[{"date_updated":"2023-02-23T10:16:13Z","type":"research_data_reference","oa_version":"Published Version","day":"23","year":"2015","citation":{"ista":"Friedlander T, Mayo AE, Tlusty T, Alon U. 2015. Supporting information text, Public Library of Science, 10.1371/journal.pcbi.1004055.s001.","short":"T. Friedlander, A.E. Mayo, T. Tlusty, U. Alon, (2015).","chicago":"Friedlander, Tamar, Avraham E. Mayo, Tsvi Tlusty, and Uri Alon. “Supporting Information Text.” Public Library of Science, 2015. https://doi.org/10.1371/journal.pcbi.1004055.s001.","ama":"Friedlander T, Mayo AE, Tlusty T, Alon U. Supporting information text. 2015. doi:10.1371/journal.pcbi.1004055.s001","ieee":"T. Friedlander, A. E. Mayo, T. Tlusty, and U. Alon, “Supporting information text.” Public Library of Science, 2015.","apa":"Friedlander, T., Mayo, A. E., Tlusty, T., & Alon, U. (2015). Supporting information text. Public Library of Science. https://doi.org/10.1371/journal.pcbi.1004055.s001","mla":"Friedlander, Tamar, et al. Supporting Information Text. Public Library of Science, 2015, doi:10.1371/journal.pcbi.1004055.s001."},"article_processing_charge":"No","author":[{"first_name":"Tamar","last_name":"Friedlander","id":"36A5845C-F248-11E8-B48F-1D18A9856A87","full_name":"Friedlander, Tamar"},{"full_name":"Mayo, Avraham E.","last_name":"Mayo","first_name":"Avraham E."},{"full_name":"Tlusty, Tsvi","last_name":"Tlusty","first_name":"Tsvi"},{"first_name":"Uri","last_name":"Alon","full_name":"Alon, Uri"}],"user_id":"6785fbc1-c503-11eb-8a32-93094b40e1cf","title":"Supporting information text","related_material":{"record":[{"status":"public","relation":"used_in_publication","id":"1827"}]},"doi":"10.1371/journal.pcbi.1004055.s001","department":[{"_id":"GaTk"}],"_id":"9718","publisher":"Public Library of Science","date_published":"2015-03-23T00:00:00Z","date_created":"2021-07-26T08:35:23Z","month":"03","status":"public"},{"publisher":"Dryad","date_published":"2015-12-21T00:00:00Z","status":"public","date_created":"2021-07-26T08:44:04Z","month":"12","day":"21","year":"2015","date_updated":"2023-09-05T13:46:04Z","type":"research_data_reference","oa_version":"Published Version","user_id":"6785fbc1-c503-11eb-8a32-93094b40e1cf","article_processing_charge":"No","author":[{"full_name":"Wielgoss, Sébastien","first_name":"Sébastien","last_name":"Wielgoss"},{"orcid":"0000-0001-5396-4346","full_name":"Bergmiller, Tobias","id":"2C471CFA-F248-11E8-B48F-1D18A9856A87","last_name":"Bergmiller","first_name":"Tobias"},{"last_name":"Bischofberger","first_name":"Anna M.","full_name":"Bischofberger, Anna M."},{"first_name":"Alex R.","last_name":"Hall","full_name":"Hall, Alex R."}],"citation":{"ista":"Wielgoss S, Bergmiller T, Bischofberger AM, Hall AR. 2015. Data from: Adaptation to parasites and costs of parasite resistance in mutator and non-mutator bacteria, Dryad, 10.5061/dryad.cj910.","chicago":"Wielgoss, Sébastien, Tobias Bergmiller, Anna M. Bischofberger, and Alex R. Hall. “Data from: Adaptation to Parasites and Costs of Parasite Resistance in Mutator and Non-Mutator Bacteria.” Dryad, 2015. https://doi.org/10.5061/dryad.cj910.","short":"S. Wielgoss, T. Bergmiller, A.M. Bischofberger, A.R. Hall, (2015).","ieee":"S. Wielgoss, T. Bergmiller, A. M. Bischofberger, and A. R. Hall, “Data from: Adaptation to parasites and costs of parasite resistance in mutator and non-mutator bacteria.” Dryad, 2015.","ama":"Wielgoss S, Bergmiller T, Bischofberger AM, Hall AR. Data from: Adaptation to parasites and costs of parasite resistance in mutator and non-mutator bacteria. 2015. doi:10.5061/dryad.cj910","mla":"Wielgoss, Sébastien, et al. Data from: Adaptation to Parasites and Costs of Parasite Resistance in Mutator and Non-Mutator Bacteria. Dryad, 2015, doi:10.5061/dryad.cj910.","apa":"Wielgoss, S., Bergmiller, T., Bischofberger, A. M., & Hall, A. R. (2015). Data from: Adaptation to parasites and costs of parasite resistance in mutator and non-mutator bacteria. Dryad. https://doi.org/10.5061/dryad.cj910"},"main_file_link":[{"open_access":"1","url":"https://doi.org/10.5061/dryad.cj910"}],"abstract":[{"lang":"eng","text":"Parasitism creates selection for resistance mechanisms in host populations and is hypothesized to promote increased host evolvability. However, the influence of these traits on host evolution when parasites are no longer present is unclear. We used experimental evolution and whole-genome sequencing of Escherichia coli to determine the effects of past and present exposure to parasitic viruses (phages) on the spread of mutator alleles, resistance, and bacterial competitive fitness. We found that mutator alleles spread rapidly during adaptation to any of four different phage species, and this pattern was even more pronounced with multiple phages present simultaneously. However, hypermutability did not detectably accelerate adaptation in the absence of phages and recovery of fitness costs associated with resistance. Several lineages evolved phage resistance through elevated mucoidy, and during subsequent evolution in phage-free conditions they rapidly reverted to nonmucoid, phage-susceptible phenotypes. Genome sequencing revealed that this phenotypic reversion was achieved by additional genetic changes rather than by genotypic reversion of the initial resistance mutations. Insertion sequence (IS) elements played a key role in both the acquisition of resistance and adaptation in the absence of parasites; unlike single nucleotide polymorphisms, IS insertions were not more frequent in mutator lineages. Our results provide a genetic explanation for rapid reversion of mucoidy, a phenotype observed in other bacterial species including human pathogens. Moreover, this demonstrates that the types of genetic change underlying adaptation to fitness costs, and consequently the impact of evolvability mechanisms such as increased point-mutation rates, depend critically on the mechanism of resistance."}],"oa":1,"doi":"10.5061/dryad.cj910","related_material":{"record":[{"relation":"used_in_publication","status":"public","id":"5749"}]},"_id":"9719","department":[{"_id":"CaGu"}],"title":"Data from: Adaptation to parasites and costs of parasite resistance in mutator and non-mutator bacteria"},{"date_updated":"2023-02-23T10:16:22Z","type":"research_data_reference","oa_version":"Published Version","day":"29","year":"2015","citation":{"ieee":"F. Theis, L. V. Ugelvig, C. Marr, and S. Cremer, “Data from: Opposing effects of allogrooming on disease transmission in ant societies.” Dryad, 2015.","ama":"Theis F, Ugelvig LV, Marr C, Cremer S. Data from: Opposing effects of allogrooming on disease transmission in ant societies. 2015. doi:10.5061/dryad.dj2bf","short":"F. Theis, L.V. Ugelvig, C. Marr, S. Cremer, (2015).","chicago":"Theis, Fabian, Line V Ugelvig, Carsten Marr, and Sylvia Cremer. “Data from: Opposing Effects of Allogrooming on Disease Transmission in Ant Societies.” Dryad, 2015. https://doi.org/10.5061/dryad.dj2bf.","ista":"Theis F, Ugelvig LV, Marr C, Cremer S. 2015. Data from: Opposing effects of allogrooming on disease transmission in ant societies, Dryad, 10.5061/dryad.dj2bf.","mla":"Theis, Fabian, et al. Data from: Opposing Effects of Allogrooming on Disease Transmission in Ant Societies. Dryad, 2015, doi:10.5061/dryad.dj2bf.","apa":"Theis, F., Ugelvig, L. V., Marr, C., & Cremer, S. (2015). Data from: Opposing effects of allogrooming on disease transmission in ant societies. Dryad. https://doi.org/10.5061/dryad.dj2bf"},"main_file_link":[{"open_access":"1","url":"https://doi.org/10.5061/dryad.dj2bf"}],"article_processing_charge":"No","user_id":"6785fbc1-c503-11eb-8a32-93094b40e1cf","author":[{"full_name":"Theis, Fabian","first_name":"Fabian","last_name":"Theis"},{"last_name":"Ugelvig","first_name":"Line V","full_name":"Ugelvig, Line V","orcid":"0000-0003-1832-8883","id":"3DC97C8E-F248-11E8-B48F-1D18A9856A87"},{"last_name":"Marr","first_name":"Carsten","full_name":"Marr, Carsten"},{"first_name":"Sylvia","last_name":"Cremer","id":"2F64EC8C-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-2193-3868","full_name":"Cremer, Sylvia"}],"abstract":[{"lang":"eng","text":"To prevent epidemics, insect societies have evolved collective disease defences that are highly effective at curing exposed individuals and limiting disease transmission to healthy group members. Grooming is an important sanitary behaviour—either performed towards oneself (self-grooming) or towards others (allogrooming)—to remove infectious agents from the body surface of exposed individuals, but at the risk of disease contraction by the groomer. We use garden ants (Lasius neglectus) and the fungal pathogen Metarhizium as a model system to study how pathogen presence affects self-grooming and allogrooming between exposed and healthy individuals. We develop an epidemiological SIS model to explore how experimentally observed grooming patterns affect disease spread within the colony, thereby providing a direct link between the expression and direction of sanitary behaviours, and their effects on colony-level epidemiology. We find that fungus-exposed ants increase self-grooming, while simultaneously decreasing allogrooming. This behavioural modulation seems universally adaptive and is predicted to contain disease spread in a great variety of host–pathogen systems. In contrast, allogrooming directed towards pathogen-exposed individuals might both increase and decrease disease risk. Our model reveals that the effect of allogrooming depends on the balance between pathogen infectiousness and efficiency of social host defences, which are likely to vary across host–pathogen systems."}],"title":"Data from: Opposing effects of allogrooming on disease transmission in ant societies","oa":1,"related_material":{"record":[{"id":"1830","relation":"used_in_publication","status":"public"}]},"doi":"10.5061/dryad.dj2bf","department":[{"_id":"SyCr"}],"_id":"9721","publisher":"Dryad","date_published":"2015-12-29T00:00:00Z","date_created":"2021-07-26T09:38:36Z","month":"12","status":"public"},{"citation":{"ama":"Symonova O, Topp C, Edelsbrunner H. Root traits computed by DynamicRoots for the maize root shown in fig 2. 2015. doi:10.1371/journal.pone.0127657.s001","ieee":"O. Symonova, C. Topp, and H. Edelsbrunner, “Root traits computed by DynamicRoots for the maize root shown in fig 2.” Public Library of Science, 2015.","chicago":"Symonova, Olga, Christopher Topp, and Herbert Edelsbrunner. “Root Traits Computed by DynamicRoots for the Maize Root Shown in Fig 2.” Public Library of Science, 2015. https://doi.org/10.1371/journal.pone.0127657.s001.","short":"O. Symonova, C. Topp, H. Edelsbrunner, (2015).","ista":"Symonova O, Topp C, Edelsbrunner H. 2015. Root traits computed by DynamicRoots for the maize root shown in fig 2, Public Library of Science, 10.1371/journal.pone.0127657.s001.","mla":"Symonova, Olga, et al. Root Traits Computed by DynamicRoots for the Maize Root Shown in Fig 2. Public Library of Science, 2015, doi:10.1371/journal.pone.0127657.s001.","apa":"Symonova, O., Topp, C., & Edelsbrunner, H. (2015). Root traits computed by DynamicRoots for the maize root shown in fig 2. Public Library of Science. https://doi.org/10.1371/journal.pone.0127657.s001"},"article_processing_charge":"No","user_id":"6785fbc1-c503-11eb-8a32-93094b40e1cf","author":[{"id":"3C0C7BC6-F248-11E8-B48F-1D18A9856A87","full_name":"Symonova, Olga","first_name":"Olga","last_name":"Symonova"},{"first_name":"Christopher","last_name":"Topp","full_name":"Topp, Christopher"},{"orcid":"0000-0002-9823-6833","full_name":"Edelsbrunner, Herbert","id":"3FB178DA-F248-11E8-B48F-1D18A9856A87","last_name":"Edelsbrunner","first_name":"Herbert"}],"oa_version":"Published Version","type":"research_data_reference","date_updated":"2023-02-23T10:14:42Z","year":"2015","day":"01","title":"Root traits computed by DynamicRoots for the maize root shown in fig 2","_id":"9737","department":[{"_id":"MaJö"},{"_id":"HeEd"}],"doi":"10.1371/journal.pone.0127657.s001","related_material":{"record":[{"id":"1793","relation":"used_in_publication","status":"public"}]},"date_published":"2015-06-01T00:00:00Z","publisher":"Public Library of Science","month":"06","date_created":"2021-07-28T06:20:13Z","status":"public"},{"_id":"9742","department":[{"_id":"SyCr"}],"doi":"10.5061/dryad.7kc79","related_material":{"record":[{"relation":"used_in_publication","status":"public","id":"2161"}]},"oa":1,"title":"Data from: Increased grooming after repeated brood care provides sanitary benefits in a clonal ant","abstract":[{"text":"Repeated pathogen exposure is a common threat in colonies of social insects, posing selection pressures on colony members to respond with improved disease-defense performance. We here tested whether experience gained by repeated tending of low-level fungus-exposed (Metarhizium robertsii) larvae may alter the performance of sanitary brood care in the clonal ant, Platythyrea punctata. We trained ants individually over nine consecutive trials to either sham-treated or fungus-exposed larvae. We then compared the larval grooming behavior of naive and trained ants and measured how effectively they removed infectious fungal conidiospores from the fungus-exposed larvae. We found that the ants changed the duration of larval grooming in response to both, larval treatment and their level of experience: (1) sham-treated larvae received longer grooming than the fungus-exposed larvae and (2) trained ants performed less self-grooming but longer larval grooming than naive ants, which was true for both, ants trained to fungus-exposed and also to sham-treated larvae. Ants that groomed the fungus-exposed larvae for longer periods removed a higher number of fungal conidiospores from the surface of the fungus-exposed larvae. As experienced ants performed longer larval grooming, they were more effective in fungal removal, thus making them better caretakers under pathogen attack of the colony. By studying this clonal ant, we can thus conclude that even in the absence of genetic variation between colony members, differences in experience levels of brood care may affect performance of sanitary brood care in social insects.","lang":"eng"}],"author":[{"last_name":"Westhus","first_name":"Claudia","full_name":"Westhus, Claudia"},{"first_name":"Line V","last_name":"Ugelvig","orcid":"0000-0003-1832-8883","full_name":"Ugelvig, Line V","id":"3DC97C8E-F248-11E8-B48F-1D18A9856A87"},{"first_name":"Edouard","last_name":"Tourdot","full_name":"Tourdot, Edouard"},{"last_name":"Heinze","first_name":"Jürgen","full_name":"Heinze, Jürgen"},{"full_name":"Doums, Claudie","first_name":"Claudie","last_name":"Doums"},{"id":"2F64EC8C-F248-11E8-B48F-1D18A9856A87","full_name":"Cremer, Sylvia","orcid":"0000-0002-2193-3868","last_name":"Cremer","first_name":"Sylvia"}],"article_processing_charge":"No","user_id":"6785fbc1-c503-11eb-8a32-93094b40e1cf","main_file_link":[{"url":"https://doi.org/10.5061/dryad.7kc79","open_access":"1"}],"citation":{"ista":"Westhus C, Ugelvig LV, Tourdot E, Heinze J, Doums C, Cremer S. 2015. Data from: Increased grooming after repeated brood care provides sanitary benefits in a clonal ant, Dryad, 10.5061/dryad.7kc79.","short":"C. Westhus, L.V. Ugelvig, E. Tourdot, J. Heinze, C. Doums, S. Cremer, (2015).","chicago":"Westhus, Claudia, Line V Ugelvig, Edouard Tourdot, Jürgen Heinze, Claudie Doums, and Sylvia Cremer. “Data from: Increased Grooming after Repeated Brood Care Provides Sanitary Benefits in a Clonal Ant.” Dryad, 2015. https://doi.org/10.5061/dryad.7kc79.","ieee":"C. Westhus, L. V. Ugelvig, E. Tourdot, J. Heinze, C. Doums, and S. Cremer, “Data from: Increased grooming after repeated brood care provides sanitary benefits in a clonal ant.” Dryad, 2015.","ama":"Westhus C, Ugelvig LV, Tourdot E, Heinze J, Doums C, Cremer S. Data from: Increased grooming after repeated brood care provides sanitary benefits in a clonal ant. 2015. doi:10.5061/dryad.7kc79","mla":"Westhus, Claudia, et al. Data from: Increased Grooming after Repeated Brood Care Provides Sanitary Benefits in a Clonal Ant. Dryad, 2015, doi:10.5061/dryad.7kc79.","apa":"Westhus, C., Ugelvig, L. V., Tourdot, E., Heinze, J., Doums, C., & Cremer, S. (2015). Data from: Increased grooming after repeated brood care provides sanitary benefits in a clonal ant. Dryad. https://doi.org/10.5061/dryad.7kc79"},"year":"2015","day":"09","oa_version":"Published Version","date_updated":"2023-02-23T10:30:52Z","type":"research_data_reference","status":"public","month":"07","date_created":"2021-07-28T08:52:53Z","date_published":"2015-07-09T00:00:00Z","publisher":"Dryad"},{"_id":"9765","department":[{"_id":"ToBo"}],"doi":"10.1371/journal.pbio.1002299.s008","related_material":{"record":[{"relation":"used_in_publication","status":"public","id":"1619"}]},"title":"Gene ontology enrichment analysis for the most sensitive gene deletion strains for all drugs","user_id":"6785fbc1-c503-11eb-8a32-93094b40e1cf","author":[{"first_name":"Guillaume","last_name":"Chevereau","full_name":"Chevereau, Guillaume","id":"424D78A0-F248-11E8-B48F-1D18A9856A87"},{"last_name":"Lukacisinova","first_name":"Marta","full_name":"Lukacisinova, Marta","orcid":"0000-0002-2519-8004","id":"4342E402-F248-11E8-B48F-1D18A9856A87"},{"first_name":"Tugce","last_name":"Batur","full_name":"Batur, Tugce"},{"first_name":"Aysegul","last_name":"Guvenek","full_name":"Guvenek, Aysegul"},{"full_name":"Ayhan, Dilay Hazal","last_name":"Ayhan","first_name":"Dilay Hazal"},{"full_name":"Toprak, Erdal","last_name":"Toprak","first_name":"Erdal"},{"full_name":"Bollenbach, Mark Tobias","orcid":"0000-0003-4398-476X","id":"3E6DB97A-F248-11E8-B48F-1D18A9856A87","last_name":"Bollenbach","first_name":"Mark Tobias"}],"article_processing_charge":"No","citation":{"mla":"Chevereau, Guillaume, et al. Gene Ontology Enrichment Analysis for the Most Sensitive Gene Deletion Strains for All Drugs. Public Library of Science, 2015, doi:10.1371/journal.pbio.1002299.s008.","apa":"Chevereau, G., Lukacisinova, M., Batur, T., Guvenek, A., Ayhan, D. H., Toprak, E., & Bollenbach, M. T. (2015). Gene ontology enrichment analysis for the most sensitive gene deletion strains for all drugs. Public Library of Science. https://doi.org/10.1371/journal.pbio.1002299.s008","short":"G. Chevereau, M. Lukacisinova, T. Batur, A. Guvenek, D.H. Ayhan, E. Toprak, M.T. Bollenbach, (2015).","chicago":"Chevereau, Guillaume, Marta Lukacisinova, Tugce Batur, Aysegul Guvenek, Dilay Hazal Ayhan, Erdal Toprak, and Mark Tobias Bollenbach. “Gene Ontology Enrichment Analysis for the Most Sensitive Gene Deletion Strains for All Drugs.” Public Library of Science, 2015. https://doi.org/10.1371/journal.pbio.1002299.s008.","ista":"Chevereau G, Lukacisinova M, Batur T, Guvenek A, Ayhan DH, Toprak E, Bollenbach MT. 2015. Gene ontology enrichment analysis for the most sensitive gene deletion strains for all drugs, Public Library of Science, 10.1371/journal.pbio.1002299.s008.","ieee":"G. Chevereau et al., “Gene ontology enrichment analysis for the most sensitive gene deletion strains for all drugs.” Public Library of Science, 2015.","ama":"Chevereau G, Lukacisinova M, Batur T, et al. Gene ontology enrichment analysis for the most sensitive gene deletion strains for all drugs. 2015. doi:10.1371/journal.pbio.1002299.s008"},"year":"2015","day":"18","oa_version":"Published Version","date_updated":"2023-02-23T10:07:02Z","type":"research_data_reference","status":"public","month":"11","date_created":"2021-08-03T07:05:16Z","date_published":"2015-11-18T00:00:00Z","publisher":"Public Library of Science"},{"date_published":"2015-05-18T00:00:00Z","publisher":"Public Library of Science","status":"public","month":"05","date_created":"2021-08-05T12:55:20Z","user_id":"6785fbc1-c503-11eb-8a32-93094b40e1cf","author":[{"full_name":"Trubenova, Barbora","orcid":"0000-0002-6873-2967","id":"42302D54-F248-11E8-B48F-1D18A9856A87","last_name":"Trubenova","first_name":"Barbora"},{"full_name":"Novak, Sebastian","id":"461468AE-F248-11E8-B48F-1D18A9856A87","first_name":"Sebastian","last_name":"Novak"},{"last_name":"Hager","first_name":"Reinmar","full_name":"Hager, Reinmar"}],"article_processing_charge":"No","citation":{"ista":"Trubenova B, Novak S, Hager R. 2015. Description of the agent based simulations, Public Library of Science, 10.1371/journal.pone.0126907.s003.","short":"B. Trubenova, S. Novak, R. Hager, (2015).","chicago":"Trubenova, Barbora, Sebastian Novak, and Reinmar Hager. “Description of the Agent Based Simulations.” Public Library of Science, 2015. https://doi.org/10.1371/journal.pone.0126907.s003.","ieee":"B. Trubenova, S. Novak, and R. Hager, “Description of the agent based simulations.” Public Library of Science, 2015.","ama":"Trubenova B, Novak S, Hager R. Description of the agent based simulations. 2015. doi:10.1371/journal.pone.0126907.s003","mla":"Trubenova, Barbora, et al. Description of the Agent Based Simulations. Public Library of Science, 2015, doi:10.1371/journal.pone.0126907.s003.","apa":"Trubenova, B., Novak, S., & Hager, R. (2015). Description of the agent based simulations. Public Library of Science. https://doi.org/10.1371/journal.pone.0126907.s003"},"year":"2015","day":"18","oa_version":"Published Version","date_updated":"2023-02-23T10:15:25Z","type":"research_data_reference","department":[{"_id":"NiBa"}],"_id":"9772","related_material":{"record":[{"status":"public","relation":"used_in_publication","id":"1809"}]},"doi":"10.1371/journal.pone.0126907.s003","title":"Description of the agent based simulations"},{"month":"03","date_created":"2021-08-05T12:58:07Z","status":"public","date_published":"2015-03-23T00:00:00Z","publisher":"Public Library of Science","title":"Evolutionary simulation code","department":[{"_id":"GaTk"}],"_id":"9773","doi":"10.1371/journal.pcbi.1004055.s002","related_material":{"record":[{"relation":"used_in_publication","status":"public","id":"1827"}]},"citation":{"ieee":"T. Friedlander, A. E. Mayo, T. Tlusty, and U. Alon, “Evolutionary simulation code.” Public Library of Science, 2015.","ama":"Friedlander T, Mayo AE, Tlusty T, Alon U. Evolutionary simulation code. 2015. doi:10.1371/journal.pcbi.1004055.s002","ista":"Friedlander T, Mayo AE, Tlusty T, Alon U. 2015. Evolutionary simulation code, Public Library of Science, 10.1371/journal.pcbi.1004055.s002.","short":"T. Friedlander, A.E. Mayo, T. Tlusty, U. Alon, (2015).","chicago":"Friedlander, Tamar, Avraham E. Mayo, Tsvi Tlusty, and Uri Alon. “Evolutionary Simulation Code.” Public Library of Science, 2015. https://doi.org/10.1371/journal.pcbi.1004055.s002.","mla":"Friedlander, Tamar, et al. Evolutionary Simulation Code. Public Library of Science, 2015, doi:10.1371/journal.pcbi.1004055.s002.","apa":"Friedlander, T., Mayo, A. E., Tlusty, T., & Alon, U. (2015). Evolutionary simulation code. Public Library of Science. https://doi.org/10.1371/journal.pcbi.1004055.s002"},"user_id":"6785fbc1-c503-11eb-8a32-93094b40e1cf","author":[{"first_name":"Tamar","last_name":"Friedlander","full_name":"Friedlander, Tamar","id":"36A5845C-F248-11E8-B48F-1D18A9856A87"},{"last_name":"Mayo","first_name":"Avraham E.","full_name":"Mayo, Avraham E."},{"full_name":"Tlusty, Tsvi","last_name":"Tlusty","first_name":"Tsvi"},{"full_name":"Alon, Uri","first_name":"Uri","last_name":"Alon"}],"article_processing_charge":"No","oa_version":"Published Version","type":"research_data_reference","date_updated":"2023-02-23T10:16:13Z","year":"2015","day":"23"},{"publist_id":"6419","intvolume":" 14","status":"public","month":"03","date_created":"2018-12-11T11:49:31Z","issue":"3","volume":14,"page":"318 - 324","date_published":"2015-03-01T00:00:00Z","publisher":"Nature Publishing Group","_id":"981","doi":"10.1038/nmat4215","oa":1,"title":"Dirac mass generation from crystal symmetry breaking on the surfaces of topological crystalline insulators","publication":"Nature Materials","abstract":[{"lang":"eng","text":"The tunability of topological surface states and controllable opening of the Dirac gap are of fundamental and practical interest in the field of topological materials. In the newly discovered topological crystalline insulators (TCIs), theory predicts that the Dirac node is protected by a crystalline symmetry and that the surface state electrons can acquire a mass if this symmetry is broken. Recent studies have detected signatures of a spontaneously generated Dirac gap in TCIs; however, the mechanism of mass formation remains elusive. In this work, we present scanning tunnelling microscopy (STM) measurements of the TCI Pb 1â'x Sn x Se for a wide range of alloy compositions spanning the topological and non-topological regimes. The STM topographies reveal a symmetry-breaking distortion on the surface, which imparts mass to the otherwise massless Dirac electrons-a mechanism analogous to the long sought-after Higgs mechanism in particle physics. Interestingly, the measured Dirac gap decreases on approaching the trivial phase, whereas the magnitude of the distortion remains nearly constant. Our data and calculations reveal that the penetration depth of Dirac surface states controls the magnitude of the Dirac mass. At the limit of the critical composition, the penetration depth is predicted to go to infinity, resulting in zero mass, consistent with our measurements. Finally, we discover the existence of surface states in the non-topological regime, which have the characteristics of gapped, double-branched Dirac fermions and could be exploited in realizing superconductivity in these materials."}],"publication_status":"published","acknowledgement":"We thank R. Buczko, C. Chamon, J. C. Seamus Davis, M. El-Batanouny, A. Mesaros, Y. Ran and A. Soumyanarayanan for useful conversations and G. McMahon for help with EDS measurements. V.M. gratefully acknowledges funding from the US Department of Energy, Scanned Probe Division under Award Number DE-FG02-12ER46880 for the support of I.Z., Y.O., W.Z. and D.W. for this project. Work at Massachusetts Institute of Technology is supported by US Department of Energy, Office of Basic Energy Sciences, Division of Materials Sciences and Engineering under Award DE-SC0010526 (L.F.), and NSF-DMR-1104498 (M.S.). H.L. acknowledges the Singapore National Research Foundation for support under NRF Award No. NRF-NRFF2013-03. Y.O. was partly supported by JSPS KAKENHI Grant Numbers 26707016 and 00707656. The work at Northeastern University is supported by the US Department of Energy grant number DE-FG02-07ER46352, and benefited from Northeastern University’s Advanced Scientific Computation Center (ASCC), theory support at the Advanced Light Source, Berkeley and the allocation of supercomputer time at the NERSC through DOE grant number DE-AC02-05CH11231. Work at Princeton University is supported by the US National Science Foundation Grant, NSF-DMR-1006492. F.C. acknowledges the support provided by MOST-Taiwan under project number NSC-102-2119-M-002-004.","author":[{"last_name":"Zeljkovic","first_name":"Ilija","full_name":"Zeljkovic, Ilija"},{"full_name":"Okada, Yoshinori","last_name":"Okada","first_name":"Yoshinori"},{"full_name":"Maksym Serbyn","orcid":"0000-0002-2399-5827","id":"47809E7E-F248-11E8-B48F-1D18A9856A87","last_name":"Serbyn","first_name":"Maksym"},{"full_name":"Sankar, Raman","last_name":"Sankar","first_name":"Raman"},{"first_name":"Daniel","last_name":"Walkup","full_name":"Walkup, Daniel"},{"full_name":"Zhou, Wenwen","last_name":"Zhou","first_name":"Wenwen"},{"last_name":"Liu","first_name":"Junwei","full_name":"Liu, Junwei"},{"first_name":"Guoqing","last_name":"Chang","full_name":"Chang, Guoqing"},{"full_name":"Wang, Yungjui","last_name":"Wang","first_name":"Yungjui"},{"last_name":"Hasan","first_name":"Md","full_name":"Hasan, Md Z"},{"first_name":"Fangcheng","last_name":"Chou","full_name":"Chou, Fangcheng"},{"full_name":"Lin, Hsin","first_name":"Hsin","last_name":"Lin"},{"full_name":"Bansil, Arun","first_name":"Arun","last_name":"Bansil"},{"full_name":"Fu, Liang","last_name":"Fu","first_name":"Liang"},{"full_name":"Madhavan, Vidya","first_name":"Vidya","last_name":"Madhavan"}],"extern":1,"quality_controlled":0,"citation":{"ama":"Zeljkovic I, Okada Y, Serbyn M, et al. Dirac mass generation from crystal symmetry breaking on the surfaces of topological crystalline insulators. Nature Materials. 2015;14(3):318-324. doi:10.1038/nmat4215","ieee":"I. Zeljkovic et al., “Dirac mass generation from crystal symmetry breaking on the surfaces of topological crystalline insulators,” Nature Materials, vol. 14, no. 3. Nature Publishing Group, pp. 318–324, 2015.","short":"I. Zeljkovic, Y. Okada, M. Serbyn, R. Sankar, D. Walkup, W. Zhou, J. Liu, G. Chang, Y. Wang, M. Hasan, F. Chou, H. Lin, A. Bansil, L. Fu, V. Madhavan, Nature Materials 14 (2015) 318–324.","chicago":"Zeljkovic, Ilija, Yoshinori Okada, Maksym Serbyn, Raman Sankar, Daniel Walkup, Wenwen Zhou, Junwei Liu, et al. “Dirac Mass Generation from Crystal Symmetry Breaking on the Surfaces of Topological Crystalline Insulators.” Nature Materials. Nature Publishing Group, 2015. https://doi.org/10.1038/nmat4215.","ista":"Zeljkovic I, Okada Y, Serbyn M, Sankar R, Walkup D, Zhou W, Liu J, Chang G, Wang Y, Hasan M, Chou F, Lin H, Bansil A, Fu L, Madhavan V. 2015. Dirac mass generation from crystal symmetry breaking on the surfaces of topological crystalline insulators. Nature Materials. 14(3), 318–324.","mla":"Zeljkovic, Ilija, et al. “Dirac Mass Generation from Crystal Symmetry Breaking on the Surfaces of Topological Crystalline Insulators.” Nature Materials, vol. 14, no. 3, Nature Publishing Group, 2015, pp. 318–24, doi:10.1038/nmat4215.","apa":"Zeljkovic, I., Okada, Y., Serbyn, M., Sankar, R., Walkup, D., Zhou, W., … Madhavan, V. (2015). Dirac mass generation from crystal symmetry breaking on the surfaces of topological crystalline insulators. Nature Materials. Nature Publishing Group. https://doi.org/10.1038/nmat4215"},"main_file_link":[{"url":"https://arxiv.org/abs/1403.4906","open_access":"1"}],"year":"2015","day":"01","date_updated":"2021-01-12T08:22:24Z","type":"journal_article"},{"title":"Criterion for many-body localization-delocalization phase transition","publication":"Physical Review X","_id":"982","doi":"10.1103/PhysRevX.5.041047","oa":1,"acknowledgement":"We acknowledge helpful discussions with Sid Parameswaran, Andrew Potter, Antonello Scardicchio, Romain Vasseur, and especially with Ehud Altman and David Huse. We would like to thank Miles Stoudenmire for the assistance with ITensor library. Research at Perimeter Institute is supported by the Government of Canada through Industry Canada and by the Province of Ontario through the Ministry of Economic Development & Innovation. This research was supported by Gordon and Betty Moore Foundation EPiQS Initiative through Grant No. GBMF4307 (M. S.), Sloan Foundation, NSERC, and Early Researcher Award of Ontario (D. A.). This work made use of the facilities of N8 HPC Centre of Excellence, provided and funded by the N8 consortium and EPSRC (Grant No. EP/K000225/1). The Centre is coordinated by the Universities of Leeds and Manchester.","abstract":[{"text":"We propose a new approach to probing ergodicity and its breakdown in one-dimensional quantum manybody systems based on their response to a local perturbation. We study the distribution of matrix elements of a local operator between the system's eigenstates, finding a qualitatively different behavior in the manybody localized (MBL) and ergodic phases. To characterize how strongly a local perturbation modifies the eigenstates, we introduce the parameter g(L) = (In (Vnm/δ)) which represents the disorder-averaged ratio of a typical matrix element of a local operator V to energy level spacing δ this parameter is reminiscent of the Thouless conductance in the single-particle localization. We show that the parameter g(L) decreases with system size L in the MBL phase and grows in the ergodic phase. We surmise that the delocalization transition occurs when g(L) is independent of system size, g(L)=gc ~ 1. We illustrate our approach by studying the many-body localization transition and resolving the many-body mobility edge in a disordered one-dimensional XXZ spin-1=2 chain using exact diagonalization and time-evolving block-decimation methods. Our criterion for the MBL transition gives insights into microscopic details of transition. Its direct physical consequences, in particular, logarithmically slow transport at the transition and extensive entanglement entropy of the eigenstates, are consistent with recent renormalization-group predictions.","lang":"eng"}],"publication_status":"published","citation":{"ieee":"M. Serbyn, Z. Papić, and D. Abanin, “Criterion for many-body localization-delocalization phase transition,” Physical Review X, vol. 5, no. 4. American Physical Society, 2015.","ama":"Serbyn M, Papić Z, Abanin D. Criterion for many-body localization-delocalization phase transition. Physical Review X. 2015;5(4). doi:10.1103/PhysRevX.5.041047","short":"M. Serbyn, Z. Papić, D. Abanin, Physical Review X 5 (2015).","chicago":"Serbyn, Maksym, Zlatko Papić, and Dmitry Abanin. “Criterion for Many-Body Localization-Delocalization Phase Transition.” Physical Review X. American Physical Society, 2015. https://doi.org/10.1103/PhysRevX.5.041047.","ista":"Serbyn M, Papić Z, Abanin D. 2015. Criterion for many-body localization-delocalization phase transition. Physical Review X. 5(4).","apa":"Serbyn, M., Papić, Z., & Abanin, D. (2015). Criterion for many-body localization-delocalization phase transition. Physical Review X. American Physical Society. https://doi.org/10.1103/PhysRevX.5.041047","mla":"Serbyn, Maksym, et al. “Criterion for Many-Body Localization-Delocalization Phase Transition.” Physical Review X, vol. 5, no. 4, American Physical Society, 2015, doi:10.1103/PhysRevX.5.041047."},"main_file_link":[{"url":"https://arxiv.org/abs/1507.01635","open_access":"1"}],"quality_controlled":0,"extern":1,"author":[{"last_name":"Serbyn","first_name":"Maksym","full_name":"Maksym Serbyn","orcid":"0000-0002-2399-5827","id":"47809E7E-F248-11E8-B48F-1D18A9856A87"},{"full_name":"Papić, Zlatko","first_name":"Zlatko","last_name":"Papić"},{"full_name":"Abanin, Dmitry A","first_name":"Dmitry","last_name":"Abanin"}],"type":"journal_article","date_updated":"2021-01-12T08:22:25Z","year":"2015","day":"01","intvolume":" 5","publist_id":"6418","month":"01","date_created":"2018-12-11T11:49:32Z","status":"public","date_published":"2015-01-01T00:00:00Z","issue":"4","volume":5,"publisher":"American Physical Society"},{"user_id":"3E5EF7F0-F248-11E8-B48F-1D18A9856A87","type":"journal_article","date_updated":"2021-01-12T08:22:28Z","oa_version":"Preprint","day":"14","language":[{"iso":"eng"}],"doi":"10.1038/nphys3461","acknowledgement":"Research support by Microsoft Project Q, the Danish National Research Foundation, the Lundbeck Foundation, the Carlsberg Foundation, and the European Commission. A.P.H. acknowledges support from the US Department of Energy, C.M.M. acknowledges support from the Villum Foundation.","date_published":"2015-09-14T00:00:00Z","external_id":{"arxiv":["1501.05155"]},"page":"1017 - 1021","arxiv":1,"citation":{"ama":"Higginbotham AP, Albrecht SM, Kiršanskas G, et al. Parity lifetime of bound states in a proximitized semiconductor nanowire. Nature Physics. 2015;11(12):1017-1021. doi:10.1038/nphys3461","ieee":"A. P. Higginbotham et al., “Parity lifetime of bound states in a proximitized semiconductor nanowire,” Nature Physics, vol. 11, no. 12. Nature Publishing Group, pp. 1017–1021, 2015.","ista":"Higginbotham AP, Albrecht SM, Kiršanskas G, Chang W, Kuemmeth F, Krogstrup P, Jespersen T, Nygård J, Flensberg K, Marcus C. 2015. Parity lifetime of bound states in a proximitized semiconductor nanowire. Nature Physics. 11(12), 1017–1021.","chicago":"Higginbotham, Andrew P, S M Albrecht, Gediminas Kiršanskas, W Chang, Ferdinand Kuemmeth, Peter Krogstrup, Thomas Jespersen, Jesper Nygård, Karsten Flensberg, and Charles Marcus. “Parity Lifetime of Bound States in a Proximitized Semiconductor Nanowire.” Nature Physics. Nature Publishing Group, 2015. https://doi.org/10.1038/nphys3461.","short":"A.P. Higginbotham, S.M. Albrecht, G. Kiršanskas, W. Chang, F. Kuemmeth, P. Krogstrup, T. Jespersen, J. Nygård, K. Flensberg, C. Marcus, Nature Physics 11 (2015) 1017–1021.","apa":"Higginbotham, A. P., Albrecht, S. M., Kiršanskas, G., Chang, W., Kuemmeth, F., Krogstrup, P., … Marcus, C. (2015). Parity lifetime of bound states in a proximitized semiconductor nanowire. Nature Physics. Nature Publishing Group. https://doi.org/10.1038/nphys3461","mla":"Higginbotham, Andrew P., et al. “Parity Lifetime of Bound States in a Proximitized Semiconductor Nanowire.” Nature Physics, vol. 11, no. 12, Nature Publishing Group, 2015, pp. 1017–21, doi:10.1038/nphys3461."},"main_file_link":[{"url":"https://arxiv.org/abs/1501.05155","open_access":"1"}],"extern":"1","quality_controlled":"1","author":[{"last_name":"Higginbotham","first_name":"Andrew P","id":"4AD6785A-F248-11E8-B48F-1D18A9856A87","full_name":"Higginbotham, Andrew P","orcid":"0000-0003-2607-2363"},{"full_name":"Albrecht, S M","last_name":"Albrecht","first_name":"S M"},{"last_name":"Kiršanskas","first_name":"Gediminas","full_name":"Kiršanskas, Gediminas"},{"full_name":"Chang, W","last_name":"Chang","first_name":"W"},{"first_name":"Ferdinand","last_name":"Kuemmeth","full_name":"Kuemmeth, Ferdinand"},{"full_name":"Krogstrup, Peter","first_name":"Peter","last_name":"Krogstrup"},{"first_name":"Thomas","last_name":"Jespersen","full_name":"Jespersen, Thomas"},{"last_name":"Nygård","first_name":"Jesper","full_name":"Nygård, Jesper"},{"last_name":"Flensberg","first_name":"Karsten","full_name":"Flensberg, Karsten"},{"first_name":"Charles","last_name":"Marcus","full_name":"Marcus, Charles"}],"year":"2015","publication":"Nature Physics","title":"Parity lifetime of bound states in a proximitized semiconductor nanowire","oa":1,"_id":"99","publication_status":"published","abstract":[{"lang":"eng","text":"Quasiparticle excitations can compromise the performance of superconducting devices, causing high-frequency dissipation, decoherence in Josephson qubits, and braiding errors in proposed Majorana-based topological quantum computers. Quasiparticle dynamics have been studied in detail in metallic superconductors but remain relatively unexplored in semiconductor-superconductor structures, which are now being intensely pursued in the context of topological superconductivity. To this end, we use a system comprising a gate-confined semiconductor nanowire with an epitaxially grown superconductor layer, yielding an isolated, proximitized nanowire segment. We identify bound states in the semiconductor by means of bias spectroscopy, determine the characteristic temperatures and magnetic fields for quasiparticle excitations, and extract a parity lifetime (poisoning time) of the bound state in the semiconductor exceeding 10 ms."}],"volume":11,"issue":"12","publisher":"Nature Publishing Group","intvolume":" 11","publist_id":"7955","date_created":"2018-12-11T11:44:37Z","month":"09","status":"public"},{"oa_version":"None","date_updated":"2021-01-12T06:48:19Z","type":"journal_article","year":"2015","day":"03","citation":{"short":"M. Isrie, M. Breuss, G. Tian, A.H. Hansen, F. Cristofoli, J. Morandell, Z.A. Kupchinsky, A. Sifrim, C. Rodriguez Rodriguez, E.P. Dapena, K. Doonanco, N. Leonard, F. Tinsa, S. Moortgat, H. Ulucan, E. Koparir, E. Karaca, N. Katsanis, V. Marton, J.R. Vermeesch, E.E. Davis, N.J. Cowan, D. Keays, H. Van Esch, The American Journal of Human Genetics 97 (2015) 790–800.","chicago":"Isrie, Mala, Martin Breuss, Guoling Tian, Andi H Hansen, Francesca Cristofoli, Jasmin Morandell, Zachari A Kupchinsky, et al. “Mutations in Either TUBB or MAPRE2 Cause Circumferential Skin Creases Kunze Type.” The American Journal of Human Genetics. Cell Press, 2015. https://doi.org/10.1016/j.ajhg.2015.10.014.","ista":"Isrie M, Breuss M, Tian G, Hansen AH, Cristofoli F, Morandell J, Kupchinsky ZA, Sifrim A, Rodriguez Rodriguez C, Dapena EP, Doonanco K, Leonard N, Tinsa F, Moortgat S, Ulucan H, Koparir E, Karaca E, Katsanis N, Marton V, Vermeesch JR, Davis EE, Cowan NJ, Keays D, Van Esch H. 2015. Mutations in either TUBB or MAPRE2 cause circumferential skin creases Kunze type. The American Journal of Human Genetics. 97(6), 790–800.","ieee":"M. Isrie et al., “Mutations in either TUBB or MAPRE2 cause circumferential skin creases Kunze type,” The American Journal of Human Genetics, vol. 97, no. 6. Cell Press, pp. 790–800, 2015.","ama":"Isrie M, Breuss M, Tian G, et al. Mutations in either TUBB or MAPRE2 cause circumferential skin creases Kunze type. The American Journal of Human Genetics. 2015;97(6):790-800. doi:10.1016/j.ajhg.2015.10.014","mla":"Isrie, Mala, et al. “Mutations in Either TUBB or MAPRE2 Cause Circumferential Skin Creases Kunze Type.” The American Journal of Human Genetics, vol. 97, no. 6, Cell Press, 2015, pp. 790–800, doi:10.1016/j.ajhg.2015.10.014.","apa":"Isrie, M., Breuss, M., Tian, G., Hansen, A. H., Cristofoli, F., Morandell, J., … Van Esch, H. (2015). Mutations in either TUBB or MAPRE2 cause circumferential skin creases Kunze type. The American Journal of Human Genetics. Cell Press. https://doi.org/10.1016/j.ajhg.2015.10.014"},"author":[{"full_name":"Isrie, Mala","first_name":"Mala","last_name":"Isrie"},{"last_name":"Breuss","first_name":"Martin","full_name":"Breuss, Martin"},{"last_name":"Tian","first_name":"Guoling","full_name":"Tian, Guoling"},{"first_name":"Andi H","last_name":"Hansen","full_name":"Hansen, Andi H","id":"38853E16-F248-11E8-B48F-1D18A9856A87"},{"full_name":"Cristofoli, Francesca","first_name":"Francesca","last_name":"Cristofoli"},{"full_name":"Morandell, Jasmin","id":"4739D480-F248-11E8-B48F-1D18A9856A87","last_name":"Morandell","first_name":"Jasmin"},{"full_name":"Kupchinsky, Zachari A","first_name":"Zachari A","last_name":"Kupchinsky"},{"last_name":"Sifrim","first_name":"Alejandro","full_name":"Sifrim, Alejandro"},{"first_name":"Celia","last_name":"Rodriguez Rodriguez","full_name":"Rodriguez Rodriguez, Celia"},{"full_name":"Dapena, Elena P","last_name":"Dapena","first_name":"Elena P"},{"last_name":"Doonanco","first_name":"Kurston","full_name":"Doonanco, Kurston"},{"last_name":"Leonard","first_name":"Norma","full_name":"Leonard, Norma"},{"full_name":"Tinsa, Faten","first_name":"Faten","last_name":"Tinsa"},{"full_name":"Moortgat, Stéphanie","last_name":"Moortgat","first_name":"Stéphanie"},{"full_name":"Ulucan, Hakan","last_name":"Ulucan","first_name":"Hakan"},{"full_name":"Koparir, Erkan","last_name":"Koparir","first_name":"Erkan"},{"full_name":"Karaca, Ender","last_name":"Karaca","first_name":"Ender"},{"full_name":"Katsanis, Nicholas","first_name":"Nicholas","last_name":"Katsanis"},{"full_name":"Marton, Valeria","first_name":"Valeria","last_name":"Marton"},{"first_name":"Joris R","last_name":"Vermeesch","full_name":"Vermeesch, Joris R"},{"last_name":"Davis","first_name":"Erica E","full_name":"Davis, Erica E"},{"full_name":"Cowan, Nicholas J","last_name":"Cowan","first_name":"Nicholas J"},{"last_name":"Keays","first_name":"David","full_name":"Keays, David"},{"full_name":"Van Esch, Hilde","first_name":"Hilde","last_name":"Van Esch"}],"quality_controlled":"1","extern":"1","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","abstract":[{"text":"Circumferential skin creases Kunze type (CSC-KT) is a specific congenital entity with an unknown genetic cause. The disease phenotype comprises characteristic circumferential skin creases accompanied by intellectual disability, a cleft palate, short stature, and dysmorphic features. Here, we report that mutations in either MAPRE2 or TUBB underlie the genetic origin of this syndrome. MAPRE2 encodes a member of the microtubule end-binding family of proteins that bind to the guanosine triphosphate cap at growing microtubule plus ends, and TUBB encodes a β-tubulin isotype that is expressed abundantly in the developing brain. Functional analyses of the TUBB mutants show multiple defects in the chaperone-dependent tubulin heterodimer folding and assembly pathway that leads to a compromised yield of native heterodimers. The TUBB mutations also have an impact on microtubule dynamics. For MAPRE2, we show that the mutations result in enhanced MAPRE2 binding to microtubules, implying an increased dwell time at microtubule plus ends. Further, in vivo analysis of MAPRE2 mutations in a zebrafish model of craniofacial development shows that the variants most likely perturb the patterning of branchial arches, either through excessive activity (under a recessive paradigm) or through haploinsufficiency (dominant de novo paradigm). Taken together, our data add CSC-KT to the growing list of tubulinopathies and highlight how multiple inheritance paradigms can affect dosage-sensitive biological systems so as to result in the same clinical defect.","lang":"eng"}],"publication_status":"published","publication":"The American Journal of Human Genetics","title":"Mutations in either TUBB or MAPRE2 cause circumferential skin creases Kunze type","_id":"1106","doi":"10.1016/j.ajhg.2015.10.014","language":[{"iso":"eng"}],"publisher":"Cell Press","date_published":"2015-12-03T00:00:00Z","issue":"6","page":"790 - 800","volume":97,"month":"12","date_created":"2018-12-11T11:50:11Z","status":"public","intvolume":" 97","publist_id":"6264"},{"publication_status":"published","abstract":[{"text":"Human cancer cells bear complex chromosome rearrangements that can be potential drivers of cancer development. However, the molecular mechanisms underlying these rearrangements have been unclear. Zhang et al. use a new technique combining live-cell imaging and single-cell sequencing to demonstrate that chromosomes mis-segregated to micronuclei frequently undergo chromothripsis-like rearrangements in the subsequent cell cycle.","lang":"eng"}],"oa":1,"_id":"11073","title":"Linking micronuclei to chromosome fragmentation","publication":"Cell","pmid":1,"year":"2015","quality_controlled":"1","extern":"1","author":[{"full_name":"Hatch, Emily M.","first_name":"Emily M.","last_name":"Hatch"},{"last_name":"HETZER","first_name":"Martin W","id":"86c0d31b-b4eb-11ec-ac5a-eae7b2e135ed","full_name":"HETZER, Martin W","orcid":"0000-0002-2111-992X"}],"main_file_link":[{"open_access":"1","url":"https://doi.org/10.1016/j.cell.2015.06.005"}],"citation":{"mla":"Hatch, Emily M., and Martin Hetzer. “Linking Micronuclei to Chromosome Fragmentation.” Cell, vol. 161, no. 7, Elsevier, 2015, pp. 1502–04, doi:10.1016/j.cell.2015.06.005.","apa":"Hatch, E. M., & Hetzer, M. (2015). Linking micronuclei to chromosome fragmentation. Cell. Elsevier. https://doi.org/10.1016/j.cell.2015.06.005","ama":"Hatch EM, Hetzer M. Linking micronuclei to chromosome fragmentation. Cell. 2015;161(7):1502-1504. doi:10.1016/j.cell.2015.06.005","ieee":"E. M. Hatch and M. Hetzer, “Linking micronuclei to chromosome fragmentation,” Cell, vol. 161, no. 7. Elsevier, pp. 1502–1504, 2015.","ista":"Hatch EM, Hetzer M. 2015. Linking micronuclei to chromosome fragmentation. Cell. 161(7), 1502–1504.","chicago":"Hatch, Emily M., and Martin Hetzer. “Linking Micronuclei to Chromosome Fragmentation.” Cell. Elsevier, 2015. https://doi.org/10.1016/j.cell.2015.06.005.","short":"E.M. Hatch, M. Hetzer, Cell 161 (2015) 1502–1504."},"status":"public","date_created":"2022-04-07T07:48:49Z","month":"06","intvolume":" 161","article_type":"original","publisher":"Elsevier","volume":161,"issue":"7","doi":"10.1016/j.cell.2015.06.005","language":[{"iso":"eng"}],"day":"18","date_updated":"2022-07-18T08:34:33Z","type":"journal_article","oa_version":"Published Version","user_id":"72615eeb-f1f3-11ec-aa25-d4573ddc34fd","article_processing_charge":"No","publication_identifier":{"issn":["0092-8674"]},"scopus_import":"1","page":"1502-1504","date_published":"2015-06-18T00:00:00Z","external_id":{"pmid":["26091034"]},"keyword":["General Biochemistry","Genetics and Molecular Biology"]},{"publisher":"Elsevier","article_type":"original","issue":"10","volume":25,"status":"public","date_created":"2022-04-07T07:49:00Z","month":"05","intvolume":" 25","year":"2015","author":[{"last_name":"Hatch","first_name":"Emily M.","full_name":"Hatch, Emily M."},{"first_name":"Martin W","last_name":"HETZER","full_name":"HETZER, Martin W","orcid":"0000-0002-2111-992X","id":"86c0d31b-b4eb-11ec-ac5a-eae7b2e135ed"}],"extern":"1","quality_controlled":"1","citation":{"short":"E.M. Hatch, M. Hetzer, Current Biology 25 (2015) PR397-R399.","chicago":"Hatch, Emily M., and Martin Hetzer. “Chromothripsis.” Current Biology. Elsevier, 2015. https://doi.org/10.1016/j.cub.2015.02.033.","ista":"Hatch EM, Hetzer M. 2015. Chromothripsis. Current Biology. 25(10), PR397-R399.","ieee":"E. M. Hatch and M. Hetzer, “Chromothripsis,” Current Biology, vol. 25, no. 10. Elsevier, pp. PR397-R399, 2015.","ama":"Hatch EM, Hetzer M. Chromothripsis. Current Biology. 2015;25(10):PR397-R399. doi:10.1016/j.cub.2015.02.033","mla":"Hatch, Emily M., and Martin Hetzer. “Chromothripsis.” Current Biology, vol. 25, no. 10, Elsevier, 2015, pp. PR397-R399, doi:10.1016/j.cub.2015.02.033.","apa":"Hatch, E. M., & Hetzer, M. (2015). Chromothripsis. Current Biology. Elsevier. https://doi.org/10.1016/j.cub.2015.02.033"},"main_file_link":[{"url":"https://doi.org/10.1016/j.cub.2015.02.033","open_access":"1"}],"publication_status":"published","oa":1,"_id":"11074","publication":"Current Biology","title":"Chromothripsis","pmid":1,"page":"PR397-R399","date_published":"2015-05-18T00:00:00Z","external_id":{"pmid":["25989073"]},"keyword":["General Agricultural and Biological Sciences","General Biochemistry","Genetics and Molecular Biology"],"publication_identifier":{"issn":["0960-9822"]},"scopus_import":"1","day":"18","date_updated":"2022-07-18T08:34:34Z","type":"journal_article","oa_version":"Published Version","user_id":"72615eeb-f1f3-11ec-aa25-d4573ddc34fd","article_processing_charge":"No","language":[{"iso":"eng"}],"doi":"10.1016/j.cub.2015.02.033"},{"doi":"10.1083/jcb.201410047","language":[{"iso":"eng"}],"day":"16","oa_version":"Published Version","date_updated":"2022-07-18T08:43:00Z","type":"journal_article","user_id":"72615eeb-f1f3-11ec-aa25-d4573ddc34fd","article_processing_charge":"No","scopus_import":"1","publication_identifier":{"eissn":["1540-8140"],"issn":["0021-9525"]},"page":"671-681","external_id":{"pmid":["25778917"]},"keyword":["Cell Biology"],"date_published":"2015-03-16T00:00:00Z","abstract":[{"text":"Previously, we identified the nucleoporin gp210/Nup210 as a critical regulator of muscle and neuronal differentiation, but how this nucleoporin exerts its function and whether it modulates nuclear pore complex (NPC) activity remain unknown. Here, we show that gp210/Nup210 mediates muscle cell differentiation in vitro via its conserved N-terminal domain that extends into the perinuclear space. Removal of the C-terminal domain, which partially mislocalizes gp210/Nup210 away from NPCs, efficiently rescues the differentiation defect caused by the knockdown of endogenous gp210/Nup210. Unexpectedly, a gp210/Nup210 mutant lacking the NPC-targeting transmembrane and C-terminal domains is sufficient for C2C12 myoblast differentiation. We demonstrate that the endoplasmic reticulum (ER) stress-specific caspase cascade is exacerbated during Nup210 depletion and that blocking ER stress-mediated apoptosis rescues differentiation of Nup210-deficient cells. Our results suggest that the role of gp210/Nup210 in cell differentiation is mediated by its large luminal domain, which can act independently of NPC association and appears to play a pivotal role in the maintenance of nuclear envelope/ER homeostasis.","lang":"eng"}],"publication_status":"published","_id":"11075","pmid":1,"publication":"Journal of Cell Biology","title":"The nucleoporin gp210/Nup210 controls muscle differentiation by regulating nuclear envelope/ER homeostasis","year":"2015","quality_controlled":"1","author":[{"last_name":"Gomez-Cavazos","first_name":"J. Sebastian","full_name":"Gomez-Cavazos, J. Sebastian"},{"id":"86c0d31b-b4eb-11ec-ac5a-eae7b2e135ed","full_name":"HETZER, Martin W","orcid":"0000-0002-2111-992X","first_name":"Martin W","last_name":"HETZER"}],"extern":"1","citation":{"ieee":"J. S. Gomez-Cavazos and M. Hetzer, “The nucleoporin gp210/Nup210 controls muscle differentiation by regulating nuclear envelope/ER homeostasis,” Journal of Cell Biology, vol. 208, no. 6. Rockefeller University Press, pp. 671–681, 2015.","ama":"Gomez-Cavazos JS, Hetzer M. The nucleoporin gp210/Nup210 controls muscle differentiation by regulating nuclear envelope/ER homeostasis. Journal of Cell Biology. 2015;208(6):671-681. doi:10.1083/jcb.201410047","short":"J.S. Gomez-Cavazos, M. Hetzer, Journal of Cell Biology 208 (2015) 671–681.","chicago":"Gomez-Cavazos, J. Sebastian, and Martin Hetzer. “The Nucleoporin Gp210/Nup210 Controls Muscle Differentiation by Regulating Nuclear Envelope/ER Homeostasis.” Journal of Cell Biology. Rockefeller University Press, 2015. https://doi.org/10.1083/jcb.201410047.","ista":"Gomez-Cavazos JS, Hetzer M. 2015. The nucleoporin gp210/Nup210 controls muscle differentiation by regulating nuclear envelope/ER homeostasis. Journal of Cell Biology. 208(6), 671–681.","mla":"Gomez-Cavazos, J. Sebastian, and Martin Hetzer. “The Nucleoporin Gp210/Nup210 Controls Muscle Differentiation by Regulating Nuclear Envelope/ER Homeostasis.” Journal of Cell Biology, vol. 208, no. 6, Rockefeller University Press, 2015, pp. 671–81, doi:10.1083/jcb.201410047.","apa":"Gomez-Cavazos, J. S., & Hetzer, M. (2015). The nucleoporin gp210/Nup210 controls muscle differentiation by regulating nuclear envelope/ER homeostasis. Journal of Cell Biology. Rockefeller University Press. https://doi.org/10.1083/jcb.201410047"},"status":"public","month":"03","date_created":"2022-04-07T07:49:10Z","intvolume":" 208","publisher":"Rockefeller University Press","article_type":"original","issue":"6","volume":208},{"language":[{"iso":"eng"}],"doi":"10.1101/gad.256495.114","user_id":"72615eeb-f1f3-11ec-aa25-d4573ddc34fd","article_processing_charge":"No","type":"journal_article","date_updated":"2022-07-18T08:43:20Z","oa_version":"Published Version","day":"01","publication_identifier":{"issn":["0890-9369"],"eissn":["1549-5477"]},"scopus_import":"1","date_published":"2015-02-01T00:00:00Z","keyword":["Developmental Biology","Genetics"],"external_id":{"pmid":["25691464"]},"page":"337-349","title":"Nuclear pore proteins and the control of genome functions","publication":"Genes & Development","pmid":1,"oa":1,"_id":"11076","publication_status":"published","abstract":[{"lang":"eng","text":"Nuclear pore complexes (NPCs) are composed of several copies of ∼30 different proteins called nucleoporins (Nups). NPCs penetrate the nuclear envelope (NE) and regulate the nucleocytoplasmic trafficking of macromolecules. Beyond this vital role, NPC components influence genome functions in a transport-independent manner. Nups play an evolutionarily conserved role in gene expression regulation that, in metazoans, extends into the nuclear interior. Additionally, in proliferative cells, Nups play a crucial role in genome integrity maintenance and mitotic progression. Here we discuss genome-related functions of Nups and their impact on essential DNA metabolism processes such as transcription, chromosome duplication, and segregation."}],"main_file_link":[{"open_access":"1","url":"https://doi.org/10.1101/gad.256495.114"}],"citation":{"short":"A. Ibarra, M. Hetzer, Genes & Development 29 (2015) 337–349.","chicago":"Ibarra, Arkaitz, and Martin Hetzer. “Nuclear Pore Proteins and the Control of Genome Functions.” Genes & Development. Cold Spring Harbor Laboratory, 2015. https://doi.org/10.1101/gad.256495.114.","ista":"Ibarra A, Hetzer M. 2015. Nuclear pore proteins and the control of genome functions. Genes & Development. 29(4), 337–349.","ama":"Ibarra A, Hetzer M. Nuclear pore proteins and the control of genome functions. Genes & Development. 2015;29(4):337-349. doi:10.1101/gad.256495.114","ieee":"A. Ibarra and M. Hetzer, “Nuclear pore proteins and the control of genome functions,” Genes & Development, vol. 29, no. 4. Cold Spring Harbor Laboratory, pp. 337–349, 2015.","mla":"Ibarra, Arkaitz, and Martin Hetzer. “Nuclear Pore Proteins and the Control of Genome Functions.” Genes & Development, vol. 29, no. 4, Cold Spring Harbor Laboratory, 2015, pp. 337–49, doi:10.1101/gad.256495.114.","apa":"Ibarra, A., & Hetzer, M. (2015). Nuclear pore proteins and the control of genome functions. Genes & Development. Cold Spring Harbor Laboratory. https://doi.org/10.1101/gad.256495.114"},"extern":"1","author":[{"first_name":"Arkaitz","last_name":"Ibarra","full_name":"Ibarra, Arkaitz"},{"last_name":"HETZER","first_name":"Martin W","id":"86c0d31b-b4eb-11ec-ac5a-eae7b2e135ed","orcid":"0000-0002-2111-992X","full_name":"HETZER, Martin W"}],"quality_controlled":"1","year":"2015","intvolume":" 29","date_created":"2022-04-07T07:49:21Z","month":"02","status":"public","volume":29,"issue":"4","article_type":"original","publisher":"Cold Spring Harbor Laboratory"},{"article_type":"original","publisher":"Cold Spring Harbor Laboratory","volume":29,"issue":"12","status":"public","month":"06","date_created":"2022-04-07T07:49:31Z","intvolume":" 29","year":"2015","quality_controlled":"1","author":[{"first_name":"Filipe V.","last_name":"Jacinto","full_name":"Jacinto, Filipe V."},{"full_name":"Benner, Chris","first_name":"Chris","last_name":"Benner"},{"last_name":"HETZER","first_name":"Martin W","id":"86c0d31b-b4eb-11ec-ac5a-eae7b2e135ed","full_name":"HETZER, Martin W","orcid":"0000-0002-2111-992X"}],"extern":"1","main_file_link":[{"url":"https://doi.org/10.1101/gad.260919.115","open_access":"1"}],"citation":{"mla":"Jacinto, Filipe V., et al. “The Nucleoporin Nup153 Regulates Embryonic Stem Cell Pluripotency through Gene Silencing.” Genes & Development, vol. 29, no. 12, Cold Spring Harbor Laboratory, 2015, pp. 1224–38, doi:10.1101/gad.260919.115.","apa":"Jacinto, F. V., Benner, C., & Hetzer, M. (2015). The nucleoporin Nup153 regulates embryonic stem cell pluripotency through gene silencing. Genes & Development. Cold Spring Harbor Laboratory. https://doi.org/10.1101/gad.260919.115","ista":"Jacinto FV, Benner C, Hetzer M. 2015. The nucleoporin Nup153 regulates embryonic stem cell pluripotency through gene silencing. Genes & Development. 29(12), 1224–1238.","chicago":"Jacinto, Filipe V., Chris Benner, and Martin Hetzer. “The Nucleoporin Nup153 Regulates Embryonic Stem Cell Pluripotency through Gene Silencing.” Genes & Development. Cold Spring Harbor Laboratory, 2015. https://doi.org/10.1101/gad.260919.115.","short":"F.V. Jacinto, C. Benner, M. Hetzer, Genes & Development 29 (2015) 1224–1238.","ieee":"F. V. Jacinto, C. Benner, and M. Hetzer, “The nucleoporin Nup153 regulates embryonic stem cell pluripotency through gene silencing,” Genes & Development, vol. 29, no. 12. Cold Spring Harbor Laboratory, pp. 1224–1238, 2015.","ama":"Jacinto FV, Benner C, Hetzer M. The nucleoporin Nup153 regulates embryonic stem cell pluripotency through gene silencing. Genes & Development. 2015;29(12):1224-1238. doi:10.1101/gad.260919.115"},"abstract":[{"lang":"eng","text":"Nucleoporins (Nups) are a family of proteins best known as the constituent building blocks of nuclear pore complexes (NPCs), membrane-embedded channels that mediate nuclear transport across the nuclear envelope. Recent evidence suggests that several Nups have additional roles in controlling the activation and silencing of developmental genes; however, the mechanistic details of these functions remain poorly understood. Here, we show that depletion of Nup153 in mouse embryonic stem cells (mESCs) causes the derepression of developmental genes and induction of early differentiation. This loss of stem cell identity is not associated with defects in the nuclear import of key pluripotency factors. Rather, Nup153 binds around the transcriptional start site (TSS) of developmental genes and mediates the recruitment of the polycomb-repressive complex 1 (PRC1) to a subset of its target loci. Our results demonstrate a chromatin-associated role of Nup153 in maintaining stem cell pluripotency by functioning in mammalian epigenetic gene silencing."}],"publication_status":"published","_id":"11077","oa":1,"pmid":1,"publication":"Genes & Development","title":"The nucleoporin Nup153 regulates embryonic stem cell pluripotency through gene silencing","page":"1224-1238","keyword":["Developmental Biology","Genetics"],"external_id":{"pmid":["26080816"]},"date_published":"2015-06-16T00:00:00Z","scopus_import":"1","publication_identifier":{"issn":["0890-9369"],"eissn":["1549-5477"]},"day":"16","oa_version":"Published Version","date_updated":"2022-07-18T08:43:51Z","type":"journal_article","user_id":"72615eeb-f1f3-11ec-aa25-d4573ddc34fd","article_processing_charge":"No","doi":"10.1101/gad.260919.115","language":[{"iso":"eng"}]},{"volume":1,"issue":"3","publisher":"Elsevier","article_type":"original","intvolume":" 1","date_created":"2022-04-07T07:49:39Z","month":"09","status":"public","main_file_link":[{"open_access":"1","url":"https://doi.org/10.1016/j.cels.2015.08.012"}],"citation":{"ama":"Ori A, Toyama BH, Harris MS, et al. Integrated transcriptome and proteome analyses reveal organ-specific proteome deterioration in old rats. Cell Systems. 2015;1(3):P224-237. doi:10.1016/j.cels.2015.08.012","ieee":"A. Ori et al., “Integrated transcriptome and proteome analyses reveal organ-specific proteome deterioration in old rats,” Cell Systems, vol. 1, no. 3. Elsevier, pp. P224-237, 2015.","short":"A. Ori, B.H. Toyama, M.S. Harris, T. Bock, M. Iskar, P. Bork, N.T. Ingolia, M. Hetzer, M. Beck, Cell Systems 1 (2015) P224-237.","chicago":"Ori, Alessandro, Brandon H. Toyama, Michael S. Harris, Thomas Bock, Murat Iskar, Peer Bork, Nicholas T. Ingolia, Martin Hetzer, and Martin Beck. “Integrated Transcriptome and Proteome Analyses Reveal Organ-Specific Proteome Deterioration in Old Rats.” Cell Systems. Elsevier, 2015. https://doi.org/10.1016/j.cels.2015.08.012.","ista":"Ori A, Toyama BH, Harris MS, Bock T, Iskar M, Bork P, Ingolia NT, Hetzer M, Beck M. 2015. Integrated transcriptome and proteome analyses reveal organ-specific proteome deterioration in old rats. Cell Systems. 1(3), P224-237.","mla":"Ori, Alessandro, et al. “Integrated Transcriptome and Proteome Analyses Reveal Organ-Specific Proteome Deterioration in Old Rats.” Cell Systems, vol. 1, no. 3, Elsevier, 2015, pp. P224-237, doi:10.1016/j.cels.2015.08.012.","apa":"Ori, A., Toyama, B. H., Harris, M. S., Bock, T., Iskar, M., Bork, P., … Beck, M. (2015). Integrated transcriptome and proteome analyses reveal organ-specific proteome deterioration in old rats. Cell Systems. Elsevier. https://doi.org/10.1016/j.cels.2015.08.012"},"author":[{"last_name":"Ori","first_name":"Alessandro","full_name":"Ori, Alessandro"},{"full_name":"Toyama, Brandon H.","last_name":"Toyama","first_name":"Brandon H."},{"first_name":"Michael S.","last_name":"Harris","full_name":"Harris, Michael S."},{"last_name":"Bock","first_name":"Thomas","full_name":"Bock, Thomas"},{"full_name":"Iskar, Murat","first_name":"Murat","last_name":"Iskar"},{"full_name":"Bork, Peer","first_name":"Peer","last_name":"Bork"},{"full_name":"Ingolia, Nicholas T.","first_name":"Nicholas T.","last_name":"Ingolia"},{"first_name":"Martin W","last_name":"HETZER","orcid":"0000-0002-2111-992X","full_name":"HETZER, Martin W","id":"86c0d31b-b4eb-11ec-ac5a-eae7b2e135ed"},{"full_name":"Beck, Martin","first_name":"Martin","last_name":"Beck"}],"quality_controlled":"1","extern":"1","year":"2015","publication":"Cell Systems","title":"Integrated transcriptome and proteome analyses reveal organ-specific proteome deterioration in old rats","pmid":1,"oa":1,"_id":"11078","publication_status":"published","abstract":[{"text":"Aging is associated with the decline of protein, cell, and organ function. Here, we use an integrated approach to characterize gene expression, bulk translation, and cell biology in the brains and livers of young and old rats. We identify 468 differences in protein abundance between young and old animals. The majority are a consequence of altered translation output, that is, the combined effect of changes in transcript abundance and translation efficiency. In addition, we identify 130 proteins whose overall abundance remains unchanged but whose sub-cellular localization, phosphorylation state, or splice-form varies. While some protein-level differences appear to be a generic property of the rats’ chronological age, the majority are specific to one organ. These may be a consequence of the organ’s physiology or the chronological age of the cells within the tissue. Taken together, our study provides an initial view of the proteome at the molecular, sub-cellular, and organ level in young and old rats.","lang":"eng"}],"date_published":"2015-09-23T00:00:00Z","keyword":["Cell Biology","Histology","Pathology and Forensic Medicine"],"external_id":{"pmid":["27135913"]},"page":"P224-237","publication_identifier":{"issn":["2405-4712"]},"scopus_import":"1","article_processing_charge":"No","user_id":"72615eeb-f1f3-11ec-aa25-d4573ddc34fd","type":"journal_article","date_updated":"2022-07-18T08:44:07Z","oa_version":"Published Version","day":"23","doi":"10.1016/j.cels.2015.08.012","language":[{"iso":"eng"}]},{"_id":"11079","oa":1,"pmid":1,"publication":"Cell Stem Cell","title":"Directly reprogrammed human neurons retain aging-associated transcriptomic signatures and reveal age-related nucleocytoplasmic defects","abstract":[{"lang":"eng","text":"Aging is a major risk factor for many human diseases, and in vitro generation of human neurons is an attractive approach for modeling aging-related brain disorders. However, modeling aging in differentiated human neurons has proved challenging. We generated neurons from human donors across a broad range of ages, either by iPSC-based reprogramming and differentiation or by direct conversion into induced neurons (iNs). While iPSCs and derived neurons did not retain aging-associated gene signatures, iNs displayed age-specific transcriptional profiles and revealed age-associated decreases in the nuclear transport receptor RanBP17. We detected an age-dependent loss of nucleocytoplasmic compartmentalization (NCC) in donor fibroblasts and corresponding iNs and found that reduced RanBP17 impaired NCC in young cells, while iPSC rejuvenation restored NCC in aged cells. These results show that iNs retain important aging-related signatures, thus allowing modeling of the aging process in vitro, and they identify impaired NCC as an important factor in human aging."}],"publication_status":"published","author":[{"last_name":"Mertens","first_name":"Jerome","full_name":"Mertens, Jerome"},{"full_name":"Paquola, Apuã C.M.","last_name":"Paquola","first_name":"Apuã C.M."},{"full_name":"Ku, Manching","last_name":"Ku","first_name":"Manching"},{"first_name":"Emily","last_name":"Hatch","full_name":"Hatch, Emily"},{"last_name":"Böhnke","first_name":"Lena","full_name":"Böhnke, Lena"},{"last_name":"Ladjevardi","first_name":"Shauheen","full_name":"Ladjevardi, Shauheen"},{"full_name":"McGrath, Sean","last_name":"McGrath","first_name":"Sean"},{"last_name":"Campbell","first_name":"Benjamin","full_name":"Campbell, Benjamin"},{"full_name":"Lee, Hyungjun","first_name":"Hyungjun","last_name":"Lee"},{"last_name":"Herdy","first_name":"Joseph R.","full_name":"Herdy, Joseph R."},{"last_name":"Gonçalves","first_name":"J. Tiago","full_name":"Gonçalves, J. Tiago"},{"first_name":"Tomohisa","last_name":"Toda","full_name":"Toda, Tomohisa"},{"full_name":"Kim, Yongsung","last_name":"Kim","first_name":"Yongsung"},{"full_name":"Winkler, Jürgen","first_name":"Jürgen","last_name":"Winkler"},{"last_name":"Yao","first_name":"Jun","full_name":"Yao, Jun"},{"last_name":"HETZER","first_name":"Martin W","full_name":"HETZER, Martin W","orcid":"0000-0002-2111-992X","id":"86c0d31b-b4eb-11ec-ac5a-eae7b2e135ed"},{"full_name":"Gage, Fred H.","last_name":"Gage","first_name":"Fred H."}],"quality_controlled":"1","extern":"1","citation":{"apa":"Mertens, J., Paquola, A. C. M., Ku, M., Hatch, E., Böhnke, L., Ladjevardi, S., … Gage, F. H. (2015). Directly reprogrammed human neurons retain aging-associated transcriptomic signatures and reveal age-related nucleocytoplasmic defects. Cell Stem Cell. Elsevier. https://doi.org/10.1016/j.stem.2015.09.001","mla":"Mertens, Jerome, et al. “Directly Reprogrammed Human Neurons Retain Aging-Associated Transcriptomic Signatures and Reveal Age-Related Nucleocytoplasmic Defects.” Cell Stem Cell, vol. 17, no. 6, Elsevier, 2015, pp. 705–18, doi:10.1016/j.stem.2015.09.001.","chicago":"Mertens, Jerome, Apuã C.M. Paquola, Manching Ku, Emily Hatch, Lena Böhnke, Shauheen Ladjevardi, Sean McGrath, et al. “Directly Reprogrammed Human Neurons Retain Aging-Associated Transcriptomic Signatures and Reveal Age-Related Nucleocytoplasmic Defects.” Cell Stem Cell. Elsevier, 2015. https://doi.org/10.1016/j.stem.2015.09.001.","short":"J. Mertens, A.C.M. Paquola, M. Ku, E. Hatch, L. Böhnke, S. Ladjevardi, S. McGrath, B. Campbell, H. Lee, J.R. Herdy, J.T. Gonçalves, T. Toda, Y. Kim, J. Winkler, J. Yao, M. Hetzer, F.H. Gage, Cell Stem Cell 17 (2015) 705–718.","ista":"Mertens J, Paquola ACM, Ku M, Hatch E, Böhnke L, Ladjevardi S, McGrath S, Campbell B, Lee H, Herdy JR, Gonçalves JT, Toda T, Kim Y, Winkler J, Yao J, Hetzer M, Gage FH. 2015. Directly reprogrammed human neurons retain aging-associated transcriptomic signatures and reveal age-related nucleocytoplasmic defects. Cell Stem Cell. 17(6), 705–718.","ieee":"J. Mertens et al., “Directly reprogrammed human neurons retain aging-associated transcriptomic signatures and reveal age-related nucleocytoplasmic defects,” Cell Stem Cell, vol. 17, no. 6. Elsevier, pp. 705–718, 2015.","ama":"Mertens J, Paquola ACM, Ku M, et al. Directly reprogrammed human neurons retain aging-associated transcriptomic signatures and reveal age-related nucleocytoplasmic defects. Cell Stem Cell. 2015;17(6):705-718. doi:10.1016/j.stem.2015.09.001"},"main_file_link":[{"open_access":"1","url":"https://doi.org/10.1016/j.stem.2015.09.001"}],"year":"2015","intvolume":" 17","status":"public","month":"12","date_created":"2022-04-07T07:49:51Z","volume":17,"issue":"6","article_type":"original","publisher":"Elsevier","language":[{"iso":"eng"}],"doi":"10.1016/j.stem.2015.09.001","user_id":"72615eeb-f1f3-11ec-aa25-d4573ddc34fd","article_processing_charge":"No","day":"03","oa_version":"Published Version","type":"journal_article","date_updated":"2022-07-18T08:44:21Z","scopus_import":"1","publication_identifier":{"issn":["1934-5909"]},"page":"705-718","external_id":{"pmid":["26456686"]},"keyword":["Cell Biology","Genetics","Molecular Medicine"],"date_published":"2015-12-03T00:00:00Z"},{"year":"2015","citation":{"ista":"Sobral D, Matthee JJ, Darvish B, Schaerer D, Mobasher B, Röttgering H, Santos S, Hemmati S. 2015. Evidence for PopIII-like stellar populations in the most luminous Lyα emitters at the epoch of reionisation: Spectroscopic confirmation. The Astrophysical Journal. 808(2), 139.","chicago":"Sobral, David, Jorryt J Matthee, Behnam Darvish, Daniel Schaerer, Bahram Mobasher, Huub Röttgering, Sérgio Santos, and Shoubaneh Hemmati. “Evidence for PopIII-like Stellar Populations in the Most Luminous Lyα Emitters at the Epoch of Reionisation: Spectroscopic Confirmation.” The Astrophysical Journal. IOP Publishing, 2015. https://doi.org/10.1088/0004-637X/808/2/139.","short":"D. Sobral, J.J. Matthee, B. Darvish, D. Schaerer, B. Mobasher, H. Röttgering, S. Santos, S. Hemmati, The Astrophysical Journal 808 (2015) 139.","ieee":"D. Sobral et al., “Evidence for PopIII-like stellar populations in the most luminous Lyα emitters at the epoch of reionisation: Spectroscopic confirmation,” The Astrophysical Journal, vol. 808, no. 2. IOP Publishing, p. 139, 2015.","ama":"Sobral D, Matthee JJ, Darvish B, et al. Evidence for PopIII-like stellar populations in the most luminous Lyα emitters at the epoch of reionisation: Spectroscopic confirmation. The Astrophysical Journal. 2015;808(2):139. doi:10.1088/0004-637X/808/2/139","mla":"Sobral, David, et al. “Evidence for PopIII-like Stellar Populations in the Most Luminous Lyα Emitters at the Epoch of Reionisation: Spectroscopic Confirmation.” The Astrophysical Journal, vol. 808, no. 2, IOP Publishing, 2015, p. 139, doi:10.1088/0004-637X/808/2/139.","apa":"Sobral, D., Matthee, J. J., Darvish, B., Schaerer, D., Mobasher, B., Röttgering, H., … Hemmati, S. (2015). Evidence for PopIII-like stellar populations in the most luminous Lyα emitters at the epoch of reionisation: Spectroscopic confirmation. The Astrophysical Journal. IOP Publishing. https://doi.org/10.1088/0004-637X/808/2/139"},"main_file_link":[{"open_access":"1","url":"https://arxiv.org/abs/1504.01734"}],"author":[{"last_name":"Sobral","first_name":"David","full_name":"Sobral, David"},{"id":"7439a258-f3c0-11ec-9501-9df22fe06720","full_name":"Matthee, Jorryt J","orcid":"0000-0003-2871-127X","last_name":"Matthee","first_name":"Jorryt J"},{"full_name":"Darvish, Behnam","last_name":"Darvish","first_name":"Behnam"},{"full_name":"Schaerer, Daniel","last_name":"Schaerer","first_name":"Daniel"},{"full_name":"Mobasher, Bahram","last_name":"Mobasher","first_name":"Bahram"},{"first_name":"Huub","last_name":"Röttgering","full_name":"Röttgering, Huub"},{"last_name":"Santos","first_name":"Sérgio","full_name":"Santos, Sérgio"},{"full_name":"Hemmati, Shoubaneh","last_name":"Hemmati","first_name":"Shoubaneh"}],"extern":"1","quality_controlled":"1","publication_status":"published","abstract":[{"lang":"eng","text":"Faint Lyα emitters become increasingly rarer toward the reionization epoch (z ∼ 6–7). However, observations from a very large (∼5 deg2) Lyα narrow-band survey at z = 6.6 show that this is not the case for the most luminous emitters, capable of ionizing their own local bubbles. Here we present follow-up observations of the two most luminous Lyα candidates in the COSMOS field: “MASOSA” and “CR7.” We used X-SHOOTER, SINFONI, and FORS2 on the Very Large Telescope, and DEIMOS on Keck, to confirm both candidates beyond any doubt. We find redshifts of z = 6.541 and z = 6.604 for “MASOSA” and “CR7,” respectively. MASOSA has a strong detection in Lyα with a line width of 386 ± 30 km s−1 (FWHM) and with very high EW0 (>200 Å), but undetected in the continuum, implying very low stellar mass and a likely young, metal-poor stellar population. “CR7,” with an observed Lyα luminosity of 1043.92±0.05 erg s−1 is the most luminous Lyα emitter ever found at z > 6 and is spatially extended (∼16 kpc). “CR7” reveals a narrow Lyα line with 266 ± 15 km s−1 FWHM, being detected in the near-infrared (NIR) (rest-frame UV; β = −2.3 ± 0.1) and in IRAC/Spitzer. We detect a narrow He II 1640 Å emission line (6σ, FWHM = 130 ± 30 km s−1 ) in CR7 which can explain the clear excess seen in the J-band photometry (EW0 ∼ 80 Å). We find no other emission lines from the UV to the NIR in our X-SHOOTER spectra (He II/O III] 1663 Å > 3 and He II/C III] 1908 Å > 2.5). We conclude that CR7 is best explained by a combination of a PopIII-like population, which dominates the rest-frame UV and the nebular emission, and a more normal stellar population, which presumably dominates the mass. Hubble Space Telescope/WFC3 observations show that the light is indeed spatially separated between a very blue component, coincident with Lyα and He II emission, and two red components (∼5 kpc away), which dominate the mass. Our findings are consistent with theoretical predictions of a PopIII wave, with PopIII star formation migrating away from the original sites of star formation."}],"title":"Evidence for PopIII-like stellar populations in the most luminous Lyα emitters at the epoch of reionisation: Spectroscopic confirmation","publication":"The Astrophysical Journal","oa":1,"_id":"11519","article_type":"original","publisher":"IOP Publishing","volume":808,"issue":"2","date_created":"2022-07-07T09:00:58Z","month":"07","status":"public","intvolume":" 808","type":"journal_article","date_updated":"2022-08-18T10:30:13Z","oa_version":"Preprint","day":"28","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","article_processing_charge":"No","acknowledgement":"We thank the anonymous reviewer for useful and constructive comments and suggestions which greatly improved the quality and clarity of our work. D.S. acknowledges financial support from the Netherlands Organisation for Scientific research (NWO) through a Veni fellowship, from FCT through a FCT Investigator Starting Grant and Start-up Grant (IF/01154/2012/CP0189/CT0010), from FCT grant UID/FIS/04434/2013, and from LSF and LKBF. J.M. acknowledges the award of a Huygens PhD fellowship. H.R. acknowledges support from the ERC Advanced Investigator program NewClusters 321271. The authors thank Mark Dijkstra, Bhaskar Agarwal, Jarrett Johnson, Andrea Ferrara, Jarle Brinchmann, Rebecca Bowler, George Becker, Emma Curtis-Lake, Milos Milosavljevic, Raffaella Schneider, Paul Shapiro, and Erik Zackrisson for interesting, stimulating and helpful discussions. The authors are extremely grateful to ESO for the award of ESO DDT time (294.A-5018 and 294.A-5039) which allowed the spectroscopic confirmation of both sources and the detailed investigation of their nature. Observations are also based on data from W.M. Keck Observatory. The W.M. Keck Observatory is operated as a scientific partnership of Caltech, the University of California and the National Aeronautics and Space Administration. Based on observations obtained with MegaPrime/Megacam, a joint project of CFHT and CEA/IRFU, at the Canada–France–Hawaii Telescope (CFHT) which is operated by the National Research Council (NRC) of Canada, the Institut National des Science de lUnivers of the Centre National de la Recherche Scientifique (CNRS) of France, and the University of Hawaii. This work is based in part on data products produced at Terapix available at the Canadian Astronomy Data Centre as part of the Canada–France–Hawaii Telescope Legacy Survey, a collaborative project of NRC and CNRS. Based on data products from observations made with ESO Telescopes at the La Silla Paranal Observatory under ESO programme IDs 294.A-5018, 294.A-5039, and 179.A-2005, and on data products produced by TERAPIX and the Cambridge Astronomy Survey Unit on behalf of the UltraVISTA consortium. The authors acknowledge the award of service time (SW2014b20) on the William Herschel Telescope (WHT). WHT and its service programme are operated on the island of La Palma by the Isaac Newton Group in the Spanish Observatorio del Roque de los Muchachos of the Instituto de Astrofisica de Canarias.","language":[{"iso":"eng"}],"doi":"10.1088/0004-637X/808/2/139","date_published":"2015-07-28T00:00:00Z","external_id":{"arxiv":["1504.01734"]},"keyword":["Space and Planetary Science","Astronomy and Astrophysics","dark ages","reionization","first stars – early universe – galaxies: evolution"],"page":"139","arxiv":1,"publication_identifier":{"issn":["0004-637X"],"eissn":["1538-4357"]},"scopus_import":"1"}]