[{"citation":{"apa":"Fernandes Redondo, R. A., de Vladar, H., Włodarski, T., &#38; Bollback, J. P. (2016). Data from evolutionary interplay between structure, energy and epistasis in the coat protein of the ϕX174 phage family. The Royal Society. <a href=\"https://doi.org/10.6084/m9.figshare.4315652.v1\">https://doi.org/10.6084/m9.figshare.4315652.v1</a>","ama":"Fernandes Redondo RA, de Vladar H, Włodarski T, Bollback JP. Data from evolutionary interplay between structure, energy and epistasis in the coat protein of the ϕX174 phage family. 2016. doi:<a href=\"https://doi.org/10.6084/m9.figshare.4315652.v1\">10.6084/m9.figshare.4315652.v1</a>","chicago":"Fernandes Redondo, Rodrigo A, Harold de Vladar, Tomasz Włodarski, and Jonathan P Bollback. “Data from Evolutionary Interplay between Structure, Energy and Epistasis in the Coat Protein of the ΦX174 Phage Family.” The Royal Society, 2016. <a href=\"https://doi.org/10.6084/m9.figshare.4315652.v1\">https://doi.org/10.6084/m9.figshare.4315652.v1</a>.","ista":"Fernandes Redondo RA, de Vladar H, Włodarski T, Bollback JP. 2016. Data from evolutionary interplay between structure, energy and epistasis in the coat protein of the ϕX174 phage family, The Royal Society, <a href=\"https://doi.org/10.6084/m9.figshare.4315652.v1\">10.6084/m9.figshare.4315652.v1</a>.","mla":"Fernandes Redondo, Rodrigo A., et al. <i>Data from Evolutionary Interplay between Structure, Energy and Epistasis in the Coat Protein of the ΦX174 Phage Family</i>. The Royal Society, 2016, doi:<a href=\"https://doi.org/10.6084/m9.figshare.4315652.v1\">10.6084/m9.figshare.4315652.v1</a>.","ieee":"R. A. Fernandes Redondo, H. de Vladar, T. Włodarski, and J. P. Bollback, “Data from evolutionary interplay between structure, energy and epistasis in the coat protein of the ϕX174 phage family.” The Royal Society, 2016.","short":"R.A. Fernandes Redondo, H. de Vladar, T. Włodarski, J.P. Bollback, (2016)."},"fulldoi":"https://doi.org/10.6084/m9.figshare.4315652.v1","main_file_link":[{"url":"https://doi.org/10.6084/m9.figshare.4315652.v1","open_access":"1"}],"month":"12","oa":1,"article_processing_charge":"No","status":"public","publisher":"The Royal Society","date_created":"2021-08-10T08:29:47Z","type":"research_data_reference","date_published":"2016-12-14T00:00:00Z","date_updated":"2026-08-27T12:09:34Z","department":[{"_id":"NiBa"},{"_id":"JoBo"}],"doi":"10.6084/m9.figshare.4315652.v1","_id":"9864","year":"2016","day":"14","title":"Data from evolutionary interplay between structure, energy and epistasis in the coat protein of the ϕX174 phage family","user_id":"317138e5-6ab7-11ef-aa6d-ffef3953e345","author":[{"full_name":"Fernandes Redondo, Rodrigo A","last_name":"Fernandes Redondo","first_name":"Rodrigo A","id":"409D5C96-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-5837-2793"},{"orcid":"0000-0002-5985-7653","id":"2A181218-F248-11E8-B48F-1D18A9856A87","first_name":"Harold","last_name":"de Vladar","full_name":"de Vladar, Harold"},{"full_name":"Włodarski, Tomasz","last_name":"Włodarski","first_name":"Tomasz"},{"first_name":"Jonathan P","full_name":"Bollback, Jonathan P","last_name":"Bollback","orcid":"0000-0002-4624-4612","id":"2C6FA9CC-F248-11E8-B48F-1D18A9856A87"}],"related_material":{"record":[{"relation":"used_in_publication","status":"public","id":"1077"}]},"oa_version":"Published Version","abstract":[{"text":"Viral capsids are structurally constrained by interactions among the amino acids (AAs) of their constituent proteins. Therefore, epistasis is expected to evolve among physically interacting sites and to influence the rates of substitution. To study the evolution of epistasis, we focused on the major structural protein of the ϕX174 phage family by, first, reconstructing the ancestral protein sequences of 18 species using a Bayesian statistical framework. The inferred ancestral reconstruction differed at eight AAs, for a total of 256 possible ancestral haplotypes. For each ancestral haplotype and the extant species, we estimated, in silico, the distribution of free energies and epistasis of the capsid structure. We found that free energy has not significantly increased but epistasis has. We decomposed epistasis up to fifth order and found that higher-order epistasis sometimes compensates pairwise interactions making the free energy seem additive. The dN/dS ratio is low, suggesting strong purifying selection, and that structure is under stabilizing selection. We synthesized phages carrying ancestral haplotypes of the coat protein gene and measured their fitness experimentally. Our findings indicate that stabilizing mutations can have higher fitness, and that fitness optima do not necessarily coincide with energy minima.","lang":"eng"}]},{"fulldoi":"https://doi.org/10.1098/rspb.2016.0811","volume":283,"tmp":{"image":"/images/cc_by.png","short":"CC BY (4.0)","legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)"},"article_processing_charge":"No","oa":1,"publication_status":"published","date_updated":"2026-08-27T12:13:27Z","date_published":"2016-06-29T00:00:00Z","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","year":"2016","external_id":{"isi":["000381247300009"]},"_id":"1262","isi":1,"quality_controlled":"1","publication":"Proceedings of the Royal Society of London Series B Biological Sciences","abstract":[{"lang":"eng","text":"Emerging infectious diseases (EIDs) have contributed significantly to the current biodiversity crisis, leading to widespread epidemics and population loss. Owing to genetic variation in pathogen virulence, a complete understanding of species decline requires the accurate identification and characterization of EIDs. We explore this issue in the Western honeybee, where increasing mortality of populations in the Northern Hemisphere has caused major concern. Specifically, we investigate the importance of genetic identity of the main suspect in mortality, deformed wing virus (DWV), in driving honeybee loss. Using laboratory experiments and a systematic field survey, we demonstrate that an emerging DWV genotype (DWV-B) is more virulent than the established DWV genotype (DWV-A) and is widespread in the landscape. Furthermore, we show in a simple model that colonies infected with DWV-B collapse sooner than colonies infected with DWV-A. We also identify potential for rapid DWV evolution by revealing extensive genome-wide recombination in vivo. The emergence of DWV-B in naive honeybee populations, including via recombination with DWV-A, could be of significant ecological and economic importance. Our findings emphasize that knowledge of pathogen genetic identity and diversity is critical to understanding drivers of species decline."}],"related_material":{"record":[{"status":"public","id":"9704","relation":"research_data"}]},"author":[{"last_name":"Mcmahon","full_name":"Mcmahon, Dino","first_name":"Dino"},{"first_name":"Myrsini","last_name":"Natsopoulou","full_name":"Natsopoulou, Myrsini"},{"last_name":"Doublet","full_name":"Doublet, Vincent","first_name":"Vincent"},{"full_name":"Fürst, Matthias","last_name":"Fürst","first_name":"Matthias","id":"393B1196-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-3712-925X"},{"first_name":"Silvio","full_name":"Weging, Silvio","last_name":"Weging"},{"first_name":"Mark","full_name":"Brown, Mark","last_name":"Brown"},{"first_name":"Andreas","last_name":"Gogol Döring","full_name":"Gogol Döring, Andreas"},{"last_name":"Paxton","full_name":"Paxton, Robert","first_name":"Robert"}],"intvolume":"       283","scopus_import":"1","citation":{"mla":"Mcmahon, Dino, et al. “Elevated Virulence of an Emerging Viral Genotype as a Driver of Honeybee Loss.” <i>Proceedings of the Royal Society of London Series B Biological Sciences</i>, vol. 283, no. 1833, 20160811, Royal Society, 2016, doi:<a href=\"https://doi.org/10.1098/rspb.2016.0811\">10.1098/rspb.2016.0811</a>.","ieee":"D. Mcmahon <i>et al.</i>, “Elevated virulence of an emerging viral genotype as a driver of honeybee loss,” <i>Proceedings of the Royal Society of London Series B Biological Sciences</i>, vol. 283, no. 1833. Royal Society, 2016.","short":"D. Mcmahon, M. Natsopoulou, V. Doublet, M. Fürst, S. Weging, M. Brown, A. Gogol Döring, R. Paxton, Proceedings of the Royal Society of London Series B Biological Sciences 283 (2016).","chicago":"Mcmahon, Dino, Myrsini Natsopoulou, Vincent Doublet, Matthias Fürst, Silvio Weging, Mark Brown, Andreas Gogol Döring, and Robert Paxton. “Elevated Virulence of an Emerging Viral Genotype as a Driver of Honeybee Loss.” <i>Proceedings of the Royal Society of London Series B Biological Sciences</i>. Royal Society, 2016. <a href=\"https://doi.org/10.1098/rspb.2016.0811\">https://doi.org/10.1098/rspb.2016.0811</a>.","apa":"Mcmahon, D., Natsopoulou, M., Doublet, V., Fürst, M., Weging, S., Brown, M., … Paxton, R. (2016). Elevated virulence of an emerging viral genotype as a driver of honeybee loss. <i>Proceedings of the Royal Society of London Series B Biological Sciences</i>. Royal Society. <a href=\"https://doi.org/10.1098/rspb.2016.0811\">https://doi.org/10.1098/rspb.2016.0811</a>","ama":"Mcmahon D, Natsopoulou M, Doublet V, et al. Elevated virulence of an emerging viral genotype as a driver of honeybee loss. <i>Proceedings of the Royal Society of London Series B Biological Sciences</i>. 2016;283(1833). doi:<a href=\"https://doi.org/10.1098/rspb.2016.0811\">10.1098/rspb.2016.0811</a>","ista":"Mcmahon D, Natsopoulou M, Doublet V, Fürst M, Weging S, Brown M, Gogol Döring A, Paxton R. 2016. Elevated virulence of an emerging viral genotype as a driver of honeybee loss. Proceedings of the Royal Society of London Series B Biological Sciences. 283(1833), 20160811."},"month":"06","file_date_updated":"2020-07-14T12:44:42Z","article_number":"20160811","status":"public","ddc":["576","592"],"issue":"1833","publisher":"Royal Society","publist_id":"6060","language":[{"iso":"eng"}],"type":"journal_article","has_accepted_license":"1","pubrep_id":"701","date_created":"2018-12-11T11:51:00Z","file":[{"checksum":"0b0d1be38b497d004064650acb3baced","content_type":"application/pdf","creator":"system","date_created":"2018-12-12T10:08:46Z","access_level":"open_access","relation":"main_file","file_size":796872,"date_updated":"2020-07-14T12:44:42Z","file_name":"IST-2016-701-v1+1_20160811.full.pdf","file_id":"4708"}],"license":"https://creativecommons.org/licenses/by/4.0/","department":[{"_id":"SyCr"}],"doi":"10.1098/rspb.2016.0811","title":"Elevated virulence of an emerging viral genotype as a driver of honeybee loss","day":"29","acknowledgement":"This work was supported by the Federal Ministry of Food, Agriculture and Consumer Protection (Germany): Fit Bee project (grant 511-06.01-28-1-71.007-10), the EU: BeeDoc (grant 244956), iDiv (2013 NGS-Fast Track grant W47004118) and the Insect Pollinators Initiative (IPI grant BB/I000100/1 and BB/I000151/1). The IPI is funded jointly by the Biotechnology and Biological Sciences Research Council, the Department for Environment, Food and Rural Affairs, the Natural Environment Research Council, the Scottish Government and the Wellcome Trust, under the Living with Environmental Change Partnership. We thank A. Abrahams, M. Husemann and A. Soro\r\nfor support in obtaining\r\nV.  destructor\r\n-free honeybees; and BBKA\r\nPresident D. Aston for access to records of colony overwinter\r\n2011–2012 mortality in the UK. We also thank the anonymous refe-\r\nrees and Stephen Martin for comments that led to substantial\r\nimprovement of the manuscript.","oa_version":"Published Version"},{"date_created":"2021-07-23T08:30:38Z","type":"research_data_reference","date_updated":"2026-08-27T12:13:28Z","date_published":"2016-05-06T00:00:00Z","doi":"10.5061/dryad.cq7t1","department":[{"_id":"SyCr"}],"_id":"9704","title":"Data from: Elevated virulence of an emerging viral genotype as a driver of honeybee loss","user_id":"317138e5-6ab7-11ef-aa6d-ffef3953e345","day":"06","year":"2016","oa_version":"Published Version","related_material":{"record":[{"relation":"used_in_publication","status":"public","id":"1262"}]},"author":[{"first_name":"Dino","last_name":"Mcmahon","full_name":"Mcmahon, Dino"},{"full_name":"Natsopoulou, Myrsini","last_name":"Natsopoulou","first_name":"Myrsini"},{"first_name":"Vincent","full_name":"Doublet, Vincent","last_name":"Doublet"},{"last_name":"Fürst","full_name":"Fürst, Matthias","first_name":"Matthias","id":"393B1196-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-3712-925X"},{"last_name":"Weging","full_name":"Weging, Silvio","first_name":"Silvio"},{"full_name":"Brown, Mark","last_name":"Brown","first_name":"Mark"},{"first_name":"Andreas","last_name":"Gogol Döring","full_name":"Gogol Döring, Andreas"},{"first_name":"Robert","full_name":"Paxton, Robert","last_name":"Paxton"}],"abstract":[{"lang":"eng","text":"Emerging infectious diseases (EIDs) have contributed significantly to the current biodiversity crisis, leading to widespread epidemics and population loss. Owing to genetic variation in pathogen virulence, a complete understanding of species decline requires the accurate identification and characterization of EIDs. We explore this issue in the Western honeybee, where increasing mortality of populations in the Northern Hemisphere has caused major concern. Specifically, we investigate the importance of genetic identity of the main suspect in mortality, deformed wing virus (DWV), in driving honeybee loss. Using laboratory experiments and a systematic field survey, we demonstrate that an emerging DWV genotype (DWV-B) is more virulent than the established DWV genotype (DWV-A) and is widespread in the landscape. Furthermore, we show in a simple model that colonies infected with DWV-B collapse sooner than colonies infected with DWV-A. We also identify potential for rapid DWV evolution by revealing extensive genome-wide recombination in vivo. The emergence of DWV-B in naive honeybee populations, including via recombination with DWV-A, could be of significant ecological and economic importance. Our findings emphasize that knowledge of pathogen genetic identity and diversity is critical to understanding drivers of species decline."}],"citation":{"ieee":"D. Mcmahon <i>et al.</i>, “Data from: Elevated virulence of an emerging viral genotype as a driver of honeybee loss.” Dryad, 2016.","short":"D. Mcmahon, M. Natsopoulou, V. Doublet, M. Fürst, S. Weging, M. Brown, A. Gogol Döring, R. Paxton, (2016).","mla":"Mcmahon, Dino, et al. <i>Data from: Elevated Virulence of an Emerging Viral Genotype as a Driver of Honeybee Loss</i>. Dryad, 2016, doi:<a href=\"https://doi.org/10.5061/dryad.cq7t1\">10.5061/dryad.cq7t1</a>.","ista":"Mcmahon D, Natsopoulou M, Doublet V, Fürst M, Weging S, Brown M, Gogol Döring A, Paxton R. 2016. Data from: Elevated virulence of an emerging viral genotype as a driver of honeybee loss, Dryad, <a href=\"https://doi.org/10.5061/dryad.cq7t1\">10.5061/dryad.cq7t1</a>.","chicago":"Mcmahon, Dino, Myrsini Natsopoulou, Vincent Doublet, Matthias Fürst, Silvio Weging, Mark Brown, Andreas Gogol Döring, and Robert Paxton. “Data from: Elevated Virulence of an Emerging Viral Genotype as a Driver of Honeybee Loss.” Dryad, 2016. <a href=\"https://doi.org/10.5061/dryad.cq7t1\">https://doi.org/10.5061/dryad.cq7t1</a>.","apa":"Mcmahon, D., Natsopoulou, M., Doublet, V., Fürst, M., Weging, S., Brown, M., … Paxton, R. (2016). Data from: Elevated virulence of an emerging viral genotype as a driver of honeybee loss. Dryad. <a href=\"https://doi.org/10.5061/dryad.cq7t1\">https://doi.org/10.5061/dryad.cq7t1</a>","ama":"Mcmahon D, Natsopoulou M, Doublet V, et al. Data from: Elevated virulence of an emerging viral genotype as a driver of honeybee loss. 2016. doi:<a href=\"https://doi.org/10.5061/dryad.cq7t1\">10.5061/dryad.cq7t1</a>"},"fulldoi":"https://doi.org/10.5061/dryad.cq7t1","main_file_link":[{"url":"https://doi.org/10.5061/dryad.cq7t1","open_access":"1"}],"month":"05","article_processing_charge":"No","oa":1,"status":"public","publisher":"Dryad"},{"project":[{"name":"International IST Postdoc Fellowship Programme","call_identifier":"FP7","_id":"25681D80-B435-11E9-9278-68D0E5697425","grant_number":"291734"}],"conference":{"start_date":"2016-12-05","end_date":"2016-12-10","location":"Barcelona, Spain","name":"NIPS: Neural Information Processing Systems"},"volume":29,"main_file_link":[{"open_access":"1","url":"https://papers.nips.cc/paper/6582-neurons-equipped-with-intrinsic-plasticity-learn-stimulus-intensity-statistics"}],"article_processing_charge":"No","oa":1,"_id":"948","year":"2016","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","author":[{"last_name":"Monk","full_name":"Monk, Travis","first_name":"Travis"},{"id":"3933349E-F248-11E8-B48F-1D18A9856A87","first_name":"Cristina","full_name":"Savin, Cristina","last_name":"Savin"},{"first_name":"Jörg","full_name":"Lücke, Jörg","last_name":"Lücke"}],"abstract":[{"text":"Experience constantly shapes neural circuits through a variety of plasticity mechanisms. While the functional roles of some plasticity mechanisms are well-understood, it remains unclear how changes in neural excitability contribute to learning. Here, we develop a normative interpretation of intrinsic plasticity (IP) as a key component of unsupervised learning. We introduce a novel generative mixture model that accounts for the class-specific statistics of stimulus intensities, and we derive a neural circuit that learns the input classes and their intensities. We will analytically show that inference and learning for our generative model can be achieved by a neural circuit with intensity-sensitive neurons equipped with a specific form of IP. Numerical experiments verify our analytical derivations and show robust behavior for artificial and natural stimuli. Our results link IP to non-trivial input statistics, in particular the statistics of stimulus intensities for classes to which a neuron is sensitive. More generally, our work paves the way toward new classification algorithms that are robust to intensity variations.","lang":"eng"}],"quality_controlled":"1","publication_status":"published","date_published":"2016-01-01T00:00:00Z","date_updated":"2026-09-17T13:00:27Z","ec_funded":1,"status":"public","publist_id":"6469","publisher":"Neural Information Processing Systems Foundation","citation":{"ista":"Monk T, Savin C, Lücke J. 2016. Neurons equipped with intrinsic plasticity learn stimulus intensity statistics. NIPS: Neural Information Processing Systems, Advances in Neural Information Processing Systems, vol. 29, 4285–4293.","chicago":"Monk, Travis, Cristina Savin, and Jörg Lücke. “Neurons Equipped with Intrinsic Plasticity Learn Stimulus Intensity Statistics,” 29:4285–93. Neural Information Processing Systems Foundation, 2016.","ama":"Monk T, Savin C, Lücke J. Neurons equipped with intrinsic plasticity learn stimulus intensity statistics. In: Vol 29. Neural Information Processing Systems Foundation; 2016:4285-4293.","apa":"Monk, T., Savin, C., &#38; Lücke, J. (2016). Neurons equipped with intrinsic plasticity learn stimulus intensity statistics (Vol. 29, pp. 4285–4293). Presented at the NIPS: Neural Information Processing Systems, Barcelona, Spain: Neural Information Processing Systems Foundation.","ieee":"T. Monk, C. Savin, and J. Lücke, “Neurons equipped with intrinsic plasticity learn stimulus intensity statistics,” presented at the NIPS: Neural Information Processing Systems, Barcelona, Spain, 2016, vol. 29, pp. 4285–4293.","short":"T. Monk, C. Savin, J. Lücke, in:, Neural Information Processing Systems Foundation, 2016, pp. 4285–4293.","mla":"Monk, Travis, et al. <i>Neurons Equipped with Intrinsic Plasticity Learn Stimulus Intensity Statistics</i>. Vol. 29, Neural Information Processing Systems Foundation, 2016, pp. 4285–93."},"scopus_import":"1","intvolume":"        29","month":"01","acknowledgement":"DFG Cluster of Excellence EXC 1077/1 (Hearing4all) and  LU 1196/5-1 (JL and TM), People Programme (Marie Curie Actions) FP7/2007-2013 grant agreement no. 291734 (CS)","day":"01","title":"Neurons equipped with intrinsic plasticity learn stimulus intensity statistics","page":"4285 - 4293","oa_version":"None","alternative_title":["Advances in Neural Information Processing Systems"],"date_created":"2018-12-11T11:49:21Z","type":"conference","language":[{"iso":"eng"}],"department":[{"_id":"GaTk"}]},{"date_created":"2023-05-05T12:54:47Z","type":"conference_abstract","has_accepted_license":"1","publication_status":"published","language":[{"iso":"eng"}],"date_published":"2016-02-24T00:00:00Z","date_updated":"2026-10-14T09:40:16Z","department":[{"_id":"ScienComp"},{"_id":"PeJo"}],"file":[{"success":1,"creator":"dernst","checksum":"4a7b00362e81358d568f5e216fa03c3e","content_type":"application/pdf","access_level":"open_access","date_created":"2023-05-16T07:03:56Z","file_id":"12968","date_updated":"2023-05-16T07:03:56Z","relation":"main_file","file_size":1073523,"file_name":"2016_AHPC_Schloegl.pdf"}],"_id":"12903","day":"24","year":"2016","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","title":"High performance computing at IST Austria: Modelling the human hippocampus","page":"37","author":[{"orcid":"0000-0002-5621-8100","id":"45BF87EE-F248-11E8-B48F-1D18A9856A87","first_name":"Alois","last_name":"Schlögl","full_name":"Schlögl, Alois"},{"first_name":"Stephan","last_name":"Stadlbauer","full_name":"Stadlbauer, Stephan","id":"4D0BC184-F248-11E8-B48F-1D18A9856A87"}],"oa_version":"Published Version","publication":"AHPC16 - Austrian HPC Meeting 2016","quality_controlled":"1","citation":{"apa":"Schlögl, A., &#38; Stadlbauer, S. (2016). High performance computing at IST Austria: Modelling the human hippocampus. In <i>AHPC16 - Austrian HPC Meeting 2016</i> (p. 37). Grundlsee, Austria: VSC - Vienna Scientific Cluster.","ama":"Schlögl A, Stadlbauer S. High performance computing at IST Austria: Modelling the human hippocampus. In: <i>AHPC16 - Austrian HPC Meeting 2016</i>. VSC - Vienna Scientific Cluster; 2016:37.","chicago":"Schlögl, Alois, and Stephan Stadlbauer. “High Performance Computing at IST Austria: Modelling the Human Hippocampus.” In <i>AHPC16 - Austrian HPC Meeting 2016</i>, 37. VSC - Vienna Scientific Cluster, 2016.","ista":"Schlögl A, Stadlbauer S. 2016. High performance computing at IST Austria: Modelling the human hippocampus. AHPC16 - Austrian HPC Meeting 2016. AHPC: Austrian HPC Meeting, 37.","mla":"Schlögl, Alois, and Stephan Stadlbauer. “High Performance Computing at IST Austria: Modelling the Human Hippocampus.” <i>AHPC16 - Austrian HPC Meeting 2016</i>, VSC - Vienna Scientific Cluster, 2016, p. 37.","short":"A. Schlögl, S. Stadlbauer, in:, AHPC16 - Austrian HPC Meeting 2016, VSC - Vienna Scientific Cluster, 2016, p. 37.","ieee":"A. Schlögl and S. Stadlbauer, “High performance computing at IST Austria: Modelling the human hippocampus,” in <i>AHPC16 - Austrian HPC Meeting 2016</i>, Grundlsee, Austria, 2016, p. 37."},"conference":{"start_date":"2016-02-22","end_date":"2016-02-24","location":"Grundlsee, Austria","name":"AHPC: Austrian HPC Meeting"},"corr_author":"1","month":"02","main_file_link":[{"open_access":"1","url":"https://asc.ac.at/fileadmin/user_upload/vsc/conferences/ahpc16/BOOKLET_AHPC16.pdf"}],"article_processing_charge":"No","oa":1,"ddc":["000"],"status":"public","file_date_updated":"2023-05-16T07:03:56Z","publisher":"VSC - Vienna Scientific Cluster"},{"article_processing_charge":"No","oa":1,"tmp":{"image":"/images/cc_by.png","short":"CC BY (4.0)","legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)"},"volume":16,"fulldoi":"https://doi.org/10.1016/j.celrep.2016.06.036","project":[{"name":"Cell- and Tissue Mechanics in Zebrafish Germ Layer Formation","call_identifier":"FWF","grant_number":"T 560-B17","_id":"2529486C-B435-11E9-9278-68D0E5697425"},{"call_identifier":"FWF","name":"Cell Cortex and Germ Layer Formation in Zebrafish Gastrulation","grant_number":"I812-B12","_id":"2527D5CC-B435-11E9-9278-68D0E5697425"},{"grant_number":"303564","_id":"25548C20-B435-11E9-9278-68D0E5697425","call_identifier":"FP7","name":"Microbial Ion Channels for Synthetic Neurobiology"}],"acknowledged_ssus":[{"_id":"SSU"}],"date_updated":"2026-10-31T23:30:34Z","ec_funded":1,"date_published":"2016-07-19T00:00:00Z","publication_status":"published","related_material":{"record":[{"relation":"dissertation_contains","status":"public","id":"961"},{"relation":"dissertation_contains","status":"public","id":"50"}]},"author":[{"id":"3BED66BE-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-6453-8075","last_name":"Sako","full_name":"Sako, Keisuke","first_name":"Keisuke"},{"last_name":"Pradhan","full_name":"Pradhan, Saurabh","first_name":"Saurabh"},{"first_name":"Vanessa","full_name":"Barone, Vanessa","last_name":"Barone","orcid":"0000-0003-2676-3367","id":"419EECCC-F248-11E8-B48F-1D18A9856A87"},{"id":"2A9DB292-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-5409-8571","full_name":"Inglés Prieto, Álvaro","last_name":"Inglés Prieto","first_name":"Álvaro"},{"full_name":"Mueller, Patrick","last_name":"Mueller","first_name":"Patrick"},{"last_name":"Ruprecht","full_name":"Ruprecht, Verena","first_name":"Verena","id":"4D71A03A-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0003-4088-8633"},{"first_name":"Daniel","last_name":"Capek","full_name":"Capek, Daniel","orcid":"0000-0001-5199-9940","id":"31C42484-F248-11E8-B48F-1D18A9856A87"},{"first_name":"Sanjeev","full_name":"Galande, Sanjeev","last_name":"Galande"},{"last_name":"Janovjak","full_name":"Janovjak, Harald L","first_name":"Harald L","id":"33BA6C30-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-8023-9315"},{"id":"39427864-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-0912-4566","last_name":"Heisenberg","full_name":"Heisenberg, Carl-Philipp J","first_name":"Carl-Philipp J"}],"publication":"Cell Reports","quality_controlled":"1","abstract":[{"lang":"eng","text":"During metazoan development, the temporal pattern of morphogen signaling is critical for organizing cell fates in space and time. Yet, tools for temporally controlling morphogen signaling within the embryo are still scarce. Here, we developed a photoactivatable Nodal receptor to determine how the temporal pattern of Nodal signaling affects cell fate specification during zebrafish gastrulation. By using this receptor to manipulate the duration of Nodal signaling in vivo by light, we show that extended Nodal signaling within the organizer promotes prechordal plate specification and suppresses endoderm differentiation. Endoderm differentiation is suppressed by extended Nodal signaling inducing expression of the transcriptional repressor goosecoid (gsc) in prechordal plate progenitors, which in turn restrains Nodal signaling from upregulating the endoderm differentiation gene sox17 within these cells. Thus, optogenetic manipulation of Nodal signaling identifies a critical role of Nodal signaling duration for organizer cell fate specification during gastrulation."}],"external_id":{"isi":["000380264200024"]},"isi":1,"_id":"1100","user_id":"317138e5-6ab7-11ef-aa6d-ffef3953e345","year":"2016","month":"07","scopus_import":"1","citation":{"ieee":"K. Sako <i>et al.</i>, “Optogenetic control of nodal signaling reveals a temporal pattern of nodal signaling regulating cell fate specification during gastrulation,” <i>Cell Reports</i>, vol. 16, no. 3. Cell Press, pp. 866–877, 2016.","short":"K. Sako, S. Pradhan, V. Barone, Á. Inglés Prieto, P. Mueller, V. Ruprecht, D. Capek, S. Galande, H.L. Janovjak, C.-P.J. Heisenberg, Cell Reports 16 (2016) 866–877.","mla":"Sako, Keisuke, et al. “Optogenetic Control of Nodal Signaling Reveals a Temporal Pattern of Nodal Signaling Regulating Cell Fate Specification during Gastrulation.” <i>Cell Reports</i>, vol. 16, no. 3, Cell Press, 2016, pp. 866–77, doi:<a href=\"https://doi.org/10.1016/j.celrep.2016.06.036\">10.1016/j.celrep.2016.06.036</a>.","ista":"Sako K, Pradhan S, Barone V, Inglés Prieto Á, Mueller P, Ruprecht V, Capek D, Galande S, Janovjak HL, Heisenberg C-PJ. 2016. Optogenetic control of nodal signaling reveals a temporal pattern of nodal signaling regulating cell fate specification during gastrulation. Cell Reports. 16(3), 866–877.","ama":"Sako K, Pradhan S, Barone V, et al. Optogenetic control of nodal signaling reveals a temporal pattern of nodal signaling regulating cell fate specification during gastrulation. <i>Cell Reports</i>. 2016;16(3):866-877. doi:<a href=\"https://doi.org/10.1016/j.celrep.2016.06.036\">10.1016/j.celrep.2016.06.036</a>","chicago":"Sako, Keisuke, Saurabh Pradhan, Vanessa Barone, Álvaro Inglés Prieto, Patrick Mueller, Verena Ruprecht, Daniel Capek, Sanjeev Galande, Harald L Janovjak, and Carl-Philipp J Heisenberg. “Optogenetic Control of Nodal Signaling Reveals a Temporal Pattern of Nodal Signaling Regulating Cell Fate Specification during Gastrulation.” <i>Cell Reports</i>. Cell Press, 2016. <a href=\"https://doi.org/10.1016/j.celrep.2016.06.036\">https://doi.org/10.1016/j.celrep.2016.06.036</a>.","apa":"Sako, K., Pradhan, S., Barone, V., Inglés Prieto, Á., Mueller, P., Ruprecht, V., … Heisenberg, C.-P. J. (2016). Optogenetic control of nodal signaling reveals a temporal pattern of nodal signaling regulating cell fate specification during gastrulation. <i>Cell Reports</i>. Cell Press. <a href=\"https://doi.org/10.1016/j.celrep.2016.06.036\">https://doi.org/10.1016/j.celrep.2016.06.036</a>"},"intvolume":"        16","publist_id":"6275","publisher":"Cell Press","ddc":["570","576"],"issue":"3","file_date_updated":"2018-12-12T10:11:04Z","status":"public","file":[{"creator":"system","content_type":"application/pdf","date_created":"2018-12-12T10:11:04Z","access_level":"open_access","file_id":"4857","file_name":"IST-2017-754-v1+1_1-s2.0-S2211124716307768-main.pdf","relation":"main_file","date_updated":"2018-12-12T10:11:04Z","file_size":3921947}],"department":[{"_id":"CaHe"},{"_id":"HaJa"}],"doi":"10.1016/j.celrep.2016.06.036","pubrep_id":"754","date_created":"2018-12-11T11:50:08Z","language":[{"iso":"eng"}],"has_accepted_license":"1","type":"journal_article","oa_version":"Published Version","acknowledgement":"We are grateful to members of the C.-P.H. and H.J. labs for discussions, R. Hauschild and the different Scientific Service Units at IST Austria for technical help, M. Dravecka for performing initial experiments, A. Schier for reading an earlier version of the manuscript, K.W. Rogers for technical help, and C. Hill, A. Bruce, and L. Solnica-Krezel for sending plasmids. This work was supported by grants from the Austrian Science Foundation (FWF): (T560-B17) and (I 812-B12) to V.R. and C.-P.H., and from the European Union (EU FP7): (6275) to H.J. A.I.-P. is supported by a Ramon Areces fellowship.","title":"Optogenetic control of nodal signaling reveals a temporal pattern of nodal signaling regulating cell fate specification during gastrulation","page":"866 - 877","day":"19"},{"user_id":"317138e5-6ab7-11ef-aa6d-ffef3953e345","year":"2016","external_id":{"isi":["000387165600018"]},"isi":1,"_id":"1321","quality_controlled":"1","publication":"Nature Cell Biology","abstract":[{"lang":"eng","text":"Most migrating cells extrude their front by the force of actin polymerization. Polymerization requires an initial nucleation step, which is mediated by factors establishing either parallel filaments in the case of filopodia or branched filaments that form the branched lamellipodial network. Branches are considered essential for regular cell motility and are initiated by the Arp2/3 complex, which in turn is activated by nucleation-promoting factors of the WASP and WAVE families. Here we employed rapid amoeboid crawling leukocytes and found that deletion of the WAVE complex eliminated actin branching and thus lamellipodia formation. The cells were left with parallel filaments at the leading edge, which translated, depending on the differentiation status of the cell, into a unipolar pointed cell shape or cells with multiple filopodia. Remarkably, unipolar cells migrated with increased speed and enormous directional persistence, while they were unable to turn towards chemotactic gradients. Cells with multiple filopodia retained chemotactic activity but their migration was progressively impaired with increasing geometrical complexity of the extracellular environment. These findings establish that diversified leading edge protrusions serve as explorative structures while they slow down actual locomotion."}],"related_material":{"record":[{"relation":"dissertation_contains","status":"public","id":"323"}]},"author":[{"orcid":"0000-0002-1073-744X","id":"3B1B77E4-F248-11E8-B48F-1D18A9856A87","first_name":"Alexander F","full_name":"Leithner, Alexander F","last_name":"Leithner"},{"first_name":"Alexander","last_name":"Eichner","full_name":"Eichner, Alexander","id":"4DFA52AE-F248-11E8-B48F-1D18A9856A87"},{"last_name":"Müller","full_name":"Müller, Jan","first_name":"Jan","id":"AD07FDB4-0F61-11EA-8158-C4CC64CEAA8D"},{"orcid":"0000-0003-0666-8928","id":"35B76592-F248-11E8-B48F-1D18A9856A87","first_name":"Anne","last_name":"Reversat","full_name":"Reversat, Anne"},{"first_name":"Markus","last_name":"Brown","full_name":"Brown, Markus","id":"3DAB9AFC-F248-11E8-B48F-1D18A9856A87"},{"id":"346C1EC6-F248-11E8-B48F-1D18A9856A87","first_name":"Jan","full_name":"Schwarz, Jan","last_name":"Schwarz"},{"first_name":"Jack","full_name":"Merrin, Jack","last_name":"Merrin","orcid":"0000-0001-5145-4609","id":"4515C308-F248-11E8-B48F-1D18A9856A87"},{"first_name":"David","full_name":"De Gorter, David","last_name":"De Gorter"},{"full_name":"Schur, Florian","last_name":"Schur","first_name":"Florian","id":"48AD8942-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0003-4790-8078"},{"last_name":"Bayerl","full_name":"Bayerl, Jonathan","first_name":"Jonathan"},{"first_name":"Ingrid","full_name":"De Vries, Ingrid","last_name":"De Vries","id":"4C7D837E-F248-11E8-B48F-1D18A9856A87"},{"orcid":"0000-0002-2670-2217","id":"355AA5A0-F248-11E8-B48F-1D18A9856A87","first_name":"Stefan","full_name":"Wieser, Stefan","last_name":"Wieser"},{"first_name":"Robert","full_name":"Hauschild, Robert","last_name":"Hauschild","orcid":"0000-0001-9843-3522","id":"4E01D6B4-F248-11E8-B48F-1D18A9856A87"},{"first_name":"Frank","full_name":"Lai, Frank","last_name":"Lai"},{"first_name":"Markus","full_name":"Moser, Markus","last_name":"Moser"},{"first_name":"Dontscho","last_name":"Kerjaschki","full_name":"Kerjaschki, Dontscho"},{"last_name":"Rottner","full_name":"Rottner, Klemens","first_name":"Klemens"},{"full_name":"Small, Victor","last_name":"Small","first_name":"Victor"},{"last_name":"Stradal","full_name":"Stradal, Theresia","first_name":"Theresia"},{"id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-6620-9179","last_name":"Sixt","full_name":"Sixt, Michael K","first_name":"Michael K"}],"article_type":"original","publication_status":"published","date_updated":"2026-10-31T23:30:39Z","ec_funded":1,"date_published":"2016-10-24T00:00:00Z","project":[{"call_identifier":"FP7","name":"Cytoskeletal force generation and force transduction of migrating leukocytes","grant_number":"281556","_id":"25A603A2-B435-11E9-9278-68D0E5697425"}],"acknowledged_ssus":[{"_id":"SSU"}],"fulldoi":"https://doi.org/10.1038/ncb3426","volume":18,"tmp":{"name":"Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC BY-NC-SA 4.0)","legal_code_url":"https://creativecommons.org/licenses/by-nc-sa/4.0/legalcode","image":"/images/cc_by_nc_sa.png","short":"CC BY-NC-SA (4.0)"},"article_processing_charge":"No","oa":1,"title":"Diversified actin protrusions promote environmental exploration but are dispensable for locomotion of leukocytes","page":"1253 - 1259","day":"24","acknowledgement":"This work was supported by the German Research Foundation (DFG) Priority Program SP 1464 to T.E.B.S. and M.S., and European Research Council (ERC GA 281556) and Human Frontiers Program grants to M.S.\r\nService Units of IST Austria for excellent technical support.","oa_version":"Submitted Version","language":[{"iso":"eng"}],"has_accepted_license":"1","type":"journal_article","date_created":"2018-12-11T11:51:21Z","file":[{"creator":"dernst","content_type":"application/pdf","checksum":"e1411cb7c99a2d9089c178a6abef25e7","file_id":"7844","file_name":"2018_NatureCell_Leithner.pdf","relation":"main_file","file_size":4433280,"date_updated":"2020-07-14T12:44:43Z","date_created":"2020-05-14T16:33:46Z","access_level":"open_access"}],"license":"https://creativecommons.org/licenses/by-nc-sa/4.0/","doi":"10.1038/ncb3426","department":[{"_id":"MiSi"},{"_id":"NanoFab"},{"_id":"Bio"}],"file_date_updated":"2020-07-14T12:44:43Z","status":"public","ddc":["570"],"publisher":"Nature Publishing Group","publist_id":"5949","intvolume":"        18","scopus_import":"1","citation":{"short":"A.F. Leithner, A. Eichner, J. Müller, A. Reversat, M. Brown, J. Schwarz, J. Merrin, D. De Gorter, F.K. Schur, J. Bayerl, I. de Vries, S. Wieser, R. Hauschild, F. Lai, M. Moser, D. Kerjaschki, K. Rottner, V. Small, T. Stradal, M.K. Sixt, Nature Cell Biology 18 (2016) 1253–1259.","ieee":"A. F. Leithner <i>et al.</i>, “Diversified actin protrusions promote environmental exploration but are dispensable for locomotion of leukocytes,” <i>Nature Cell Biology</i>, vol. 18. Nature Publishing Group, pp. 1253–1259, 2016.","mla":"Leithner, Alexander F., et al. “Diversified Actin Protrusions Promote Environmental Exploration but Are Dispensable for Locomotion of Leukocytes.” <i>Nature Cell Biology</i>, vol. 18, Nature Publishing Group, 2016, pp. 1253–59, doi:<a href=\"https://doi.org/10.1038/ncb3426\">10.1038/ncb3426</a>.","ista":"Leithner AF, Eichner A, Müller J, Reversat A, Brown M, Schwarz J, Merrin J, De Gorter D, Schur FK, Bayerl J, de Vries I, Wieser S, Hauschild R, Lai F, Moser M, Kerjaschki D, Rottner K, Small V, Stradal T, Sixt MK. 2016. Diversified actin protrusions promote environmental exploration but are dispensable for locomotion of leukocytes. Nature Cell Biology. 18, 1253–1259.","ama":"Leithner AF, Eichner A, Müller J, et al. Diversified actin protrusions promote environmental exploration but are dispensable for locomotion of leukocytes. <i>Nature Cell Biology</i>. 2016;18:1253-1259. doi:<a href=\"https://doi.org/10.1038/ncb3426\">10.1038/ncb3426</a>","chicago":"Leithner, Alexander F, Alexander Eichner, Jan Müller, Anne Reversat, Markus Brown, Jan Schwarz, Jack Merrin, et al. “Diversified Actin Protrusions Promote Environmental Exploration but Are Dispensable for Locomotion of Leukocytes.” <i>Nature Cell Biology</i>. Nature Publishing Group, 2016. <a href=\"https://doi.org/10.1038/ncb3426\">https://doi.org/10.1038/ncb3426</a>.","apa":"Leithner, A. F., Eichner, A., Müller, J., Reversat, A., Brown, M., Schwarz, J., … Sixt, M. K. (2016). Diversified actin protrusions promote environmental exploration but are dispensable for locomotion of leukocytes. <i>Nature Cell Biology</i>. Nature Publishing Group. <a href=\"https://doi.org/10.1038/ncb3426\">https://doi.org/10.1038/ncb3426</a>"},"month":"10","corr_author":"1"},{"publisher":"Cell Press","publist_id":"6170","file_date_updated":"2020-07-14T12:44:37Z","status":"public","ddc":["576","616"],"issue":"6","month":"12","intvolume":"       167","scopus_import":"1","citation":{"short":"D.-C. Tarlungeanu, E. Deliu, C. Dotter, M. Kara, P. Janiesch, M. Scalise, M. Galluccio, M. Tesulov, E. Morelli, F. Sönmez, K. Bilgüvar, R. Ohgaki, Y. Kanai, A. Johansen, S. Esharif, T. Ben Omran, M. Topcu, A. Schlessinger, C. Indiveri, K. Duncan, A. Caglayan, M. Günel, J. Gleeson, G. Novarino, Cell 167 (2016) 1481–1494.","ieee":"D.-C. Tarlungeanu <i>et al.</i>, “Impaired amino acid transport at the blood brain barrier is a cause of autism spectrum disorder,” <i>Cell</i>, vol. 167, no. 6. Cell Press, pp. 1481–1494, 2016.","mla":"Tarlungeanu, Dora-Clara, et al. “Impaired Amino Acid Transport at the Blood Brain Barrier Is a Cause of Autism Spectrum Disorder.” <i>Cell</i>, vol. 167, no. 6, Cell Press, 2016, pp. 1481–94, doi:<a href=\"https://doi.org/10.1016/j.cell.2016.11.013\">10.1016/j.cell.2016.11.013</a>.","ista":"Tarlungeanu D-C, Deliu E, Dotter C, Kara M, Janiesch P, Scalise M, Galluccio M, Tesulov M, Morelli E, Sönmez F, Bilgüvar K, Ohgaki R, Kanai Y, Johansen A, Esharif S, Ben Omran T, Topcu M, Schlessinger A, Indiveri C, Duncan K, Caglayan A, Günel M, Gleeson J, Novarino G. 2016. Impaired amino acid transport at the blood brain barrier is a cause of autism spectrum disorder. Cell. 167(6), 1481–1494.","apa":"Tarlungeanu, D.-C., Deliu, E., Dotter, C., Kara, M., Janiesch, P., Scalise, M., … Novarino, G. (2016). Impaired amino acid transport at the blood brain barrier is a cause of autism spectrum disorder. <i>Cell</i>. Cell Press. <a href=\"https://doi.org/10.1016/j.cell.2016.11.013\">https://doi.org/10.1016/j.cell.2016.11.013</a>","ama":"Tarlungeanu D-C, Deliu E, Dotter C, et al. Impaired amino acid transport at the blood brain barrier is a cause of autism spectrum disorder. <i>Cell</i>. 2016;167(6):1481-1494. doi:<a href=\"https://doi.org/10.1016/j.cell.2016.11.013\">10.1016/j.cell.2016.11.013</a>","chicago":"Tarlungeanu, Dora-Clara, Elena Deliu, Christoph Dotter, Majdi Kara, Philipp Janiesch, Mariafrancesca Scalise, Michele Galluccio, et al. “Impaired Amino Acid Transport at the Blood Brain Barrier Is a Cause of Autism Spectrum Disorder.” <i>Cell</i>. Cell Press, 2016. <a href=\"https://doi.org/10.1016/j.cell.2016.11.013\">https://doi.org/10.1016/j.cell.2016.11.013</a>."},"oa_version":"Submitted Version","page":"1481 - 1494","title":"Impaired amino acid transport at the blood brain barrier is a cause of autism spectrum disorder","day":"01","acknowledgement":"This work was supported by NICHD (P01HD070494) and SFARI (grant 275275) to J.G.G., and FWF (SFB35_3523) to G.N.\r\nWe thank A.C. Manzano, Mike Liu, and F. Marr for technical assistance, and R. Shigemoto and the IST Austria Electron Microscopy (EM) Facility for assistance. We acknowledge support from CIDR for genome-wide SNP analysis (X01HG008823) and Broad Institute Center for Mendelian Disorders (UM1HG008900 to D. MacArthur), the Yale Center for Mendelian Disorders (U54HG006504 to M.G.), the Gregory M. Kiez and Mehmet Kutman Foundation (M.G.), Italian Ministry of Instruction University and Research (PON01_00937 to C.I.), and NIH (R01-GM108911 to A.S.). This work was supported by NICHD (P01HD070494) and SFARI (grant 275275) to J.G.G., and FWF (SFB35_3523) to G.N.\r\n\r\n#EMFacility","file":[{"creator":"system","content_type":"application/pdf","checksum":"7fe01ab12a6610d3db421e0136db2f77","date_created":"2018-12-12T10:13:44Z","access_level":"open_access","file_id":"5030","file_name":"IST-2017-771-v1+1_Tarlungeanu_et_al._Final_edited.pdf","file_size":73907957,"date_updated":"2020-07-14T12:44:37Z","relation":"main_file"}],"department":[{"_id":"GaNo"}],"doi":"10.1016/j.cell.2016.11.013","language":[{"iso":"eng"}],"has_accepted_license":"1","type":"journal_article","pubrep_id":"771","date_created":"2018-12-11T11:50:35Z","project":[{"name":"Transmembrane Transporters in Health and Disease","call_identifier":"FWF","_id":"25473368-B435-11E9-9278-68D0E5697425","grant_number":"F03523"}],"oa":1,"article_processing_charge":"No","volume":167,"fulldoi":"https://doi.org/10.1016/j.cell.2016.11.013","publication":"Cell","quality_controlled":"1","abstract":[{"text":"Autism spectrum disorders (ASD) are a group of genetic disorders often overlapping with other neurological conditions. We previously described abnormalities in the branched-chain amino acid (BCAA) catabolic pathway as a cause of ASD. Here, we show that the solute carrier transporter 7a5 (SLC7A5), a large neutral amino acid transporter localized at the blood brain barrier (BBB), has an essential role in maintaining normal levels of brain BCAAs. In mice, deletion of Slc7a5 from the endothelial cells of the BBB leads to atypical brain amino acid profile, abnormal mRNA translation, and severe neurological abnormalities. Furthermore, we identified several patients with autistic traits and motor delay carrying deleterious homozygous mutations in the SLC7A5 gene. Finally, we demonstrate that BCAA intracerebroventricular administration ameliorates abnormal behaviors in adult mutant mice. Our data elucidate a neurological syndrome defined by SLC7A5 mutations and support an essential role for the BCAA in human brain function.","lang":"eng"}],"related_material":{"record":[{"relation":"dissertation_contains","id":"395","status":"public"}]},"author":[{"id":"2ABCE612-F248-11E8-B48F-1D18A9856A87","full_name":"Tarlungeanu, Dora-Clara","last_name":"Tarlungeanu","first_name":"Dora-Clara"},{"first_name":"Elena","full_name":"Deliu, Elena","last_name":"Deliu","orcid":"0000-0002-7370-5293","id":"37A40D7E-F248-11E8-B48F-1D18A9856A87"},{"last_name":"Dotter","full_name":"Dotter, Christoph","first_name":"Christoph","id":"4C66542E-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-9033-9096"},{"last_name":"Kara","full_name":"Kara, Majdi","first_name":"Majdi"},{"full_name":"Janiesch, Philipp","last_name":"Janiesch","first_name":"Philipp"},{"last_name":"Scalise","full_name":"Scalise, Mariafrancesca","first_name":"Mariafrancesca"},{"first_name":"Michele","full_name":"Galluccio, Michele","last_name":"Galluccio"},{"last_name":"Tesulov","full_name":"Tesulov, Mateja","first_name":"Mateja"},{"id":"3F4D1282-F248-11E8-B48F-1D18A9856A87","first_name":"Emanuela","last_name":"Morelli","full_name":"Morelli, Emanuela"},{"full_name":"Sönmez, Fatma","last_name":"Sönmez","first_name":"Fatma"},{"first_name":"Kaya","last_name":"Bilgüvar","full_name":"Bilgüvar, Kaya"},{"full_name":"Ohgaki, Ryuichi","last_name":"Ohgaki","first_name":"Ryuichi"},{"last_name":"Kanai","full_name":"Kanai, Yoshikatsu","first_name":"Yoshikatsu"},{"first_name":"Anide","full_name":"Johansen, Anide","last_name":"Johansen"},{"full_name":"Esharif, Seham","last_name":"Esharif","first_name":"Seham"},{"first_name":"Tawfeg","full_name":"Ben Omran, Tawfeg","last_name":"Ben Omran"},{"last_name":"Topcu","full_name":"Topcu, Meral","first_name":"Meral"},{"first_name":"Avner","full_name":"Schlessinger, Avner","last_name":"Schlessinger"},{"last_name":"Indiveri","full_name":"Indiveri, Cesare","first_name":"Cesare"},{"full_name":"Duncan, Kent","last_name":"Duncan","first_name":"Kent"},{"first_name":"Ahmet","full_name":"Caglayan, Ahmet","last_name":"Caglayan"},{"first_name":"Murat","full_name":"Günel, Murat","last_name":"Günel"},{"full_name":"Gleeson, Joseph","last_name":"Gleeson","first_name":"Joseph"},{"first_name":"Gaia","last_name":"Novarino","full_name":"Novarino, Gaia","orcid":"0000-0002-7673-7178","id":"3E57A680-F248-11E8-B48F-1D18A9856A87"}],"article_type":"original","user_id":"317138e5-6ab7-11ef-aa6d-ffef3953e345","year":"2016","external_id":{"isi":["000389470500012"]},"_id":"1183","isi":1,"date_updated":"2026-10-31T23:30:39Z","date_published":"2016-12-01T00:00:00Z","publication_status":"published"},{"project":[{"_id":"25832EC2-B435-11E9-9278-68D0E5697425","grant_number":"S 11407_N23","name":"Rigorous Systems Engineering","call_identifier":"FWF"},{"name":"Quantitative Graph Games: Theory and Applications","call_identifier":"FP7","grant_number":"279307","_id":"2581B60A-B435-11E9-9278-68D0E5697425"}],"conference":{"name":"POPL: Principles of Programming Languages","location":"St. Petersburg, FL, USA","end_date":"2016-01-22","start_date":"2016-01-20"},"volume":"20-22","fulldoi":"https://doi.org/10.1145/2837614.2837624","main_file_link":[{"open_access":"1","url":"http://arxiv.org/abs/1510.07565"}],"oa":1,"_id":"1437","external_id":{"arxiv":["1510.07565"]},"year":"2016","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","author":[{"orcid":"0000-0002-4561-241X","id":"2E5DCA20-F248-11E8-B48F-1D18A9856A87","first_name":"Krishnendu","full_name":"Chatterjee, Krishnendu","last_name":"Chatterjee"},{"first_name":"Amir","full_name":"Goharshady, Amir","last_name":"Goharshady","orcid":"0000-0003-1702-6584","id":"391365CE-F248-11E8-B48F-1D18A9856A87"},{"id":"3B699956-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0003-4783-0389","last_name":"Ibsen-Jensen","full_name":"Ibsen-Jensen, Rasmus","first_name":"Rasmus"},{"full_name":"Pavlogiannis, Andreas","last_name":"Pavlogiannis","first_name":"Andreas","id":"49704004-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-8943-0722"}],"related_material":{"record":[{"relation":"earlier_version","status":"public","id":"5441"},{"relation":"earlier_version","status":"public","id":"5442"},{"relation":"later_version","id":"6009","status":"public"},{"id":"821","status":"public","relation":"dissertation_contains"},{"relation":"dissertation_contains","id":"8934","status":"public"}]},"abstract":[{"text":"We study algorithmic questions for concurrent systems where the transitions are labeled from a complete, closed semiring, and path properties are algebraic with semiring operations. The algebraic path properties can model dataflow analysis problems, the shortest path problem, and many other natural problems that arise in program analysis. We consider that each component of the concurrent system is a graph with constant treewidth, a property satisfied by the controlflow graphs of most programs. We allow for multiple possible queries, which arise naturally in demand driven dataflow analysis. The study of multiple queries allows us to consider the tradeoff between the resource usage of the one-time preprocessing and for each individual query. The traditional approach constructs the product graph of all components and applies the best-known graph algorithm on the product. In this approach, even the answer to a single query requires the transitive closure (i.e., the results of all possible queries), which provides no room for tradeoff between preprocessing and query time. Our main contributions are algorithms that significantly improve the worst-case running time of the traditional approach, and provide various tradeoffs depending on the number of queries. For example, in a concurrent system of two components, the traditional approach requires hexic time in the worst case for answering one query as well as computing the transitive closure, whereas we show that with one-time preprocessing in almost cubic time, each subsequent query can be answered in at most linear time, and even the transitive closure can be computed in almost quartic time. Furthermore, we establish conditional optimality results showing that the worst-case running time of our algorithms cannot be improved without achieving major breakthroughs in graph algorithms (i.e., improving the worst-case bound for the shortest path problem in general graphs). Preliminary experimental results show that our algorithms perform favorably on several benchmarks.","lang":"eng"}],"quality_controlled":"1","publication_status":"published","date_published":"2016-01-11T00:00:00Z","ec_funded":1,"date_updated":"2026-10-31T23:30:48Z","status":"public","arxiv":1,"publist_id":"5761","publisher":"ACM","citation":{"mla":"Chatterjee, Krishnendu, et al. <i>Algorithms for Algebraic Path Properties in Concurrent Systems of Constant Treewidth Components</i>. Vol. 20–22, ACM, 2016, pp. 733–47, doi:<a href=\"https://doi.org/10.1145/2837614.2837624\">10.1145/2837614.2837624</a>.","ieee":"K. Chatterjee, A. K. Goharshady, R. Ibsen-Jensen, and A. Pavlogiannis, “Algorithms for algebraic path properties in concurrent systems of constant treewidth components,” presented at the POPL: Principles of Programming Languages, St. Petersburg, FL, USA, 2016, vol. 20–22, pp. 733–747.","short":"K. Chatterjee, A.K. Goharshady, R. Ibsen-Jensen, A. Pavlogiannis, in:, ACM, 2016, pp. 733–747.","ama":"Chatterjee K, Goharshady AK, Ibsen-Jensen R, Pavlogiannis A. Algorithms for algebraic path properties in concurrent systems of constant treewidth components. In: Vol 20-22. ACM; 2016:733-747. doi:<a href=\"https://doi.org/10.1145/2837614.2837624\">10.1145/2837614.2837624</a>","apa":"Chatterjee, K., Goharshady, A. K., Ibsen-Jensen, R., &#38; Pavlogiannis, A. (2016). Algorithms for algebraic path properties in concurrent systems of constant treewidth components (Vol. 20–22, pp. 733–747). Presented at the POPL: Principles of Programming Languages, St. Petersburg, FL, USA: ACM. <a href=\"https://doi.org/10.1145/2837614.2837624\">https://doi.org/10.1145/2837614.2837624</a>","chicago":"Chatterjee, Krishnendu, Amir Kafshdar Goharshady, Rasmus Ibsen-Jensen, and Andreas Pavlogiannis. “Algorithms for Algebraic Path Properties in Concurrent Systems of Constant Treewidth Components,” 20–22:733–47. ACM, 2016. <a href=\"https://doi.org/10.1145/2837614.2837624\">https://doi.org/10.1145/2837614.2837624</a>.","ista":"Chatterjee K, Goharshady AK, Ibsen-Jensen R, Pavlogiannis A. 2016. Algorithms for algebraic path properties in concurrent systems of constant treewidth components. POPL: Principles of Programming Languages, POPL, vol. 20–22, 733–747."},"scopus_import":1,"corr_author":"1","month":"01","day":"11","page":"733 - 747","title":"Algorithms for algebraic path properties in concurrent systems of constant treewidth components","oa_version":"Preprint","date_created":"2018-12-11T11:52:01Z","alternative_title":["POPL"],"type":"conference","language":[{"iso":"eng"}],"doi":"10.1145/2837614.2837624","department":[{"_id":"KrCh"}]},{"abstract":[{"text":"We consider nondeterministic probabilistic programs with the most basic liveness property of termination. We present efficient methods for termination analysis of nondeterministic probabilistic programs with polynomial guards and assignments. Our approach is through synthesis of polynomial ranking supermartingales, that on one hand significantly generalizes linear ranking supermartingales and on the other hand is a counterpart of polynomial ranking-functions for proving termination of nonprobabilistic programs. The approach synthesizes polynomial ranking-supermartingales through Positivstellensatz's, yielding an efficient method which is not only sound, but also semi-complete over a large subclass of programs. We show experimental results to demonstrate that our approach can handle several classical programs with complex polynomial guards and assignments, and can synthesize efficient quadratic ranking-supermartingales when a linear one does not exist even for simple affine programs.","lang":"eng"}],"quality_controlled":"1","author":[{"id":"2E5DCA20-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-4561-241X","full_name":"Chatterjee, Krishnendu","last_name":"Chatterjee","first_name":"Krishnendu"},{"id":"3AAD03D6-F248-11E8-B48F-1D18A9856A87","full_name":"Fu, Hongfei","last_name":"Fu","first_name":"Hongfei"},{"first_name":"Amir","full_name":"Goharshady, Amir","last_name":"Goharshady","orcid":"0000-0003-1702-6584","id":"391365CE-F248-11E8-B48F-1D18A9856A87"}],"related_material":{"record":[{"status":"public","id":"8934","relation":"dissertation_contains"}]},"year":"2016","user_id":"317138e5-6ab7-11ef-aa6d-ffef3953e345","isi":1,"_id":"1386","external_id":{"isi":["000387731200001"],"arxiv":["1604.07169"]},"date_published":"2016-07-01T00:00:00Z","date_updated":"2026-10-31T23:30:49Z","ec_funded":1,"publication_status":"published","project":[{"name":"Rigorous Systems Engineering","call_identifier":"FWF","_id":"25832EC2-B435-11E9-9278-68D0E5697425","grant_number":"S 11407_N23"},{"grant_number":"279307","_id":"2581B60A-B435-11E9-9278-68D0E5697425","name":"Quantitative Graph Games: Theory and Applications","call_identifier":"FP7"},{"_id":"25EE3708-B435-11E9-9278-68D0E5697425","grant_number":"267989","call_identifier":"FP7","name":"Quantitative Reactive Modeling"}],"article_processing_charge":"No","oa":1,"main_file_link":[{"url":"http://arxiv.org/abs/1604.07169","open_access":"1"}],"fulldoi":"https://doi.org/10.1007/978-3-319-41528-4_1","volume":9779,"conference":{"end_date":"2016-07-23","start_date":"2016-07-17","name":"CAV: Computer Aided Verification","location":"Toronto, Canada"},"oa_version":"Preprint","day":"01","title":"Termination analysis of probabilistic programs through Positivstellensatz's","page":"3 - 22","doi":"10.1007/978-3-319-41528-4_1","department":[{"_id":"KrCh"}],"type":"conference","language":[{"iso":"eng"}],"alternative_title":["LNCS"],"date_created":"2018-12-11T11:51:43Z","publisher":"Springer","publist_id":"5824","status":"public","arxiv":1,"corr_author":"1","month":"07","intvolume":"      9779","citation":{"ista":"Chatterjee K, Fu H, Goharshady AK. 2016. Termination analysis of probabilistic programs through Positivstellensatz’s. CAV: Computer Aided Verification, LNCS, vol. 9779, 3–22.","chicago":"Chatterjee, Krishnendu, Hongfei Fu, and Amir Kafshdar Goharshady. “Termination Analysis of Probabilistic Programs through Positivstellensatz’s,” 9779:3–22. Springer, 2016. <a href=\"https://doi.org/10.1007/978-3-319-41528-4_1\">https://doi.org/10.1007/978-3-319-41528-4_1</a>.","ama":"Chatterjee K, Fu H, Goharshady AK. Termination analysis of probabilistic programs through Positivstellensatz’s. In: Vol 9779. Springer; 2016:3-22. doi:<a href=\"https://doi.org/10.1007/978-3-319-41528-4_1\">10.1007/978-3-319-41528-4_1</a>","apa":"Chatterjee, K., Fu, H., &#38; Goharshady, A. K. (2016). Termination analysis of probabilistic programs through Positivstellensatz’s (Vol. 9779, pp. 3–22). Presented at the CAV: Computer Aided Verification, Toronto, Canada: Springer. <a href=\"https://doi.org/10.1007/978-3-319-41528-4_1\">https://doi.org/10.1007/978-3-319-41528-4_1</a>","short":"K. Chatterjee, H. Fu, A.K. Goharshady, in:, Springer, 2016, pp. 3–22.","ieee":"K. Chatterjee, H. Fu, and A. K. Goharshady, “Termination analysis of probabilistic programs through Positivstellensatz’s,” presented at the CAV: Computer Aided Verification, Toronto, Canada, 2016, vol. 9779, pp. 3–22.","mla":"Chatterjee, Krishnendu, et al. <i>Termination Analysis of Probabilistic Programs through Positivstellensatz’s</i>. Vol. 9779, Springer, 2016, pp. 3–22, doi:<a href=\"https://doi.org/10.1007/978-3-319-41528-4_1\">10.1007/978-3-319-41528-4_1</a>."},"scopus_import":"1"}]