to probe cell type specific imprinted expression in other tissues in mouse, particularly in extra-embryonic tissues.","lang":"eng"}],"publication_status":"published","date_created":"2021-02-23T12:31:43Z","external_id":{"isi":["000635575000005"],"pmid":["33600873"]},"scopus_import":"1"},{"article_processing_charge":"Yes","citation":{"apa":"Nagy-Staron, A. A., Tomasek, K., Caruso Carter, C., Sonnleitner, E., Kavcic, B., Paixão, T., &#38; Guet, C. C. (2021). Local genetic context shapes the function of a gene regulatory network. <i>ELife</i>. eLife Sciences Publications. <a href=\"https://doi.org/10.7554/elife.65993\">https://doi.org/10.7554/elife.65993</a>","ieee":"A. A. Nagy-Staron <i>et al.</i>, “Local genetic context shapes the function of a gene regulatory network,” <i>eLife</i>, vol. 10. eLife Sciences Publications, 2021.","chicago":"Nagy-Staron, Anna A, Kathrin Tomasek, Caroline Caruso Carter, Elisabeth Sonnleitner, Bor Kavcic, Tiago Paixão, and Calin C Guet. “Local Genetic Context Shapes the Function of a Gene Regulatory Network.” <i>ELife</i>. eLife Sciences Publications, 2021. <a href=\"https://doi.org/10.7554/elife.65993\">https://doi.org/10.7554/elife.65993</a>.","mla":"Nagy-Staron, Anna A., et al. “Local Genetic Context Shapes the Function of a Gene Regulatory Network.” <i>ELife</i>, vol. 10, e65993, eLife Sciences Publications, 2021, doi:<a href=\"https://doi.org/10.7554/elife.65993\">10.7554/elife.65993</a>.","short":"A.A. Nagy-Staron, K. Tomasek, C. Caruso Carter, E. Sonnleitner, B. Kavcic, T. Paixão, C.C. Guet, ELife 10 (2021).","ama":"Nagy-Staron AA, Tomasek K, Caruso Carter C, et al. Local genetic context shapes the function of a gene regulatory network. <i>eLife</i>. 2021;10. doi:<a href=\"https://doi.org/10.7554/elife.65993\">10.7554/elife.65993</a>","ista":"Nagy-Staron AA, Tomasek K, Caruso Carter C, Sonnleitner E, Kavcic B, Paixão T, Guet CC. 2021. Local genetic context shapes the function of a gene regulatory network. eLife. 10, e65993."},"has_accepted_license":"1","publisher":"eLife Sciences Publications","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)"},"related_material":{"record":[{"id":"8951","relation":"research_data","status":"public"}]},"file":[{"checksum":"3c2f44058c2dd45a5a1027f09d263f8e","creator":"bkavcic","date_created":"2021-03-23T10:12:58Z","access_level":"open_access","file_id":"9284","relation":"main_file","file_name":"elife-65993-v2.pdf","file_size":1390469,"success":1,"date_updated":"2021-03-23T10:12:58Z","content_type":"application/pdf"}],"date_updated":"2024-02-21T12:41:57Z","oa_version":"Published Version","isi":1,"ddc":["570"],"month":"03","status":"public","publication_status":"published","date_created":"2021-03-23T10:11:46Z","external_id":{"isi":["000631050900001"]},"file_date_updated":"2021-03-23T10:12:58Z","abstract":[{"lang":"eng","text":"Gene expression levels are influenced by multiple coexisting molecular mechanisms. Some of these interactions such as those of transcription factors and promoters have been studied extensively. However, predicting phenotypes of gene regulatory networks (GRNs) remains a major challenge. Here, we use a well-defined synthetic GRN to study in Escherichia coli how network phenotypes depend on local genetic context, i.e. the genetic neighborhood of a transcription factor and its relative position. We show that one GRN with fixed topology can display not only quantitatively but also qualitatively different phenotypes, depending solely on the local genetic context of its components. Transcriptional read-through is the main molecular mechanism that places one transcriptional unit (TU) within two separate regulons without the need for complex regulatory sequences. We propose that relative order of individual TUs, with its potential for combinatorial complexity, plays an important role in shaping phenotypes of GRNs."}],"intvolume":"        10","date_published":"2021-03-08T00:00:00Z","author":[{"orcid":"0000-0002-1391-8377","full_name":"Nagy-Staron, Anna A","id":"3ABC5BA6-F248-11E8-B48F-1D18A9856A87","first_name":"Anna A","last_name":"Nagy-Staron"},{"last_name":"Tomasek","orcid":"0000-0003-3768-877X","id":"3AEC8556-F248-11E8-B48F-1D18A9856A87","first_name":"Kathrin","full_name":"Tomasek, Kathrin"},{"last_name":"Caruso Carter","first_name":"Caroline","full_name":"Caruso Carter, Caroline"},{"full_name":"Sonnleitner, Elisabeth","first_name":"Elisabeth","last_name":"Sonnleitner"},{"id":"350F91D2-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0001-6041-254X","full_name":"Kavcic, Bor","first_name":"Bor","last_name":"Kavcic"},{"full_name":"Paixão, Tiago","first_name":"Tiago","last_name":"Paixão"},{"last_name":"Guet","orcid":"0000-0001-6220-2052","first_name":"Calin C","full_name":"Guet, Calin C","id":"47F8433E-F248-11E8-B48F-1D18A9856A87"}],"volume":10,"quality_controlled":"1","_id":"9283","keyword":["Genetics and Molecular Biology"],"oa":1,"publication_identifier":{"issn":["2050-084X"]},"language":[{"iso":"eng"}],"article_number":"e65993","ec_funded":1,"article_type":"original","publication":"eLife","day":"08","doi":"10.7554/elife.65993","user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","title":"Local genetic context shapes the function of a gene regulatory network","project":[{"call_identifier":"FP7","_id":"2517526A-B435-11E9-9278-68D0E5697425","name":"The Systems Biology of Transcriptional Read-Through in Bacteria: from Synthetic Networks to Genomic Studies","grant_number":"628377"},{"call_identifier":"FWF","_id":"268BFA92-B435-11E9-9278-68D0E5697425","name":"CyberCircuits: Cybergenetic circuits to test composability of gene networks","grant_number":"I03901"}],"acknowledgement":"We thank J Bollback, L Hurst, M Lagator, C Nizak, O Rivoire, M Savageau, G Tkacik, and B Vicozo\r\nfor helpful discussions; A Dolinar and A Greshnova for technical assistance; T Bollenbach for supplying the strain JW0336; C Rusnac, and members of the Guet lab for comments. The research leading to these results has received funding from the People Programme (Marie Curie Actions) of the European Union’s Seventh Framework Programme (FP7/2007-2013) under REA grant agreement n˚\r\n628377 (ANS) and an Austrian Science Fund (FWF) grant n˚ I 3901-B32 (CCG).","year":"2021","department":[{"_id":"GaTk"},{"_id":"CaGu"}]},{"abstract":[{"text":"We report the complete analysis of a deterministic model of deleterious mutations and negative selection against them at two haploid loci without recombination. As long as mutation is a weaker force than selection, mutant alleles remain rare at the only stable equilibrium, and otherwise, a variety of dynamics are possible. If the mutation-free genotype is absent, generally the only stable equilibrium is the one that corresponds to fixation of the mutant allele at the locus where it is less deleterious. This result suggests that fixation of a deleterious allele that follows a click of the Muller’s ratchet is governed by natural selection, instead of random drift.","lang":"eng"}],"external_id":{"isi":["000659161500002"]},"date_created":"2021-05-12T05:58:42Z","publication_status":"published","volume":524,"author":[{"full_name":"Khudiakova, Kseniia","id":"4E6DC800-AE37-11E9-AC72-31CAE5697425","orcid":"0000-0002-6246-1465","first_name":"Kseniia","last_name":"Khudiakova"},{"full_name":"Neretina, Tatiana Yu.","first_name":"Tatiana Yu.","last_name":"Neretina"},{"first_name":"Alexey S.","full_name":"Kondrashov, Alexey S.","last_name":"Kondrashov"}],"date_published":"2021-04-24T00:00:00Z","intvolume":"       524","_id":"9387","quality_controlled":"1","publisher":"Elsevier ","citation":{"ama":"Khudiakova K, Neretina TY, Kondrashov AS. Two linked loci under mutation-selection balance and Muller’s ratchet. <i>Journal of Theoretical Biology</i>. 2021;524. doi:<a href=\"https://doi.org/10.1016/j.jtbi.2021.110729\">10.1016/j.jtbi.2021.110729</a>","ista":"Khudiakova K, Neretina TY, Kondrashov AS. 2021. Two linked loci under mutation-selection balance and Muller’s ratchet. Journal of Theoretical Biology. 524, 110729.","mla":"Khudiakova, Kseniia, et al. “Two Linked Loci under Mutation-Selection Balance and Muller’s Ratchet.” <i>Journal of Theoretical Biology</i>, vol. 524, 110729, Elsevier , 2021, doi:<a href=\"https://doi.org/10.1016/j.jtbi.2021.110729\">10.1016/j.jtbi.2021.110729</a>.","short":"K. Khudiakova, T.Y. Neretina, A.S. Kondrashov, Journal of Theoretical Biology 524 (2021).","chicago":"Khudiakova, Kseniia, Tatiana Yu. Neretina, and Alexey S. Kondrashov. “Two Linked Loci under Mutation-Selection Balance and Muller’s Ratchet.” <i>Journal of Theoretical Biology</i>. Elsevier , 2021. <a href=\"https://doi.org/10.1016/j.jtbi.2021.110729\">https://doi.org/10.1016/j.jtbi.2021.110729</a>.","ieee":"K. Khudiakova, T. Y. Neretina, and A. S. Kondrashov, “Two linked loci under mutation-selection balance and Muller’s ratchet,” <i>Journal of Theoretical Biology</i>, vol. 524. Elsevier , 2021.","apa":"Khudiakova, K., Neretina, T. Y., &#38; Kondrashov, A. S. (2021). Two linked loci under mutation-selection balance and Muller’s ratchet. <i>Journal of Theoretical Biology</i>. Elsevier . <a href=\"https://doi.org/10.1016/j.jtbi.2021.110729\">https://doi.org/10.1016/j.jtbi.2021.110729</a>"},"article_processing_charge":"No","type":"journal_article","status":"public","month":"04","isi":1,"oa_version":"Preprint","date_updated":"2023-08-08T13:32:40Z","title":"Two linked loci under mutation-selection balance and Muller’s ratchet","main_file_link":[{"open_access":"1","url":"https://www.biorxiv.org/content/10.1101/477489v1"}],"department":[{"_id":"GradSch"}],"year":"2021","acknowledgement":"This work was supported by the Russian Science Foundation grant N 16-14-10173.","language":[{"iso":"eng"}],"publication_identifier":{"issn":["0022-5193"]},"oa":1,"keyword":["General Biochemistry","Genetics and Molecular Biology","Modelling and Simulation","Statistics and Probability","General Immunology and Microbiology","Applied Mathematics","General Agricultural and Biological Sciences","General Medicine"],"article_type":"original","article_number":"110729","day":"24","publication":"Journal of Theoretical Biology","user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","doi":"10.1016/j.jtbi.2021.110729"},{"article_type":"original","keyword":["History and Philosophy of Science","General Biochemistry","Genetics and Molecular Biology","General Neuroscience"],"oa":1,"publication_identifier":{"issn":["0077-8923"],"eissn":["1749-6632"]},"language":[{"iso":"eng"}],"doi":"10.1111/nyas.14674","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","publication":"Annals of the New York Academy of Sciences","day":"01","main_file_link":[{"url":"https://doi.org/10.1111/nyas.14674","open_access":"1"}],"title":"Morphology control in crystalline nanoparticle–polymer aggregates","year":"2021","extern":"1","pmid":1,"type":"journal_article","article_processing_charge":"No","citation":{"chicago":"Bian, Tong, and Rafal Klajn. “Morphology Control in Crystalline Nanoparticle–Polymer Aggregates.” <i>Annals of the New York Academy of Sciences</i>. Wiley, 2021. <a href=\"https://doi.org/10.1111/nyas.14674\">https://doi.org/10.1111/nyas.14674</a>.","apa":"Bian, T., &#38; Klajn, R. (2021). Morphology control in crystalline nanoparticle–polymer aggregates. <i>Annals of the New York Academy of Sciences</i>. Wiley. <a href=\"https://doi.org/10.1111/nyas.14674\">https://doi.org/10.1111/nyas.14674</a>","ieee":"T. Bian and R. Klajn, “Morphology control in crystalline nanoparticle–polymer aggregates,” <i>Annals of the New York Academy of Sciences</i>, vol. 1505, no. 1. Wiley, pp. 191–201, 2021.","ama":"Bian T, Klajn R. Morphology control in crystalline nanoparticle–polymer aggregates. <i>Annals of the New York Academy of Sciences</i>. 2021;1505(1):191-201. doi:<a href=\"https://doi.org/10.1111/nyas.14674\">10.1111/nyas.14674</a>","ista":"Bian T, Klajn R. 2021. Morphology control in crystalline nanoparticle–polymer aggregates. Annals of the New York Academy of Sciences. 1505(1), 191–201.","mla":"Bian, Tong, and Rafal Klajn. “Morphology Control in Crystalline Nanoparticle–Polymer Aggregates.” <i>Annals of the New York Academy of Sciences</i>, vol. 1505, no. 1, Wiley, 2021, pp. 191–201, doi:<a href=\"https://doi.org/10.1111/nyas.14674\">10.1111/nyas.14674</a>.","short":"T. Bian, R. Klajn, Annals of the New York Academy of Sciences 1505 (2021) 191–201."},"publisher":"Wiley","date_updated":"2023-08-07T10:01:10Z","oa_version":"Published Version","ddc":["540"],"month":"12","status":"public","scopus_import":"1","publication_status":"published","date_created":"2023-08-01T09:33:39Z","external_id":{"pmid":["34427923"]},"abstract":[{"text":"Self-assembly of nanoparticles can be mediated by polymers, but has so far led almost exclusively to nanoparticle aggregates that are amorphous. Here, we employed Coulombic interactions to generate a range of composite materials from mixtures of charged nanoparticles and oppositely charged polymers. The assembly behavior of these nanoparticle/polymer composites depends on their order of addition: polymers added to nanoparticles give rise to stable aggregates, but nanoparticles added to polymers disassemble the initially formed aggregates. The amorphous aggregates were transformed into crystalline ones by transiently increasing the ionic strength of the solution. The morphology of the resulting crystals depended on the length of the polymer: short polymer chains mediated the self-assembly of nanoparticles into strongly faceted crystals, whereas long chains led to pseudospherical nanoparticle/polymer assemblies, within which the crystalline order of nanoparticles was retained.","lang":"eng"}],"quality_controlled":"1","issue":"1","_id":"13356","intvolume":"      1505","date_published":"2021-12-01T00:00:00Z","volume":1505,"author":[{"first_name":"Tong","full_name":"Bian, Tong","last_name":"Bian"},{"full_name":"Klajn, Rafal","first_name":"Rafal","id":"8e84690e-1e48-11ed-a02b-a1e6fb8bb53b","last_name":"Klajn"}],"page":"191-201"},{"date_created":"2021-10-20T14:40:32Z","publication_status":"published","external_id":{"isi":["000709050300001"]},"file_date_updated":"2021-10-21T13:51:49Z","abstract":[{"text":"The C-terminal domain (CTD) of the largest subunit of RNA polymerase II (Pol II) is a regulatory hub for transcription and RNA processing. Here, we identify PHD-finger protein 3 (PHF3) as a regulator of transcription and mRNA stability that docks onto Pol II CTD through its SPOC domain. We characterize SPOC as a CTD reader domain that preferentially binds two phosphorylated Serine-2 marks in adjacent CTD repeats. PHF3 drives liquid-liquid phase separation of phosphorylated Pol II, colocalizes with Pol II clusters and tracks with Pol II across the length of genes. PHF3 knock-out or SPOC deletion in human cells results in increased Pol II stalling, reduced elongation rate and an increase in mRNA stability, with marked derepression of neuronal genes. Key neuronal genes are aberrantly expressed in Phf3 knock-out mouse embryonic stem cells, resulting in impaired neuronal differentiation. Our data suggest that PHF3 acts as a prominent effector of neuronal gene regulation by bridging transcription with mRNA decay.","lang":"eng"}],"intvolume":"        12","date_published":"2021-10-19T00:00:00Z","volume":12,"author":[{"full_name":"Appel, Lisa-Marie","first_name":"Lisa-Marie","last_name":"Appel"},{"first_name":"Vedran","full_name":"Franke, Vedran","last_name":"Franke"},{"full_name":"Bruno, Melania","first_name":"Melania","last_name":"Bruno"},{"full_name":"Grishkovskaya, Irina","first_name":"Irina","last_name":"Grishkovskaya"},{"last_name":"Kasiliauskaite","full_name":"Kasiliauskaite, Aiste","first_name":"Aiste"},{"last_name":"Kaufmann","first_name":"Tanja","full_name":"Kaufmann, Tanja"},{"full_name":"Schoeberl, Ursula E.","first_name":"Ursula E.","last_name":"Schoeberl"},{"last_name":"Puchinger","full_name":"Puchinger, Martin G.","first_name":"Martin G."},{"last_name":"Kostrhon","full_name":"Kostrhon, Sebastian","first_name":"Sebastian"},{"last_name":"Ebenwaldner","first_name":"Carmen","full_name":"Ebenwaldner, Carmen"},{"last_name":"Sebesta","full_name":"Sebesta, Marek","first_name":"Marek"},{"last_name":"Beltzung","first_name":"Etienne","full_name":"Beltzung, Etienne"},{"full_name":"Mechtler, Karl","first_name":"Karl","last_name":"Mechtler"},{"last_name":"Lin","full_name":"Lin, Gen","first_name":"Gen"},{"last_name":"Vlasova","full_name":"Vlasova, Anna","first_name":"Anna"},{"first_name":"Martin","full_name":"Leeb, Martin","last_name":"Leeb"},{"full_name":"Pavri, Rushad","first_name":"Rushad","last_name":"Pavri"},{"first_name":"Alexander","full_name":"Stark, Alexander","last_name":"Stark"},{"first_name":"Altuna","full_name":"Akalin, Altuna","last_name":"Akalin"},{"first_name":"Richard","full_name":"Stefl, Richard","last_name":"Stefl"},{"last_name":"Bernecky","full_name":"Bernecky, Carrie A","id":"2CB9DFE2-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0003-0893-7036","first_name":"Carrie A"},{"last_name":"Djinovic-Carugo","first_name":"Kristina","full_name":"Djinovic-Carugo, Kristina"},{"first_name":"Dea","full_name":"Slade, Dea","last_name":"Slade"}],"issue":"1","quality_controlled":"1","_id":"10163","article_processing_charge":"No","citation":{"short":"L.-M. Appel, V. Franke, M. Bruno, I. Grishkovskaya, A. Kasiliauskaite, T. Kaufmann, U.E. Schoeberl, M.G. Puchinger, S. Kostrhon, C. Ebenwaldner, M. Sebesta, E. Beltzung, K. Mechtler, G. Lin, A. Vlasova, M. Leeb, R. Pavri, A. Stark, A. Akalin, R. Stefl, C. Bernecky, K. Djinovic-Carugo, D. Slade, Nature Communications 12 (2021).","mla":"Appel, Lisa-Marie, et al. “PHF3 Regulates Neuronal Gene Expression through the Pol II CTD Reader Domain SPOC.” <i>Nature Communications</i>, vol. 12, no. 1, 6078, Springer Nature, 2021, doi:<a href=\"https://doi.org/10.1038/s41467-021-26360-2\">10.1038/s41467-021-26360-2</a>.","ama":"Appel L-M, Franke V, Bruno M, et al. PHF3 regulates neuronal gene expression through the Pol II CTD reader domain SPOC. <i>Nature Communications</i>. 2021;12(1). doi:<a href=\"https://doi.org/10.1038/s41467-021-26360-2\">10.1038/s41467-021-26360-2</a>","ista":"Appel L-M, Franke V, Bruno M, Grishkovskaya I, Kasiliauskaite A, Kaufmann T, Schoeberl UE, Puchinger MG, Kostrhon S, Ebenwaldner C, Sebesta M, Beltzung E, Mechtler K, Lin G, Vlasova A, Leeb M, Pavri R, Stark A, Akalin A, Stefl R, Bernecky C, Djinovic-Carugo K, Slade D. 2021. PHF3 regulates neuronal gene expression through the Pol II CTD reader domain SPOC. Nature Communications. 12(1), 6078.","ieee":"L.-M. Appel <i>et al.</i>, “PHF3 regulates neuronal gene expression through the Pol II CTD reader domain SPOC,” <i>Nature Communications</i>, vol. 12, no. 1. Springer Nature, 2021.","apa":"Appel, L.-M., Franke, V., Bruno, M., Grishkovskaya, I., Kasiliauskaite, A., Kaufmann, T., … Slade, D. (2021). PHF3 regulates neuronal gene expression through the Pol II CTD reader domain SPOC. <i>Nature Communications</i>. Springer Nature. <a href=\"https://doi.org/10.1038/s41467-021-26360-2\">https://doi.org/10.1038/s41467-021-26360-2</a>","chicago":"Appel, Lisa-Marie, Vedran Franke, Melania Bruno, Irina Grishkovskaya, Aiste Kasiliauskaite, Tanja Kaufmann, Ursula E. Schoeberl, et al. “PHF3 Regulates Neuronal Gene Expression through the Pol II CTD Reader Domain SPOC.” <i>Nature Communications</i>. Springer Nature, 2021. <a href=\"https://doi.org/10.1038/s41467-021-26360-2\">https://doi.org/10.1038/s41467-021-26360-2</a>."},"publisher":"Springer Nature","has_accepted_license":"1","type":"journal_article","related_material":{"link":[{"description":"Preprint ","url":"https://www.biorxiv.org/content/10.1101/2020.02.11.943159","relation":"earlier_version"}]},"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)"},"file":[{"checksum":"d99fcd51aebde19c21314e3de0148007","creator":"cchlebak","date_created":"2021-10-21T13:51:49Z","access_level":"open_access","file_id":"10169","relation":"main_file","file_name":"2021_NatComm_Appel.pdf","success":1,"file_size":5111706,"content_type":"application/pdf","date_updated":"2021-10-21T13:51:49Z"}],"date_updated":"2023-08-14T08:02:31Z","oa_version":"Published Version","ddc":["610"],"isi":1,"month":"10","status":"public","title":"PHF3 regulates neuronal gene expression through the Pol II CTD reader domain SPOC","acknowledgement":"D.S. thanks Claudine Kraft, Renée Schroeder, Verena Jantsch, Franz Klein and Peter Schlögelhofer for support. We thank Anita Testa Salmazo for help with purifying Pol II; Matthias Geyer and Robert Düster for sharing DYRK1A kinase; Felix Hartmann and Clemens Plaschka for help with mass photometry; Goran Kokic for design of the arrest assay sequences; Petra van der Lelij for help with generating mESC KO; Maximilian Freilinger for help with the purification of mEGFP-CTD; Stefan Ameres, Nina Fasching and Brian Reichholf for advice on SLAM-seq and for sharing reagents; Laura Gallego Valle for advice regarding LLPS assays; Krzysztof Chylinski for advice regarding CRISPR/Cas9 methodology; VBCF Protein Technologies facility for purifying PHF3 and providing gRNAs and Cas9; VBCF NGS facility for sequencing; Monoclonal antibody facility at the Helmholtz center for Pol II antibodies; Friedrich Propst and Elzbieta Kowalska for advice and for sharing materials; Egon Ogris for sharing materials; Martin Eilers for recommending a ChIP-grade TFIIS antibody; Susanne Opravil, Otto Hudecz, Markus Hartl and Natascha Hartl for mass spectrometry analysis; staff of the X-ray beamlines at the ESRF in Grenoble for their excellent support; Christa Bücker, Anton Meinhart, Clemens Plaschka and members of the Slade lab for critical comments on the manuscript; Life Science Editors for editing assistance. M.B. and D.S. acknowledge support by the FWF-funded DK ‘Chromosome Dynamics’. T.K. is a recipient of the DOC fellowship from the Austrian Academy of Sciences. U.S. is supported by the L’Oreal for Women in Science Austria Fellowship and the Austrian Science Fund (FWF T 795-B30). M.L is supported by the Vienna Science and Technology Fund (WWTF, VRG14-006). R.S. is supported by the Czech Science Foundation (15-17670 S and 21-24460 S), Ministry of Education, Youths and Sports of the Czech Republic (CEITEC 2020 project (LQ1601)), and the European Research Council (ERC) under the European Union’s Horizon 2020 research and innovation programme (Grant agreement no. 649030); this publication reflects only the author’s view and the Research Executive Agency is not responsible for any use that may be made of the information it contains. M.S. is supported by the Czech Science Foundation (GJ20-21581Y). K.D.C. research is supported by the Austrian Science Fund (FWF) Projects I525 and I1593, P22276, P19060, and W1221, Federal Ministry of Economy, Family and Youth through the initiative ‘Laura Bassi Centres of Expertise’, funding from the Centre of Optimized Structural Studies No. 253275, the Wellcome Trust Collaborative Award (201543/Z/16), COST action BM1405 Non-globular proteins - from sequence to structure, function and application in molecular physiopathology (NGP-NET), the Vienna Science and Technology Fund (WWTF LS17-008), and by the University of Vienna. This project was funded by the MFPL start-up grant, the Vienna Science and Technology Fund (WWTF LS14-001), and the Austrian Science Fund (P31546-B28 and W1258 “DK: Integrative Structural Biology”) to D.S.","year":"2021","department":[{"_id":"CaBe"}],"keyword":["general physics and astronomy","general biochemistry","genetics and molecular biology","general chemistry"],"oa":1,"language":[{"iso":"eng"}],"publication_identifier":{"eissn":["2041-1723"]},"article_number":"6078","article_type":"original","publication":"Nature Communications","day":"19","doi":"10.1038/s41467-021-26360-2","user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8"},{"user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","doi":"10.1016/j.jsb.2021.107808","day":"03","publication":"Journal of Structural Biology","article_type":"original","article_number":"107808","publication_identifier":{"issn":["1047-8477"]},"language":[{"iso":"eng"}],"keyword":["Structural Biology"],"oa":1,"department":[{"_id":"FlSc"}],"year":"2021","acknowledgement":"This research was supported by the Scientific Service Units (SSUs) of IST Austria through resources provided by Scientific Computing (SciComp), the Life Science Facility (LSF), the BioImaging Facility (BIF), and the Electron Microscopy Facility (EMF). We also thank Victor-Valentin Hodirnau for help with cryo-ET data acquisition. The authors acknowledge support from IST Austria and from the Austrian Science Fund (FWF): M02495 to G.D. and Austrian Science Fund (FWF): P33367 to F.K.M.S.","project":[{"name":"Structure and isoform diversity of the Arp2/3 complex","_id":"9B954C5C-BA93-11EA-9121-9846C619BF3A","grant_number":"P33367"},{"call_identifier":"FWF","grant_number":"M02495","_id":"2674F658-B435-11E9-9278-68D0E5697425","name":"Protein structure and function in filopodia across scales"}],"acknowledged_ssus":[{"_id":"ScienComp"},{"_id":"LifeSc"},{"_id":"Bio"},{"_id":"EM-Fac"}],"title":"Computational toolbox for ultrastructural quantitative analysis of filament networks in cryo-ET data","month":"11","status":"public","ddc":["572"],"isi":1,"oa_version":"Published Version","date_updated":"2023-11-21T08:36:02Z","file":[{"date_updated":"2021-11-15T13:11:27Z","content_type":"application/pdf","success":1,"file_size":16818304,"file_name":"2021_JournalStructBiol_Dimchev.pdf","relation":"main_file","file_id":"10291","access_level":"open_access","date_created":"2021-11-15T13:11:27Z","checksum":"6b209e4d44775d4e02b50f78982c15fa","creator":"cchlebak"}],"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)"},"related_material":{"record":[{"relation":"software","id":"14502","status":"public"}]},"type":"journal_article","publisher":"Elsevier ","has_accepted_license":"1","citation":{"chicago":"Dimchev, Georgi A, Behnam Amiri, Florian Fäßler, Martin Falcke, and Florian KM Schur. “Computational Toolbox for Ultrastructural Quantitative Analysis of Filament Networks in Cryo-ET Data.” <i>Journal of Structural Biology</i>. Elsevier , 2021. <a href=\"https://doi.org/10.1016/j.jsb.2021.107808\">https://doi.org/10.1016/j.jsb.2021.107808</a>.","ieee":"G. A. Dimchev, B. Amiri, F. Fäßler, M. Falcke, and F. K. Schur, “Computational toolbox for ultrastructural quantitative analysis of filament networks in cryo-ET data,” <i>Journal of Structural Biology</i>, vol. 213, no. 4. Elsevier , 2021.","apa":"Dimchev, G. A., Amiri, B., Fäßler, F., Falcke, M., &#38; Schur, F. K. (2021). Computational toolbox for ultrastructural quantitative analysis of filament networks in cryo-ET data. <i>Journal of Structural Biology</i>. Elsevier . <a href=\"https://doi.org/10.1016/j.jsb.2021.107808\">https://doi.org/10.1016/j.jsb.2021.107808</a>","ama":"Dimchev GA, Amiri B, Fäßler F, Falcke M, Schur FK. Computational toolbox for ultrastructural quantitative analysis of filament networks in cryo-ET data. <i>Journal of Structural Biology</i>. 2021;213(4). doi:<a href=\"https://doi.org/10.1016/j.jsb.2021.107808\">10.1016/j.jsb.2021.107808</a>","ista":"Dimchev GA, Amiri B, Fäßler F, Falcke M, Schur FK. 2021. Computational toolbox for ultrastructural quantitative analysis of filament networks in cryo-ET data. Journal of Structural Biology. 213(4), 107808.","mla":"Dimchev, Georgi A., et al. “Computational Toolbox for Ultrastructural Quantitative Analysis of Filament Networks in Cryo-ET Data.” <i>Journal of Structural Biology</i>, vol. 213, no. 4, 107808, Elsevier , 2021, doi:<a href=\"https://doi.org/10.1016/j.jsb.2021.107808\">10.1016/j.jsb.2021.107808</a>.","short":"G.A. Dimchev, B. Amiri, F. Fäßler, M. Falcke, F.K. Schur, Journal of Structural Biology 213 (2021)."},"article_processing_charge":"Yes (via OA deal)","_id":"10290","issue":"4","quality_controlled":"1","volume":213,"author":[{"orcid":"0000-0001-8370-6161","id":"38C393BE-F248-11E8-B48F-1D18A9856A87","full_name":"Dimchev, Georgi A","first_name":"Georgi A","last_name":"Dimchev"},{"full_name":"Amiri, Behnam","first_name":"Behnam","last_name":"Amiri"},{"last_name":"Fäßler","full_name":"Fäßler, Florian","first_name":"Florian","orcid":"0000-0001-7149-769X","id":"404F5528-F248-11E8-B48F-1D18A9856A87"},{"last_name":"Falcke","first_name":"Martin","full_name":"Falcke, Martin"},{"full_name":"Schur, Florian KM","first_name":"Florian KM","orcid":"0000-0003-4790-8078","id":"48AD8942-F248-11E8-B48F-1D18A9856A87","last_name":"Schur"}],"date_published":"2021-11-03T00:00:00Z","intvolume":"       213","scopus_import":"1","abstract":[{"lang":"eng","text":"A precise quantitative description of the ultrastructural characteristics underlying biological mechanisms is often key to their understanding. This is particularly true for dynamic extra- and intracellular filamentous assemblies, playing a role in cell motility, cell integrity, cytokinesis, tissue formation and maintenance. For example, genetic manipulation or modulation of actin regulatory proteins frequently manifests in changes of the morphology, dynamics, and ultrastructural architecture of actin filament-rich cell peripheral structures, such as lamellipodia or filopodia. However, the observed ultrastructural effects often remain subtle and require sufficiently large datasets for appropriate quantitative analysis. The acquisition of such large datasets has been enabled by recent advances in high-throughput cryo-electron tomography (cryo-ET) methods. This also necessitates the development of complementary approaches to maximize the extraction of relevant biological information. We have developed a computational toolbox for the semi-automatic quantification of segmented and vectorized filamentous networks from pre-processed cryo-electron tomograms, facilitating the analysis and cross-comparison of multiple experimental conditions. GUI-based components simplify the processing of data and allow users to obtain a large number of ultrastructural parameters describing filamentous assemblies. We demonstrate the feasibility of this workflow by analyzing cryo-ET data of untreated and chemically perturbed branched actin filament networks and that of parallel actin filament arrays. In principle, the computational toolbox presented here is applicable for data analysis comprising any type of filaments in regular (i.e. parallel) or random arrangement. We show that it can ease the identification of key differences between experimental groups and facilitate the in-depth analysis of ultrastructural data in a time-efficient manner."}],"file_date_updated":"2021-11-15T13:11:27Z","external_id":{"isi":["000720259500002"]},"date_created":"2021-11-15T12:21:42Z","publication_status":"published"},{"article_number":"e71575","article_type":"original","oa":1,"keyword":["general immunology and microbiology","general biochemistry","genetics and molecular biology","general medicine","general neuroscience"],"publication_identifier":{"issn":["2050-084X"]},"language":[{"iso":"eng"}],"doi":"10.7554/elife.71575","user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","publication":"eLife","day":"17","title":"Control of protein synthesis and memory by GluN3A-NMDA receptors through inhibition of GIT1/mTORC1 assembly","acknowledgement":"We thank Stuart Lipton and Nobuki Nakanishi for providing the Grin3a knockout mice, Beverly Davidson for the AAV-caRheb, Jose Esteban for help with behavioral and biochemical experiments, and Noelia Campillo, Rebeca Martínez-Turrillas, and Ana Navarro for expert technical help. Work was funded by the UTE project CIMA; fellowships from the Fundación Tatiana Pérez de Guzmán el Bueno, FEBS, and IBRO (to M.J.C.D.), Generalitat Valenciana (to O.E.-Z.), Juan de la Cierva (to L.G.R.), FPI-MINECO (to E.R.V., to S.N.) and Intertalentum postdoctoral program (to V.B.); ANR (GluBrain3A) and ERC Advanced Grants (#693021) (to P.P.); Ramón y Cajal program RYC2014-15784, RETOS-MINECO SAF2016-76565-R, ERANET-Neuron JTC 2019 ISCIII AC19/00077 FEDER funds (to R.A.); RETOS-MINECO SAF2017-87928-R (to A.B.); an NIH grant (NS76637) and UTHSC College of Medicine funds (to S.J.T.); and NARSAD Independent Investigator Award and grants from the MINECO (CSD2008-00005, SAF2013-48983R, SAF2016-80895-R), Generalitat Valenciana (PROMETEO 2019/020)(to I.P.O.) and Severo-Ochoa Excellence Awards (SEV-2013-0317, SEV-2017-0723).","year":"2021","department":[{"_id":"GaNo"}],"type":"journal_article","article_processing_charge":"No","citation":{"ama":"Conde-Dusman MJ, Dey PN, Elía-Zudaire Ó, et al. Control of protein synthesis and memory by GluN3A-NMDA receptors through inhibition of GIT1/mTORC1 assembly. <i>eLife</i>. 2021;10. doi:<a href=\"https://doi.org/10.7554/elife.71575\">10.7554/elife.71575</a>","ista":"Conde-Dusman MJ, Dey PN, Elía-Zudaire Ó, Garcia Rabaneda LE, García-Lira C, Grand T, Briz V, Velasco ER, Andero Galí R, Niñerola S, Barco A, Paoletti P, Wesseling JF, Gardoni F, Tavalin SJ, Perez-Otaño I. 2021. Control of protein synthesis and memory by GluN3A-NMDA receptors through inhibition of GIT1/mTORC1 assembly. eLife. 10, e71575.","short":"M.J. Conde-Dusman, P.N. Dey, Ó. Elía-Zudaire, L.E. Garcia Rabaneda, C. García-Lira, T. Grand, V. Briz, E.R. Velasco, R. Andero Galí, S. Niñerola, A. Barco, P. Paoletti, J.F. Wesseling, F. Gardoni, S.J. Tavalin, I. Perez-Otaño, ELife 10 (2021).","mla":"Conde-Dusman, María J., et al. “Control of Protein Synthesis and Memory by GluN3A-NMDA Receptors through Inhibition of GIT1/MTORC1 Assembly.” <i>ELife</i>, vol. 10, e71575, eLife Sciences Publications, 2021, doi:<a href=\"https://doi.org/10.7554/elife.71575\">10.7554/elife.71575</a>.","chicago":"Conde-Dusman, María J, Partha N Dey, Óscar Elía-Zudaire, Luis E Garcia Rabaneda, Carmen García-Lira, Teddy Grand, Victor Briz, et al. “Control of Protein Synthesis and Memory by GluN3A-NMDA Receptors through Inhibition of GIT1/MTORC1 Assembly.” <i>ELife</i>. eLife Sciences Publications, 2021. <a href=\"https://doi.org/10.7554/elife.71575\">https://doi.org/10.7554/elife.71575</a>.","apa":"Conde-Dusman, M. J., Dey, P. N., Elía-Zudaire, Ó., Garcia Rabaneda, L. E., García-Lira, C., Grand, T., … Perez-Otaño, I. (2021). Control of protein synthesis and memory by GluN3A-NMDA receptors through inhibition of GIT1/mTORC1 assembly. <i>ELife</i>. eLife Sciences Publications. <a href=\"https://doi.org/10.7554/elife.71575\">https://doi.org/10.7554/elife.71575</a>","ieee":"M. J. Conde-Dusman <i>et al.</i>, “Control of protein synthesis and memory by GluN3A-NMDA receptors through inhibition of GIT1/mTORC1 assembly,” <i>eLife</i>, vol. 10. eLife Sciences Publications, 2021."},"has_accepted_license":"1","publisher":"eLife Sciences Publications","date_updated":"2023-08-14T11:50:50Z","oa_version":"Published Version","isi":1,"ddc":["570"],"month":"11","status":"public","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)"},"file":[{"relation":"main_file","file_name":"elife-71575-v1.pdf","date_updated":"2021-11-18T07:02:02Z","content_type":"application/pdf","file_size":2477302,"success":1,"checksum":"59318e9e41507cec83c2f4070e6ad540","creator":"lgarciar","access_level":"open_access","date_created":"2021-11-18T07:02:02Z","file_id":"10302"}],"publication_status":"published","date_created":"2021-11-18T06:59:45Z","external_id":{"isi":["000720945900001"]},"file_date_updated":"2021-11-18T07:02:02Z","abstract":[{"text":"De novo protein synthesis is required for synapse modifications underlying stable memory encoding. Yet neurons are highly compartmentalized cells and how protein synthesis can be regulated at the synapse level is unknown. Here, we characterize neuronal signaling complexes formed by the postsynaptic scaffold GIT1, the mechanistic target of rapamycin (mTOR) kinase, and Raptor that couple synaptic stimuli to mTOR-dependent protein synthesis; and identify NMDA receptors containing GluN3A subunits as key negative regulators of GIT1 binding to mTOR. Disruption of GIT1/mTOR complexes by enhancing GluN3A expression or silencing GIT1 inhibits synaptic mTOR activation and restricts the mTOR-dependent translation of specific activity-regulated mRNAs. Conversely, GluN3A removal enables complex formation, potentiates mTOR-dependent protein synthesis, and facilitates the consolidation of associative and spatial memories in mice. The memory enhancement becomes evident with light or spaced training, can be achieved by selectively deleting GluN3A from excitatory neurons during adulthood, and does not compromise other aspects of cognition such as memory flexibility or extinction. Our findings provide mechanistic insight into synaptic translational control and reveal a potentially selective target for cognitive enhancement.","lang":"eng"}],"quality_controlled":"1","_id":"10301","date_published":"2021-11-17T00:00:00Z","intvolume":"        10","volume":10,"author":[{"first_name":"María J","full_name":"Conde-Dusman, María J","last_name":"Conde-Dusman"},{"last_name":"Dey","first_name":"Partha N","full_name":"Dey, Partha N"},{"last_name":"Elía-Zudaire","first_name":"Óscar","full_name":"Elía-Zudaire, Óscar"},{"id":"33D1B084-F248-11E8-B48F-1D18A9856A87","full_name":"Garcia Rabaneda, Luis E","first_name":"Luis E","last_name":"Garcia Rabaneda"},{"last_name":"García-Lira","full_name":"García-Lira, Carmen","first_name":"Carmen"},{"last_name":"Grand","full_name":"Grand, Teddy","first_name":"Teddy"},{"first_name":"Victor","full_name":"Briz, Victor","last_name":"Briz"},{"first_name":"Eric R","full_name":"Velasco, Eric R","last_name":"Velasco"},{"first_name":"Raül","full_name":"Andero Galí, Raül","last_name":"Andero Galí"},{"full_name":"Niñerola, Sergio","first_name":"Sergio","last_name":"Niñerola"},{"last_name":"Barco","full_name":"Barco, Angel","first_name":"Angel"},{"full_name":"Paoletti, Pierre","first_name":"Pierre","last_name":"Paoletti"},{"first_name":"John F","full_name":"Wesseling, John F","last_name":"Wesseling"},{"last_name":"Gardoni","first_name":"Fabrizio","full_name":"Gardoni, Fabrizio"},{"first_name":"Steven J","full_name":"Tavalin, Steven J","last_name":"Tavalin"},{"last_name":"Perez-Otaño","first_name":"Isabel","full_name":"Perez-Otaño, Isabel"}]},{"title":"Cryo-EM structure of a functional monomeric Photosystem I from Thermosynechococcus elongatus reveals red chlorophyll cluster","pmid":1,"year":"2021","department":[{"_id":"LeSa"}],"acknowledgement":"We are grateful for additional support and valuable scientific input for this project by Yuko Misumi, Jiannan Li, Hisako Kubota-Kawai, Takeshi Kawabata, Mian Wu, Eiki Yamashita, Atsushi Nakagawa, Volker Hartmann, Melanie Völkel and Matthias Rögner. Parts of this research were funded by the German Research Council (DFG) within the framework of GRK 2341 (Microbial Substrate Conversion) to M.M.N., the Platform Project for Supporting Drug Discovery and Life Science Research [Basis for Supporting Innovative Drug Discovery and Life Science Research (BINDS)] from AMED under grant number JP20am0101117 (K.N.), JP16K07266 to Atsunori Oshima and C.G., a Grants-in-Aid for Scientific Research under grant number JP 25000013 (K.N.), 17H03647 (C.G.) and 16H06560 (G.K.) from MEXT-KAKENHI, the International Joint Research Promotion Program from Osaka University to M.M.N., C.G. and G.K., and the Cyclic Innovation for Clinical Empowerment (CiCLE) Grant Number JP17pc0101020 from AMED to K.N. and G.K.","publication_identifier":{"issn":["2399-3642"]},"language":[{"iso":"eng"}],"oa":1,"keyword":["general agricultural and biological Sciences","general biochemistry","genetics and molecular biology","medicine (miscellaneous)"],"article_type":"original","article_number":"304","publication":"Communications Biology","day":"08","user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","doi":"10.1038/s42003-021-01808-9","file_date_updated":"2021-11-19T15:09:18Z","abstract":[{"text":"A high-resolution structure of trimeric cyanobacterial Photosystem I (PSI) from Thermosynechococcus elongatus was reported as the first atomic model of PSI almost 20 years ago. However, the monomeric PSI structure has not yet been reported despite long-standing interest in its structure and extensive spectroscopic characterization of the loss of red chlorophylls upon monomerization. Here, we describe the structure of monomeric PSI from Thermosynechococcus elongatus BP-1. Comparison with the trimer structure gave detailed insights into monomerization-induced changes in both the central trimerization domain and the peripheral regions of the complex. Monomerization-induced loss of red chlorophylls is assigned to a cluster of chlorophylls adjacent to PsaX. Based on our findings, we propose a role of PsaX in the stabilization of red chlorophylls and that lipids of the surrounding membrane present a major source of thermal energy for uphill excitation energy transfer from red chlorophylls to P700.","lang":"eng"}],"external_id":{"isi":["000627440700001"],"pmid":["33686186"]},"date_created":"2021-11-19T11:37:29Z","publication_status":"published","scopus_import":"1","date_published":"2021-03-08T00:00:00Z","intvolume":"         4","author":[{"full_name":"Çoruh, Mehmet Orkun","orcid":"0000-0002-3219-2022","first_name":"Mehmet Orkun","id":"d25163e5-8d53-11eb-a251-e6dd8ea1b8ef","last_name":"Çoruh"},{"full_name":"Frank, Anna","first_name":"Anna","last_name":"Frank"},{"last_name":"Tanaka","full_name":"Tanaka, Hideaki","first_name":"Hideaki"},{"first_name":"Akihiro","full_name":"Kawamoto, Akihiro","last_name":"Kawamoto"},{"last_name":"El-Mohsnawy","first_name":"Eithar","full_name":"El-Mohsnawy, Eithar"},{"full_name":"Kato, Takayuki","first_name":"Takayuki","last_name":"Kato"},{"first_name":"Keiichi","full_name":"Namba, Keiichi","last_name":"Namba"},{"first_name":"Christoph","full_name":"Gerle, Christoph","last_name":"Gerle"},{"last_name":"Nowaczyk","full_name":"Nowaczyk, Marc M.","first_name":"Marc M."},{"full_name":"Kurisu, Genji","first_name":"Genji","last_name":"Kurisu"}],"volume":4,"_id":"10310","issue":"1","quality_controlled":"1","citation":{"ieee":"M. O. Çoruh <i>et al.</i>, “Cryo-EM structure of a functional monomeric Photosystem I from Thermosynechococcus elongatus reveals red chlorophyll cluster,” <i>Communications Biology</i>, vol. 4, no. 1. Springer , 2021.","apa":"Çoruh, M. O., Frank, A., Tanaka, H., Kawamoto, A., El-Mohsnawy, E., Kato, T., … Kurisu, G. (2021). Cryo-EM structure of a functional monomeric Photosystem I from Thermosynechococcus elongatus reveals red chlorophyll cluster. <i>Communications Biology</i>. Springer . <a href=\"https://doi.org/10.1038/s42003-021-01808-9\">https://doi.org/10.1038/s42003-021-01808-9</a>","chicago":"Çoruh, Mehmet Orkun, Anna Frank, Hideaki Tanaka, Akihiro Kawamoto, Eithar El-Mohsnawy, Takayuki Kato, Keiichi Namba, Christoph Gerle, Marc M. Nowaczyk, and Genji Kurisu. “Cryo-EM Structure of a Functional Monomeric Photosystem I from Thermosynechococcus Elongatus Reveals Red Chlorophyll Cluster.” <i>Communications Biology</i>. Springer , 2021. <a href=\"https://doi.org/10.1038/s42003-021-01808-9\">https://doi.org/10.1038/s42003-021-01808-9</a>.","mla":"Çoruh, Mehmet Orkun, et al. “Cryo-EM Structure of a Functional Monomeric Photosystem I from Thermosynechococcus Elongatus Reveals Red Chlorophyll Cluster.” <i>Communications Biology</i>, vol. 4, no. 1, 304, Springer , 2021, doi:<a href=\"https://doi.org/10.1038/s42003-021-01808-9\">10.1038/s42003-021-01808-9</a>.","short":"M.O. Çoruh, A. Frank, H. Tanaka, A. Kawamoto, E. El-Mohsnawy, T. Kato, K. Namba, C. Gerle, M.M. Nowaczyk, G. Kurisu, Communications Biology 4 (2021).","ama":"Çoruh MO, Frank A, Tanaka H, et al. Cryo-EM structure of a functional monomeric Photosystem I from Thermosynechococcus elongatus reveals red chlorophyll cluster. <i>Communications Biology</i>. 2021;4(1). doi:<a href=\"https://doi.org/10.1038/s42003-021-01808-9\">10.1038/s42003-021-01808-9</a>","ista":"Çoruh MO, Frank A, Tanaka H, Kawamoto A, El-Mohsnawy E, Kato T, Namba K, Gerle C, Nowaczyk MM, Kurisu G. 2021. Cryo-EM structure of a functional monomeric Photosystem I from Thermosynechococcus elongatus reveals red chlorophyll cluster. Communications Biology. 4(1), 304."},"publisher":"Springer ","has_accepted_license":"1","article_processing_charge":"No","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)"},"file":[{"access_level":"open_access","date_created":"2021-11-19T15:09:18Z","creator":"cchlebak","checksum":"8ffd39f2bba7152a2441802ff313bf0b","file_id":"10318","relation":"main_file","content_type":"application/pdf","date_updated":"2021-11-19T15:09:18Z","file_size":6030261,"success":1,"file_name":"2021_CommBio_Çoruh.pdf"}],"ddc":["570"],"isi":1,"status":"public","month":"03","date_updated":"2023-08-14T11:51:19Z","oa_version":"Published Version"},{"_id":"10337","issue":"6","quality_controlled":"1","volume":220,"author":[{"first_name":"Longhui","full_name":"Zeng, Longhui","last_name":"Zeng"},{"last_name":"Palaia","full_name":"Palaia, Ivan","first_name":"Ivan"},{"first_name":"Anđela","orcid":"0000-0002-7854-2139","id":"bf63d406-f056-11eb-b41d-f263a6566d8b","full_name":"Šarić, Anđela","last_name":"Šarić"},{"last_name":"Su","full_name":"Su, Xiaolei","first_name":"Xiaolei"}],"date_published":"2021-04-30T00:00:00Z","intvolume":"       220","scopus_import":"1","abstract":[{"lang":"eng","text":"The T cell receptor (TCR) pathway receives, processes, and amplifies the signal from pathogenic antigens to the activation of T cells. Although major components in this pathway have been identified, the knowledge on how individual components cooperate to effectively transduce signals remains limited. Phase separation emerges as a biophysical principle in organizing signaling molecules into liquid-like condensates. Here, we report that phospholipase Cγ1 (PLCγ1) promotes phase separation of LAT, a key adaptor protein in the TCR pathway. PLCγ1 directly cross-links LAT through its two SH2 domains. PLCγ1 also protects LAT from dephosphorylation by the phosphatase CD45 and promotes LAT-dependent ERK activation and SLP76 phosphorylation. Intriguingly, a nonmonotonic effect of PLCγ1 on LAT clustering was discovered. Computer simulations, based on patchy particles, revealed how the cluster size is regulated by protein compositions. Together, these results define a critical function of PLCγ1 in promoting phase separation of the LAT complex and TCR signal transduction."}],"external_id":{"pmid":["33929486"]},"publication_status":"published","date_created":"2021-11-25T15:21:30Z","status":"public","month":"04","oa_version":"None","date_updated":"2021-11-25T15:33:08Z","tmp":{"legal_code_url":"https://creativecommons.org/licenses/by-nc-sa/4.0/legalcode","short":"CC BY-NC-SA (4.0)","name":"Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC BY-NC-SA 4.0)","image":"/images/cc_by_nc_sa.png"},"type":"journal_article","publisher":"Rockefeller University Press","citation":{"ama":"Zeng L, Palaia I, Šarić A, Su X. PLCγ1 promotes phase separation of T cell signaling components. <i>Journal of Cell Biology</i>. 2021;220(6). doi:<a href=\"https://doi.org/10.1083/jcb.202009154\">10.1083/jcb.202009154</a>","ista":"Zeng L, Palaia I, Šarić A, Su X. 2021. PLCγ1 promotes phase separation of T cell signaling components. Journal of Cell Biology. 220(6), e202009154.","mla":"Zeng, Longhui, et al. “PLCγ1 Promotes Phase Separation of T Cell Signaling Components.” <i>Journal of Cell Biology</i>, vol. 220, no. 6, e202009154, Rockefeller University Press, 2021, doi:<a href=\"https://doi.org/10.1083/jcb.202009154\">10.1083/jcb.202009154</a>.","short":"L. Zeng, I. Palaia, A. Šarić, X. Su, Journal of Cell Biology 220 (2021).","chicago":"Zeng, Longhui, Ivan Palaia, Anđela Šarić, and Xiaolei Su. “PLCγ1 Promotes Phase Separation of T Cell Signaling Components.” <i>Journal of Cell Biology</i>. Rockefeller University Press, 2021. <a href=\"https://doi.org/10.1083/jcb.202009154\">https://doi.org/10.1083/jcb.202009154</a>.","apa":"Zeng, L., Palaia, I., Šarić, A., &#38; Su, X. (2021). PLCγ1 promotes phase separation of T cell signaling components. <i>Journal of Cell Biology</i>. Rockefeller University Press. <a href=\"https://doi.org/10.1083/jcb.202009154\">https://doi.org/10.1083/jcb.202009154</a>","ieee":"L. Zeng, I. Palaia, A. Šarić, and X. Su, “PLCγ1 promotes phase separation of T cell signaling components,” <i>Journal of Cell Biology</i>, vol. 220, no. 6. Rockefeller University Press, 2021."},"article_processing_charge":"No","year":"2021","acknowledgement":"Charles H. Hood Foundation (NO AWARD) ; Rally Foundation (NO AWARD)","pmid":1,"extern":"1","title":"PLCγ1 promotes phase separation of T cell signaling components","user_id":"8b945eb4-e2f2-11eb-945a-df72226e66a9","doi":"10.1083/jcb.202009154","day":"30","publication":"Journal of Cell Biology","article_type":"original","article_number":"e202009154","publication_identifier":{"eissn":["1540-8140"],"issn":["0021-9525"]},"language":[{"iso":"eng"}],"keyword":["cell biology"]},{"article_number":"e72676","article_type":"original","ec_funded":1,"oa":1,"keyword":["genetics and molecular biology"],"publication_identifier":{"issn":["2050-084X"]},"language":[{"iso":"eng"}],"doi":"10.7554/elife.72676","user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","day":"01","publication":"eLife","title":"Histone H1 prevents non-CG methylation-mediated small RNA biogenesis in Arabidopsis heterochromatin","acknowledgement":"We thank X Feng for helpful comments on the manuscript. This work was supported by a European Research Council grant MaintainMeth (725746) to DZ.","project":[{"call_identifier":"H2020","grant_number":"725746","name":"Quantitative analysis of DNA methylation maintenance with chromatin","_id":"62935a00-2b32-11ec-9570-eff30fa39068"}],"department":[{"_id":"DaZi"}],"year":"2021","pmid":1,"type":"journal_article","article_processing_charge":"No","has_accepted_license":"1","publisher":"eLife Sciences Publications","citation":{"ama":"Choi J, Lyons DB, Zilberman D. Histone H1 prevents non-CG methylation-mediated small RNA biogenesis in Arabidopsis heterochromatin. <i>eLife</i>. 2021;10. doi:<a href=\"https://doi.org/10.7554/elife.72676\">10.7554/elife.72676</a>","ista":"Choi J, Lyons DB, Zilberman D. 2021. Histone H1 prevents non-CG methylation-mediated small RNA biogenesis in Arabidopsis heterochromatin. eLife. 10, e72676.","short":"J. Choi, D.B. Lyons, D. Zilberman, ELife 10 (2021).","mla":"Choi, Jaemyung, et al. “Histone H1 Prevents Non-CG Methylation-Mediated Small RNA Biogenesis in Arabidopsis Heterochromatin.” <i>ELife</i>, vol. 10, e72676, eLife Sciences Publications, 2021, doi:<a href=\"https://doi.org/10.7554/elife.72676\">10.7554/elife.72676</a>.","chicago":"Choi, Jaemyung, David B Lyons, and Daniel Zilberman. “Histone H1 Prevents Non-CG Methylation-Mediated Small RNA Biogenesis in Arabidopsis Heterochromatin.” <i>ELife</i>. eLife Sciences Publications, 2021. <a href=\"https://doi.org/10.7554/elife.72676\">https://doi.org/10.7554/elife.72676</a>.","apa":"Choi, J., Lyons, D. B., &#38; Zilberman, D. (2021). Histone H1 prevents non-CG methylation-mediated small RNA biogenesis in Arabidopsis heterochromatin. <i>ELife</i>. eLife Sciences Publications. <a href=\"https://doi.org/10.7554/elife.72676\">https://doi.org/10.7554/elife.72676</a>","ieee":"J. Choi, D. B. Lyons, and D. Zilberman, “Histone H1 prevents non-CG methylation-mediated small RNA biogenesis in Arabidopsis heterochromatin,” <i>eLife</i>, vol. 10. eLife Sciences Publications, 2021."},"oa_version":"Published Version","date_updated":"2023-08-17T06:21:08Z","status":"public","month":"12","isi":1,"ddc":["570"],"file":[{"file_id":"11384","creator":"dernst","checksum":"22ed4c55fb550f6da02ae55c359be651","date_created":"2022-05-16T10:42:22Z","access_level":"open_access","file_name":"2021_eLife_Choi.pdf","success":1,"file_size":2715200,"date_updated":"2022-05-16T10:42:22Z","content_type":"application/pdf","relation":"main_file"}],"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)"},"scopus_import":"1","external_id":{"isi":["000754832000001"],"pmid":["34850679"]},"date_created":"2021-12-10T13:12:08Z","publication_status":"published","abstract":[{"text":"Flowering plants utilize small RNA molecules to guide DNA methyltransferases to genomic sequences. This RNA-directed DNA methylation (RdDM) pathway preferentially targets euchromatic transposable elements. However, RdDM is thought to be recruited by methylation of histone H3 at lysine 9 (H3K9me), a hallmark of heterochromatin. How RdDM is targeted to euchromatin despite an affinity for H3K9me is unclear. Here we show that loss of histone H1 enhances heterochromatic RdDM, preferentially at nucleosome linker DNA. Surprisingly, this does not require SHH1, the RdDM component that binds H3K9me. Furthermore, H3K9me is dispensable for RdDM, as is CG DNA methylation. Instead, we find that non-CG methylation is specifically associated with small RNA biogenesis, and without H1 small RNA production quantitatively expands to non-CG methylated loci. Our results demonstrate that H1 enforces the separation of euchromatic and heterochromatic DNA methylation pathways by excluding the small RNA-generating branch of RdDM from non-CG methylated heterochromatin.","lang":"eng"}],"file_date_updated":"2022-05-16T10:42:22Z","quality_controlled":"1","_id":"10533","author":[{"full_name":"Choi, Jaemyung","first_name":"Jaemyung","last_name":"Choi"},{"last_name":"Lyons","full_name":"Lyons, David B","first_name":"David B"},{"last_name":"Zilberman","orcid":"0000-0002-0123-8649","first_name":"Daniel","full_name":"Zilberman, Daniel","id":"6973db13-dd5f-11ea-814e-b3e5455e9ed1"}],"volume":10,"date_published":"2021-12-01T00:00:00Z","intvolume":"        10"},{"title":"Cul3 regulates cytoskeleton protein homeostasis and cell migration during a critical window of brain development","acknowledgement":"We thank A. Coll Manzano, F. Freeman, M. Ladron de Guevara, and A. Ç. Yahya for technical assistance, S. Deixler, A. Lepold, and A. Schlerka for the management of our animal colony, as well as M. Schunn and the Preclinical Facility team for technical assistance. We thank K. Heesom and her team at the University of Bristol Proteomics Facility for the proteomics sample preparation, data generation, and analysis support. We thank Y. B. Simon for kindly providing the plasmid for lentiviral labeling. Further, we thank M. Sixt for his advice regarding cell migration and the fruitful discussions. This work was supported by the ISTPlus postdoctoral fellowship (Grant Agreement No. 754411) to B.B., by the European Union’s Horizon 2020 research and innovation program (ERC) grant 715508 (REVERSEAUTISM), and by the Austrian Science Fund (FWF) to G.N. (DK W1232-B24 and SFB F7807-B) and to J.G.D (I3600-B27).","project":[{"grant_number":"754411","_id":"260C2330-B435-11E9-9278-68D0E5697425","name":"ISTplus - Postdoctoral Fellowships","call_identifier":"H2020"},{"grant_number":"715508","name":"Probing the Reversibility of Autism Spectrum Disorders by Employing in vivo and in vitro Models","_id":"25444568-B435-11E9-9278-68D0E5697425","call_identifier":"H2020"},{"_id":"2548AE96-B435-11E9-9278-68D0E5697425","name":"Molecular Drug Targets","grant_number":"W1232-B24","call_identifier":"FWF"},{"grant_number":"F07807","name":"Neural stem cells in autism and epilepsy","_id":"05A0D778-7A3F-11EA-A408-12923DDC885E"},{"call_identifier":"FWF","_id":"265CB4D0-B435-11E9-9278-68D0E5697425","name":"Optical control of synaptic function via adhesion molecules","grant_number":"I03600"}],"department":[{"_id":"GaNo"},{"_id":"JoDa"},{"_id":"FlSc"},{"_id":"MiSi"},{"_id":"LifeSc"},{"_id":"Bio"}],"year":"2021","acknowledged_ssus":[{"_id":"PreCl"}],"article_number":"3058","ec_funded":1,"article_type":"original","keyword":["General Biochemistry","Genetics and Molecular Biology"],"oa":1,"publication_identifier":{"eissn":["2041-1723"]},"language":[{"iso":"eng"}],"doi":"10.1038/s41467-021-23123-x","user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","day":"24","publication":"Nature Communications","date_created":"2021-05-28T11:49:46Z","publication_status":"published","external_id":{"isi":["000658769900010"]},"abstract":[{"lang":"eng","text":"De novo loss of function mutations in the ubiquitin ligase-encoding gene Cullin3 lead to autism spectrum disorder (ASD). In mouse, constitutive haploinsufficiency leads to motor coordination deficits as well as ASD-relevant social and cognitive impairments. However, induction of Cul3 haploinsufficiency later in life does not lead to ASD-relevant behaviors, pointing to an important role of Cul3 during a critical developmental window. Here we show that Cul3 is essential to regulate neuronal migration and, therefore, constitutive Cul3 heterozygous mutant mice display cortical lamination abnormalities. At the molecular level, we found that Cul3 controls neuronal migration by tightly regulating the amount of Plastin3 (Pls3), a previously unrecognized player of neural migration. Furthermore, we found that Pls3 cell-autonomously regulates cell migration by regulating actin cytoskeleton organization, and its levels are inversely proportional to neural migration speed. Finally, we provide evidence that cellular phenotypes associated with autism-linked gene haploinsufficiency can be rescued by transcriptional activation of the intact allele in vitro, offering a proof of concept for a potential therapeutic approach for ASDs."}],"file_date_updated":"2021-05-28T12:39:43Z","issue":"1","quality_controlled":"1","_id":"9429","volume":12,"author":[{"last_name":"Morandell","id":"4739D480-F248-11E8-B48F-1D18A9856A87","full_name":"Morandell, Jasmin","first_name":"Jasmin"},{"id":"29A8453C-F248-11E8-B48F-1D18A9856A87","full_name":"Schwarz, Lena A","first_name":"Lena A","last_name":"Schwarz"},{"last_name":"Basilico","first_name":"Bernadette","full_name":"Basilico, Bernadette","orcid":"0000-0003-1843-3173","id":"36035796-5ACA-11E9-A75E-7AF2E5697425"},{"last_name":"Tasciyan","orcid":"0000-0003-1671-393X","id":"4323B49C-F248-11E8-B48F-1D18A9856A87","full_name":"Tasciyan, Saren","first_name":"Saren"},{"last_name":"Dimchev","full_name":"Dimchev, Georgi A","orcid":"0000-0001-8370-6161","first_name":"Georgi A","id":"38C393BE-F248-11E8-B48F-1D18A9856A87"},{"last_name":"Nicolas","id":"2A103192-F248-11E8-B48F-1D18A9856A87","full_name":"Nicolas, Armel","first_name":"Armel"},{"first_name":"Christoph M","full_name":"Sommer, Christoph M","orcid":"0000-0003-1216-9105","id":"4DF26D8C-F248-11E8-B48F-1D18A9856A87","last_name":"Sommer"},{"full_name":"Kreuzinger, Caroline","first_name":"Caroline","id":"382077BA-F248-11E8-B48F-1D18A9856A87","last_name":"Kreuzinger"},{"id":"4C66542E-F248-11E8-B48F-1D18A9856A87","full_name":"Dotter, Christoph","first_name":"Christoph","orcid":"0000-0002-9033-9096","last_name":"Dotter"},{"id":"3B2ABCF4-F248-11E8-B48F-1D18A9856A87","first_name":"Lisa","full_name":"Knaus, Lisa","last_name":"Knaus"},{"last_name":"Dobler","id":"D23090A2-9057-11EA-883A-A8396FC7A38F","full_name":"Dobler, Zoe","first_name":"Zoe"},{"first_name":"Emanuele","full_name":"Cacci, Emanuele","last_name":"Cacci"},{"first_name":"Florian KM","id":"48AD8942-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0003-4790-8078","full_name":"Schur, Florian KM","last_name":"Schur"},{"last_name":"Danzl","id":"42EFD3B6-F248-11E8-B48F-1D18A9856A87","full_name":"Danzl, Johann G","orcid":"0000-0001-8559-3973","first_name":"Johann G"},{"last_name":"Novarino","id":"3E57A680-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-7673-7178","first_name":"Gaia","full_name":"Novarino, Gaia"}],"intvolume":"        12","date_published":"2021-05-24T00:00:00Z","type":"journal_article","article_processing_charge":"No","publisher":"Springer Nature","has_accepted_license":"1","citation":{"ista":"Morandell J, Schwarz LA, Basilico B, Tasciyan S, Dimchev GA, Nicolas A, Sommer CM, Kreuzinger C, Dotter C, Knaus L, Dobler Z, Cacci E, Schur FK, Danzl JG, Novarino G. 2021. Cul3 regulates cytoskeleton protein homeostasis and cell migration during a critical window of brain development. Nature Communications. 12(1), 3058.","ama":"Morandell J, Schwarz LA, Basilico B, et al. Cul3 regulates cytoskeleton protein homeostasis and cell migration during a critical window of brain development. <i>Nature Communications</i>. 2021;12(1). doi:<a href=\"https://doi.org/10.1038/s41467-021-23123-x\">10.1038/s41467-021-23123-x</a>","short":"J. Morandell, L.A. Schwarz, B. Basilico, S. Tasciyan, G.A. Dimchev, A. Nicolas, C.M. Sommer, C. Kreuzinger, C. Dotter, L. Knaus, Z. Dobler, E. Cacci, F.K. Schur, J.G. Danzl, G. Novarino, Nature Communications 12 (2021).","mla":"Morandell, Jasmin, et al. “Cul3 Regulates Cytoskeleton Protein Homeostasis and Cell Migration during a Critical Window of Brain Development.” <i>Nature Communications</i>, vol. 12, no. 1, 3058, Springer Nature, 2021, doi:<a href=\"https://doi.org/10.1038/s41467-021-23123-x\">10.1038/s41467-021-23123-x</a>.","chicago":"Morandell, Jasmin, Lena A Schwarz, Bernadette Basilico, Saren Tasciyan, Georgi A Dimchev, Armel Nicolas, Christoph M Sommer, et al. “Cul3 Regulates Cytoskeleton Protein Homeostasis and Cell Migration during a Critical Window of Brain Development.” <i>Nature Communications</i>. Springer Nature, 2021. <a href=\"https://doi.org/10.1038/s41467-021-23123-x\">https://doi.org/10.1038/s41467-021-23123-x</a>.","ieee":"J. Morandell <i>et al.</i>, “Cul3 regulates cytoskeleton protein homeostasis and cell migration during a critical window of brain development,” <i>Nature Communications</i>, vol. 12, no. 1. Springer Nature, 2021.","apa":"Morandell, J., Schwarz, L. A., Basilico, B., Tasciyan, S., Dimchev, G. A., Nicolas, A., … Novarino, G. (2021). Cul3 regulates cytoskeleton protein homeostasis and cell migration during a critical window of brain development. <i>Nature Communications</i>. Springer Nature. <a href=\"https://doi.org/10.1038/s41467-021-23123-x\">https://doi.org/10.1038/s41467-021-23123-x</a>"},"oa_version":"Published Version","date_updated":"2024-09-10T12:04:26Z","month":"05","status":"public","isi":1,"ddc":["572"],"file":[{"file_id":"9430","creator":"kschuh","checksum":"337e0f7959c35ec959984cacdcb472ba","date_created":"2021-05-28T12:39:43Z","access_level":"open_access","file_name":"2021_NatureCommunications_Morandell.pdf","success":1,"file_size":9358599,"date_updated":"2021-05-28T12:39:43Z","content_type":"application/pdf","relation":"main_file"}],"related_material":{"link":[{"relation":"press_release","url":"https://ist.ac.at/en/news/defective-gene-slows-down-brain-cells/"}],"record":[{"status":"public","id":"7800","relation":"earlier_version"},{"status":"public","relation":"dissertation_contains","id":"12401"}]},"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)"}},{"issue":"1","quality_controlled":"1","_id":"9431","volume":12,"author":[{"last_name":"Obr","full_name":"Obr, Martin","id":"4741CA5A-F248-11E8-B48F-1D18A9856A87","first_name":"Martin"},{"first_name":"Clifton L.","full_name":"Ricana, Clifton L.","last_name":"Ricana"},{"last_name":"Nikulin","full_name":"Nikulin, Nadia","first_name":"Nadia"},{"first_name":"Jon-Philip R.","full_name":"Feathers, Jon-Philip R.","last_name":"Feathers"},{"last_name":"Klanschnig","full_name":"Klanschnig, Marco","first_name":"Marco"},{"full_name":"Thader, Andreas","id":"3A18A7B8-F248-11E8-B48F-1D18A9856A87","first_name":"Andreas","last_name":"Thader"},{"last_name":"Johnson","full_name":"Johnson, Marc C.","first_name":"Marc C."},{"first_name":"Volker M.","full_name":"Vogt, Volker M.","last_name":"Vogt"},{"last_name":"Schur","full_name":"Schur, Florian KM","first_name":"Florian KM","id":"48AD8942-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0003-4790-8078"},{"full_name":"Dick, Robert A.","first_name":"Robert A.","last_name":"Dick"}],"date_published":"2021-05-28T00:00:00Z","intvolume":"        12","scopus_import":"1","date_created":"2021-05-28T14:25:50Z","publication_status":"published","external_id":{"isi":["000659145000011"]},"file_date_updated":"2021-06-09T15:21:14Z","abstract":[{"lang":"eng","text":"Inositol hexakisphosphate (IP6) is an assembly cofactor for HIV-1. We report here that IP6 is also used for assembly of Rous sarcoma virus (RSV), a retrovirus from a different genus. IP6 is ~100-fold more potent at promoting RSV mature capsid protein (CA) assembly than observed for HIV-1 and removal of IP6 in cells reduces infectivity by 100-fold. Here, visualized by cryo-electron tomography and subtomogram averaging, mature capsid-like particles show an IP6-like density in the CA hexamer, coordinated by rings of six lysines and six arginines. Phosphate and IP6 have opposing effects on CA in vitro assembly, inducing formation of T = 1 icosahedrons and tubes, respectively, implying that phosphate promotes pentamer and IP6 hexamer formation. Subtomogram averaging and classification optimized for analysis of pleomorphic retrovirus particles reveal that the heterogeneity of mature RSV CA polyhedrons results from an unexpected, intrinsic CA hexamer flexibility. In contrast, the CA pentamer forms rigid units organizing the local architecture. These different features of hexamers and pentamers determine the structural mechanism to form CA polyhedrons of variable shape in mature RSV particles."}],"oa_version":"Published Version","date_updated":"2023-08-08T13:53:53Z","month":"05","status":"public","isi":1,"ddc":["570"],"file":[{"file_id":"9538","access_level":"open_access","date_created":"2021-06-09T15:21:14Z","checksum":"53ccc53d09a9111143839dbe7784e663","creator":"kschuh","date_updated":"2021-06-09T15:21:14Z","content_type":"application/pdf","success":1,"file_size":6166295,"file_name":"2021_NatureCommunications_Obr.pdf","relation":"main_file"}],"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)"},"related_material":{"link":[{"relation":"press_release","description":"News on IST Homepage","url":"https://ist.ac.at/en/news/how-retroviruses-become-infectious/"}]},"type":"journal_article","article_processing_charge":"No","has_accepted_license":"1","publisher":"Nature Research","citation":{"apa":"Obr, M., Ricana, C. L., Nikulin, N., Feathers, J.-P. R., Klanschnig, M., Thader, A., … Dick, R. A. (2021). Structure of the mature Rous sarcoma virus lattice reveals a role for IP6 in the formation of the capsid hexamer. <i>Nature Communications</i>. Nature Research. <a href=\"https://doi.org/10.1038/s41467-021-23506-0\">https://doi.org/10.1038/s41467-021-23506-0</a>","ieee":"M. Obr <i>et al.</i>, “Structure of the mature Rous sarcoma virus lattice reveals a role for IP6 in the formation of the capsid hexamer,” <i>Nature Communications</i>, vol. 12, no. 1. Nature Research, 2021.","chicago":"Obr, Martin, Clifton L. Ricana, Nadia Nikulin, Jon-Philip R. Feathers, Marco Klanschnig, Andreas Thader, Marc C. Johnson, Volker M. Vogt, Florian KM Schur, and Robert A. Dick. “Structure of the Mature Rous Sarcoma Virus Lattice Reveals a Role for IP6 in the Formation of the Capsid Hexamer.” <i>Nature Communications</i>. Nature Research, 2021. <a href=\"https://doi.org/10.1038/s41467-021-23506-0\">https://doi.org/10.1038/s41467-021-23506-0</a>.","mla":"Obr, Martin, et al. “Structure of the Mature Rous Sarcoma Virus Lattice Reveals a Role for IP6 in the Formation of the Capsid Hexamer.” <i>Nature Communications</i>, vol. 12, no. 1, 3226, Nature Research, 2021, doi:<a href=\"https://doi.org/10.1038/s41467-021-23506-0\">10.1038/s41467-021-23506-0</a>.","short":"M. Obr, C.L. Ricana, N. Nikulin, J.-P.R. Feathers, M. Klanschnig, A. Thader, M.C. Johnson, V.M. Vogt, F.K. Schur, R.A. Dick, Nature Communications 12 (2021).","ista":"Obr M, Ricana CL, Nikulin N, Feathers J-PR, Klanschnig M, Thader A, Johnson MC, Vogt VM, Schur FK, Dick RA. 2021. Structure of the mature Rous sarcoma virus lattice reveals a role for IP6 in the formation of the capsid hexamer. Nature Communications. 12(1), 3226.","ama":"Obr M, Ricana CL, Nikulin N, et al. Structure of the mature Rous sarcoma virus lattice reveals a role for IP6 in the formation of the capsid hexamer. <i>Nature Communications</i>. 2021;12(1). doi:<a href=\"https://doi.org/10.1038/s41467-021-23506-0\">10.1038/s41467-021-23506-0</a>"},"acknowledgement":"This work was funded by the National Institute of Allergy and Infectious Diseases under awards R01AI147890 to R.A.D., R01AI150454 to V.M.V, R35GM136258 in support of J-P.R.F, and the Austrian Science Fund (FWF) grant P31445 to F.K.M.S. Access to high-resolution cryo-ET data acquisition at EMBL Heidelberg was supported by iNEXT (grant no. 653706), funded by the Horizon 2020 program of the European Union (PID 4246). We thank Wim Hagen and Felix Weis at EMBL Heidelberg for support in cryo-ET data acquisition. This work made use of the Cornell Center for Materials Research Shared Facilities, which are supported through the NSF MRSEC program (DMR-179875). This research was also supported by the Scientific Service Units (SSUs) of IST Austria through resources provided by Scientific Computing (SciComp), the Life Science Facility (LSF), and the Electron Microscopy Facility (EMF).","project":[{"call_identifier":"FWF","_id":"26736D6A-B435-11E9-9278-68D0E5697425","name":"Structural conservation and diversity in retroviral capsid","grant_number":"P31445"}],"department":[{"_id":"FlSc"}],"year":"2021","acknowledged_ssus":[{"_id":"ScienComp"},{"_id":"LifeSc"},{"_id":"EM-Fac"}],"title":"Structure of the mature Rous sarcoma virus lattice reveals a role for IP6 in the formation of the capsid hexamer","doi":"10.1038/s41467-021-23506-0","user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","day":"28","publication":"Nature Communications","article_number":"3226","article_type":"original","keyword":["General Biochemistry","Genetics and Molecular Biology","General Physics and Astronomy","General Chemistry"],"oa":1,"publication_identifier":{"eissn":["2041-1723"]},"language":[{"iso":"eng"}]}]