[{"oa_version":"Published Version","fulldoi":"https://doi.org/10.15479/AT:ISTA:th_1032","publication_status":"published","OA_place":"publisher","article_processing_charge":"No","oa":1,"department":[{"_id":"RySh"},{"_id":"GradSch"}],"degree_awarded":"PhD","title":"From the left to the right: A tale of asymmetries, environments, and hippocampal development","_id":"51","publication_identifier":{"issn":["2663-337X"]},"date_created":"2018-12-11T11:44:22Z","pubrep_id":"1032","abstract":[{"lang":"eng","text":"Asymmetries have long been known about in the central nervous system. From gross anatomical differences, such as the presence of the parapineal organ in only one hemisphere of the developing zebrafish, to more subtle differences in activity between both hemispheres, as seen in freely roaming animals or human participants under PET and fMRI imaging analysis. The presence of asymmetries has been demonstrated to have huge behavioural implications, with their disruption often leading to the generation of neurological disorders, memory problems, changes in personality, and in an organism's health and well-being. For my Ph.D. work I aimed to tackle two important avenues of research. The first being the process of input-side dependency in the hippocampus, with the goal of finding a key gene responsible for its development (Gene X). The second project was to do with experience-induced laterality formation in the hippocampus. Specifically, how laterality in the synapse density of the CA1 stratum radiatum (s.r.) could be induced purely through environmental enrichment. Through unilateral tracer injections into the CA3, I was able to selectively measure the properties of synapses within the CA1 and investigate how they differed based upon which hemisphere the presynaptic neurone originated. Having found the existence of a previously unreported reversed (left-isomerism) i.v. mutant, through morpholocal examination of labelled terminals in the CA1 s.r., I aimed to elucidate a key gene responsible for the process of left or right determination of inputs to the CA1 s.r.. This work relates to the previous finding of input-side dependent asymmetry in the wild-type rodent, where the origin of the projecting neurone to the CA1 will determine the morphology of a synapse, to a greater degree than the hemisphere in which the projection terminates. Using left- and right-isomerism i.v. mice, in combination with whole genome sequence analysis, I highlight Ena/VASP-like (Evl) as a potential target for Gene X. In relation to this topic, I also highlight my work in the recently published paper of how knockout of PirB can lead to a lack of input-side dependency in the murine hippocampus. For the second question, I show that the environmental enrichment paradigm will lead to an asymmetry in the synapse densities in the hippocampus of mice. I also highlight that the nature of the enrichment is of less consequence than the process of enrichment itself. I demonstrate that the CA3 region will dramatically alter its projection targets, in relation to environmental stimulation, with the asymmetry in synaptic density, caused by enrichment, relying heavily on commissural fibres. I also highlight the vital importance of input-side dependent asymmetry, as a necessary component of experience-dependent laterality formation in the CA1 s.r.. However, my results suggest that it isn't the only cause, as there appears to be a CA1 dependent mechanism also at play. Upon further investigation, I highlight the significant, and highly important, finding that the changes seen in the CA1 s.r. were predominantly caused through projections from the left-CA3, with the right-CA3 having less involvement in this mechanism."}],"page":"186","date_updated":"2026-07-31T09:40:17Z","file":[{"access_level":"closed","file_name":"2018_Thesis_Case_Source.doc","date_updated":"2021-02-11T23:30:13Z","relation":"source_file","content_type":"application/msword","checksum":"dcc7b55619d8509dd62b8e99d6cdee44","file_id":"6251","creator":"dernst","embargo_to":"open_access","date_created":"2019-04-09T07:16:26Z","file_size":141270528},{"file_name":"2018_Thesis_Case.pdf","access_level":"open_access","relation":"main_file","date_updated":"2021-02-11T11:17:14Z","creator":"dernst","checksum":"f69fdd5c8709c4e618aa8c1a1221153d","content_type":"application/pdf","file_id":"6252","file_size":15193621,"date_created":"2019-04-09T07:16:23Z","embargo":"2019-07-05"}],"doi_confirm":"1","publist_id":"8003","publisher":"Institute of Science and Technology Austria","type":"dissertation","year":"2018","language":[{"iso":"eng"}],"day":"27","supervisor":[{"id":"499F3ABC-F248-11E8-B48F-1D18A9856A87","full_name":"Shigemoto, Ryuichi","orcid":"0000-0001-8761-9444","first_name":"Ryuichi","last_name":"Shigemoto"}],"alternative_title":["ISTA Thesis"],"doi":"10.15479/AT:ISTA:th_1032","user_id":"8b945eb4-e2f2-11eb-945a-df72226e66a9","related_material":{"record":[{"status":"public","relation":"part_of_dissertation","id":"682"}]},"ddc":["571","576"],"month":"06","status":"public","author":[{"first_name":"Matthew J","id":"44B7CA5A-F248-11E8-B48F-1D18A9856A87","full_name":"Case, Matthew J","last_name":"Case"}],"citation":{"ama":"Case MJ. From the left to the right: A tale of asymmetries, environments, and hippocampal development. 2018. doi:<a href=\"https://doi.org/10.15479/AT:ISTA:th_1032\">10.15479/AT:ISTA:th_1032</a>","ieee":"M. J. Case, “From the left to the right: A tale of asymmetries, environments, and hippocampal development,” Institute of Science and Technology Austria, 2018.","chicago":"Case, Matthew J. “From the Left to the Right: A Tale of Asymmetries, Environments, and Hippocampal Development.” Institute of Science and Technology Austria, 2018. <a href=\"https://doi.org/10.15479/AT:ISTA:th_1032\">https://doi.org/10.15479/AT:ISTA:th_1032</a>.","short":"M.J. Case, From the Left to the Right: A Tale of Asymmetries, Environments, and Hippocampal Development, Institute of Science and Technology Austria, 2018.","ista":"Case MJ. 2018. From the left to the right: A tale of asymmetries, environments, and hippocampal development. Institute of Science and Technology Austria.","apa":"Case, M. J. (2018). <i>From the left to the right: A tale of asymmetries, environments, and hippocampal development</i>. Institute of Science and Technology Austria. <a href=\"https://doi.org/10.15479/AT:ISTA:th_1032\">https://doi.org/10.15479/AT:ISTA:th_1032</a>","mla":"Case, Matthew J. <i>From the Left to the Right: A Tale of Asymmetries, Environments, and Hippocampal Development</i>. Institute of Science and Technology Austria, 2018, doi:<a href=\"https://doi.org/10.15479/AT:ISTA:th_1032\">10.15479/AT:ISTA:th_1032</a>."},"corr_author":"1","date_published":"2018-06-27T00:00:00Z","has_accepted_license":"1","file_date_updated":"2021-02-11T23:30:13Z"},{"abstract":[{"lang":"eng","text":"Genomic imprinting is an epigenetic process that leads to parent of origin-specific gene expression in a subset of genes. Imprinted genes are essential for brain development, and deregulation of imprinting is associated with neurodevelopmental diseases and the pathogenesis of psychiatric disorders. However, the cell-type specificity of imprinting at single cell resolution, and how imprinting and thus gene dosage regulates neuronal circuit assembly is still largely unknown. Here, MADM (Mosaic Analysis with Double Markers) technology was employed to assess genomic imprinting at single cell level. By visualizing MADM-induced uniparental disomies (UPDs) in distinct colors at single cell level in genetic mosaic animals, this experimental paradigm provides a unique quantitative platform to systematically assay the UPD-mediated imbalances in imprinted gene expression at unprecedented resolution. An experimental pipeline based on FACS, RNA-seq and bioinformatics analysis was established and applied to systematically map cell-type-specific ‘imprintomes’ in the mouse brain. The results revealed that parental-specific expression of imprinted genes per se is rarely cell-type-specific even at the individual cell level. Conversely, when we extended the comparison to downstream responses resulting from imbalanced imprinted gene expression, we discovered an unexpectedly high degree of cell-type specificity. Furthermore, we determined a novel function of genomic imprinting in cortical astrocyte production and in olfactory bulb (OB) granule cell generation. These results suggest important functional implication of genomic imprinting for generating cell-type diversity in the brain. In addition, MADM provides a powerful tool to study candidate genes by concomitant genetic manipulation and fluorescent labelling of single cells. MADM-based candidate gene approach was utilized to identify potential imprinted genes involved in the generation of cortical astrocytes and OB granule cells. We investigated p57Kip2, a maternally expressed gene and known cell cycle regulator. Although we found that p57Kip2 does not play a role in these processes, we detected an unexpected function of the paternal allele previously thought to be silent. Finally, we took advantage of a key property of MADM which is to allow unambiguous investigation of environmental impact on single cells. The experimental pipeline based on FACS and RNA-seq analysis of MADM-labeled cells was established to probe the functional differences of single cell loss of gene function compared to global loss of function on a transcriptional level. With this method, both common and distinct responses were isolated due to cell-autonomous and non-autonomous effects acting on genotypically identical cells. As a result, transcriptional changes were identified which result solely from the surrounding environment. Using the MADM technology to study genomic imprinting at single cell resolution, we have identified cell-type-specific gene expression, novel gene function and the impact of environment on single cell transcriptomes. Together, these provide important insights to the understanding of mechanisms regulating cell-type specificity and thus diversity in the brain."}],"pubrep_id":"1057","page":"1 - 139","date_updated":"2026-07-29T13:40:27Z","file":[{"date_created":"2019-05-10T07:47:04Z","file_size":17949175,"file_name":"Thesis_LaukoterSusanne_FINAL.docx","access_level":"closed","date_updated":"2019-11-23T23:30:03Z","relation":"source_file","content_type":"application/vnd.openxmlformats-officedocument.wordprocessingml.document","checksum":"41fdbf5fdce312802935d88a8ad9932c","file_id":"6396","embargo_to":"open_access","creator":"dernst"},{"date_created":"2019-05-10T07:47:04Z","file_size":21187245,"embargo":"2019-11-21","access_level":"open_access","file_name":"Thesis_LaukoterSusanne_FINAL.pdf","date_updated":"2021-02-11T11:17:16Z","relation":"main_file","checksum":"53001a9a0c9e570e598d861bb0af28aa","content_type":"application/pdf","file_id":"6397","creator":"dernst"}],"publist_id":"8046","doi_confirm":"1","type":"dissertation","publisher":"Institute of Science and Technology Austria","language":[{"iso":"eng"}],"year":"2018","fulldoi":"https://doi.org/10.15479/AT:ISTA:th1057","oa_version":"Published Version","OA_place":"publisher","publication_status":"published","article_processing_charge":"No","oa":1,"degree_awarded":"PhD","department":[{"_id":"SiHi"},{"_id":"GradSch"}],"_id":"10","title":"Role of genomic imprinting in cerebral cortex development","publication_identifier":{"issn":["2663-337X"]},"date_created":"2018-12-11T11:44:08Z","citation":{"ama":"Laukoter S. Role of genomic imprinting in cerebral cortex development. 2018:1-139. doi:<a href=\"https://doi.org/10.15479/AT:ISTA:th1057\">10.15479/AT:ISTA:th1057</a>","ieee":"S. Laukoter, “Role of genomic imprinting in cerebral cortex development,” Institute of Science and Technology Austria, 2018.","mla":"Laukoter, Susanne. <i>Role of Genomic Imprinting in Cerebral Cortex Development</i>. Institute of Science and Technology Austria, 2018, pp. 1–139, doi:<a href=\"https://doi.org/10.15479/AT:ISTA:th1057\">10.15479/AT:ISTA:th1057</a>.","apa":"Laukoter, S. (2018). <i>Role of genomic imprinting in cerebral cortex development</i>. Institute of Science and Technology Austria. <a href=\"https://doi.org/10.15479/AT:ISTA:th1057\">https://doi.org/10.15479/AT:ISTA:th1057</a>","short":"S. Laukoter, Role of Genomic Imprinting in Cerebral Cortex Development, Institute of Science and Technology Austria, 2018.","ista":"Laukoter S. 2018. Role of genomic imprinting in cerebral cortex development. Institute of Science and Technology Austria.","chicago":"Laukoter, Susanne. “Role of Genomic Imprinting in Cerebral Cortex Development.” Institute of Science and Technology Austria, 2018. <a href=\"https://doi.org/10.15479/AT:ISTA:th1057\">https://doi.org/10.15479/AT:ISTA:th1057</a>."},"corr_author":"1","date_published":"2018-11-21T00:00:00Z","file_date_updated":"2021-02-11T11:17:16Z","has_accepted_license":"1","day":"21","supervisor":[{"last_name":"Vicoso","first_name":"Beatriz","full_name":"Vicoso, Beatriz","orcid":"0000-0002-4579-8306","id":"49E1C5C6-F248-11E8-B48F-1D18A9856A87"}],"alternative_title":["ISTA Thesis"],"user_id":"8b945eb4-e2f2-11eb-945a-df72226e66a9","doi":"10.15479/AT:ISTA:th1057","author":[{"last_name":"Laukoter","first_name":"Susanne","id":"2D6B7A9A-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-7903-3010","full_name":"Laukoter, Susanne"}],"month":"11","status":"public","ddc":["570"]},{"type":"dissertation","publisher":"Institute of Science and Technology Austria","language":[{"iso":"eng"}],"year":"2018","publist_id":"7277","doi_confirm":"1","date_updated":"2026-07-29T13:30:01Z","file":[{"creator":"dernst","embargo_to":"open_access","checksum":"0c9d6d1c80d9857e6e545213467bbcb2","content_type":"application/vnd.openxmlformats-officedocument.wordprocessingml.document","file_id":"6226","file_name":"2018_Hurny_thesis_source.docx","access_level":"closed","date_updated":"2020-12-02T23:30:08Z","relation":"source_file","file_size":28112114,"date_created":"2019-04-05T09:37:56Z"},{"checksum":"ecbe481a1413d270bd501b872c7ed54f","content_type":"application/pdf","file_id":"6227","creator":"dernst","access_level":"open_access","file_name":"2018_Hurny_thesis.pdf","date_updated":"2020-12-02T09:52:16Z","relation":"main_file","embargo":"2019-07-10","date_created":"2019-04-05T09:37:55Z","file_size":12524427}],"abstract":[{"lang":"eng","text":"The whole life cycle of plants as well as their responses to environmental stimuli is governed by a complex network of hormonal regulations. A number of studies have demonstrated an essential role of both auxin and cytokinin in the regulation of many aspects of plant growth and development including embryogenesis, postembryonic organogenic processes such as root, and shoot branching, root and shoot apical meristem activity and phyllotaxis. Over the last decades essential knowledge on the key molecular factors and pathways that spatio-temporally define auxin and cytokinin activities in the plant body has accumulated. However, how both hormonal pathways are interconnected by a complex network of interactions and feedback circuits that determines the final outcome of the individual hormone actions is still largely unknown. Root system architecture establishment and in particular formation of lateral organs is prime example of developmental process at whose regulation both auxin and cytokinin pathways converge. To dissect convergence points and pathways that tightly balance auxin - cytokinin antagonistic activities that determine the root branching pattern transcriptome profiling was applied. Genome wide expression analyses of the xylem pole pericycle, a tissue giving rise to lateral roots, led to identification of genes that are highly responsive to combinatorial auxin and cytokinin treatments and play an essential function in the auxin-cytokinin regulated root branching. SYNERGISTIC AUXIN CYTOKININ 1 (SYAC1) gene, which encodes for a protein of unknown function, was detected among the top candidate genes of which expression was synergistically up-regulated by simultaneous hormonal treatment. Plants with modulated SYAC1 activity exhibit severe defects in the root system establishment and attenuate developmental responses to both auxin and cytokinin. To explore the biological function of the SYAC1, we employed different strategies including expression pattern analysis, subcellular localization and phenotypic analyses of the syac1 loss-of-function and gain-of-function transgenic lines along with the identification of the SYAC1 interaction partners. Detailed functional characterization revealed that SYAC1 acts as a developmentally specific regulator of the secretory pathway to control deposition of cell wall components and thereby rapidly fine tune elongation growth."}],"pubrep_id":"930","page":"147","publication_identifier":{"issn":["2663-337X"]},"date_created":"2018-12-11T11:47:03Z","degree_awarded":"PhD","department":[{"_id":"EvBe"},{"_id":"GradSch"}],"_id":"539","title":"Identification and characterization of novel auxin-cytokinin cross-talk components","article_processing_charge":"No","oa":1,"fulldoi":"https://doi.org/10.15479/AT:ISTA:th_930","oa_version":"Published Version","OA_place":"publisher","publication_status":"published","date_published":"2018-01-01T00:00:00Z","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)"},"file_date_updated":"2020-12-02T23:30:08Z","has_accepted_license":"1","corr_author":"1","citation":{"ama":"Hurny A. Identification and characterization of novel auxin-cytokinin cross-talk components. 2018. doi:<a href=\"https://doi.org/10.15479/AT:ISTA:th_930\">10.15479/AT:ISTA:th_930</a>","ieee":"A. Hurny, “Identification and characterization of novel auxin-cytokinin cross-talk components,” Institute of Science and Technology Austria, 2018.","chicago":"Hurny, Andrej. “Identification and Characterization of Novel Auxin-Cytokinin Cross-Talk Components.” Institute of Science and Technology Austria, 2018. <a href=\"https://doi.org/10.15479/AT:ISTA:th_930\">https://doi.org/10.15479/AT:ISTA:th_930</a>.","mla":"Hurny, Andrej. <i>Identification and Characterization of Novel Auxin-Cytokinin Cross-Talk Components</i>. Institute of Science and Technology Austria, 2018, doi:<a href=\"https://doi.org/10.15479/AT:ISTA:th_930\">10.15479/AT:ISTA:th_930</a>.","ista":"Hurny A. 2018. Identification and characterization of novel auxin-cytokinin cross-talk components. Institute of Science and Technology Austria.","short":"A. Hurny, Identification and Characterization of Novel Auxin-Cytokinin Cross-Talk Components, Institute of Science and Technology Austria, 2018.","apa":"Hurny, A. (2018). <i>Identification and characterization of novel auxin-cytokinin cross-talk components</i>. Institute of Science and Technology Austria. <a href=\"https://doi.org/10.15479/AT:ISTA:th_930\">https://doi.org/10.15479/AT:ISTA:th_930</a>"},"author":[{"last_name":"Hurny","full_name":"Hurny, Andrej","orcid":"0000-0003-3638-1426","id":"4DC4AF46-F248-11E8-B48F-1D18A9856A87","first_name":"Andrej"}],"ddc":["570"],"month":"01","status":"public","related_material":{"record":[{"id":"1024","relation":"part_of_dissertation","status":"public"}]},"alternative_title":["ISTA Thesis"],"user_id":"8b945eb4-e2f2-11eb-945a-df72226e66a9","doi":"10.15479/AT:ISTA:th_930","day":"01","supervisor":[{"id":"38F4F166-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-8510-9739","full_name":"Benková, Eva","first_name":"Eva","last_name":"Benková"}]},{"day":"01","user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","doi":"10.1534/g3.117.300452","publication":"G3: Genes, Genomes, Genetics","quality_controlled":"1","related_material":{"record":[{"id":"6530","relation":"research_paper"},{"id":"6543","relation":"research_paper"},{"id":"11193","status":"public","relation":"dissertation_contains"},{"id":"6546","status":"public","relation":"dissertation_contains"}]},"author":[{"last_name":"György","id":"3BCEDBE0-F248-11E8-B48F-1D18A9856A87","full_name":"György, Attila","orcid":"0000-0002-1819-198X","first_name":"Attila"},{"last_name":"Roblek","first_name":"Marko","id":"3047D808-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0001-9588-1389","full_name":"Roblek, Marko"},{"first_name":"Aparna","id":"2F064CFE-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0001-7190-0776","full_name":"Ratheesh, Aparna","last_name":"Ratheesh"},{"last_name":"Valosková","first_name":"Katarina","id":"46F146FC-F248-11E8-B48F-1D18A9856A87","full_name":"Valosková, Katarina","orcid":"0000-0002-7926-0221"},{"last_name":"Belyaeva","first_name":"Vera","id":"47F080FE-F248-11E8-B48F-1D18A9856A87","full_name":"Belyaeva, Vera"},{"first_name":"Stephanie","id":"2A95E7B0-F248-11E8-B48F-1D18A9856A87","full_name":"Wachner, Stephanie","last_name":"Wachner"},{"full_name":"Matsubayashi, Yutaka","first_name":"Yutaka","last_name":"Matsubayashi"},{"first_name":"Besaiz","full_name":"Sanchez Sanchez, Besaiz","last_name":"Sanchez Sanchez"},{"full_name":"Stramer, Brian","first_name":"Brian","last_name":"Stramer"},{"first_name":"Daria E","id":"3D224B9E-F248-11E8-B48F-1D18A9856A87","full_name":"Siekhaus, Daria E","orcid":"0000-0001-8323-8353","last_name":"Siekhaus"}],"ddc":["570"],"status":"public","month":"03","isi":1,"issue":"3","citation":{"ama":"György A, Roblek M, Ratheesh A, et al. Tools allowing independent visualization and genetic manipulation of Drosophila melanogaster macrophages and surrounding tissues. <i>G3: Genes, Genomes, Genetics</i>. 2018;8(3):845-857. doi:<a href=\"https://doi.org/10.1534/g3.117.300452\">10.1534/g3.117.300452</a>","ieee":"A. György <i>et al.</i>, “Tools allowing independent visualization and genetic manipulation of Drosophila melanogaster macrophages and surrounding tissues,” <i>G3: Genes, Genomes, Genetics</i>, vol. 8, no. 3. Genetics Society of America, pp. 845–857, 2018.","short":"A. György, M. Roblek, A. Ratheesh, K. Valosková, V. Belyaeva, S. Wachner, Y. Matsubayashi, B. Sanchez Sanchez, B. Stramer, D.E. Siekhaus, G3: Genes, Genomes, Genetics 8 (2018) 845–857.","ista":"György A, Roblek M, Ratheesh A, Valosková K, Belyaeva V, Wachner S, Matsubayashi Y, Sanchez Sanchez B, Stramer B, Siekhaus DE. 2018. Tools allowing independent visualization and genetic manipulation of Drosophila melanogaster macrophages and surrounding tissues. G3: Genes, Genomes, Genetics. 8(3), 845–857.","apa":"György, A., Roblek, M., Ratheesh, A., Valosková, K., Belyaeva, V., Wachner, S., … Siekhaus, D. E. (2018). Tools allowing independent visualization and genetic manipulation of Drosophila melanogaster macrophages and surrounding tissues. <i>G3: Genes, Genomes, Genetics</i>. Genetics Society of America. <a href=\"https://doi.org/10.1534/g3.117.300452\">https://doi.org/10.1534/g3.117.300452</a>","mla":"György, Attila, et al. “Tools Allowing Independent Visualization and Genetic Manipulation of Drosophila Melanogaster Macrophages and Surrounding Tissues.” <i>G3: Genes, Genomes, Genetics</i>, vol. 8, no. 3, Genetics Society of America, 2018, pp. 845–57, doi:<a href=\"https://doi.org/10.1534/g3.117.300452\">10.1534/g3.117.300452</a>.","chicago":"György, Attila, Marko Roblek, Aparna Ratheesh, Katarina Valosková, Vera Belyaeva, Stephanie Wachner, Yutaka Matsubayashi, Besaiz Sanchez Sanchez, Brian Stramer, and Daria E Siekhaus. “Tools Allowing Independent Visualization and Genetic Manipulation of Drosophila Melanogaster Macrophages and Surrounding Tissues.” <i>G3: Genes, Genomes, Genetics</i>. Genetics Society of America, 2018. <a href=\"https://doi.org/10.1534/g3.117.300452\">https://doi.org/10.1534/g3.117.300452</a>."},"ec_funded":1,"scopus_import":"1","corr_author":"1","external_id":{"isi":["000426693300011"]},"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)"},"date_published":"2018-03-01T00:00:00Z","acknowledgement":" A. Ratheesh also by Marie Curie IIF GA-2012-32950BB:DICJI, Marko Roblek by the provincial government of Lower Austria, K. Valoskova and S. Wachner by DOC Fellowships from the Austrian Academy of Sciences, ","file_date_updated":"2020-07-14T12:46:56Z","has_accepted_license":"1","fulldoi":"https://doi.org/10.1534/g3.117.300452","oa_version":"Published Version","publication_status":"published","article_processing_charge":"No","oa":1,"department":[{"_id":"DaSi"}],"_id":"544","title":"Tools allowing independent visualization and genetic manipulation of Drosophila melanogaster macrophages and surrounding tissues","date_created":"2018-12-11T11:47:05Z","abstract":[{"text":"Drosophila melanogaster plasmatocytes, the phagocytic cells among hemocytes, are essential for immune responses, but also play key roles from early development to death through their interactions with other cell types. They regulate homeostasis and signaling during development, stem cell proliferation, metabolism, cancer, wound responses and aging, displaying intriguing molecular and functional conservation with vertebrate macrophages. Given the relative ease of genetics in Drosophila compared to vertebrates, tools permitting visualization and genetic manipulation of plasmatocytes and surrounding tissues independently at all stages would greatly aid in fully understanding these processes, but are lacking. Here we describe a comprehensive set of transgenic lines that allow this. These include extremely brightly fluorescing mCherry-based lines that allow GAL4-independent visualization of plasmatocyte nuclei, cytoplasm or actin cytoskeleton from embryonic Stage 8 through adulthood in both live and fixed samples even as heterozygotes, greatly facilitating screening. These lines allow live visualization and tracking of embryonic plasmatocytes, as well as larval plasmatocytes residing at the body wall or flowing with the surrounding hemolymph. With confocal imaging, interactions of plasmatocytes and inner tissues can be seen in live or fixed embryos, larvae and adults. They permit efficient GAL4-independent FACS analysis/sorting of plasmatocytes throughout life. To facilitate genetic analysis of reciprocal signaling, we have also made a plasmatocyte-expressing QF2 line that in combination with extant GAL4 drivers allows independent genetic manipulation of both plasmatocytes and surrounding tissues, and a GAL80 line that blocks GAL4 drivers from affecting plasmatocytes, both of which function from the early embryo to the adult.","lang":"eng"}],"pubrep_id":"990","page":"845 - 857","volume":8,"intvolume":"         8","date_updated":"2026-10-05T22:31:08Z","acknowledged_ssus":[{"_id":"LifeSc"}],"file":[{"date_created":"2018-12-12T10:11:48Z","file_size":2251222,"checksum":"7d9d28b915159078a4ca7add568010e8","content_type":"application/pdf","file_id":"4905","creator":"system","file_name":"IST-2018-990-v1+1_2018_Gyoergy_Tools_allowing.pdf","access_level":"open_access","relation":"main_file","date_updated":"2020-07-14T12:46:56Z"}],"publist_id":"7271","type":"journal_article","publisher":"Genetics Society of America","language":[{"iso":"eng"}],"project":[{"name":"The role of Drosophila TNF alpha in immune cell invasion","_id":"253B6E48-B435-11E9-9278-68D0E5697425","call_identifier":"FWF","grant_number":"P29638"},{"_id":"253B6E48-B435-11E9-9278-68D0E5697425","name":"The role of Drosophila TNF alpha in immune cell invasion","call_identifier":"FWF","grant_number":"P29638"},{"name":"Investigating the role of the novel major superfamily facilitator transporter family member MFSD1 in metastasis","_id":"2637E9C0-B435-11E9-9278-68D0E5697425","grant_number":"LSC16-021"},{"grant_number":"334077","_id":"2536F660-B435-11E9-9278-68D0E5697425","name":"Investigating the role of transporters in invasive migration through junctions","call_identifier":"FP7"}],"year":"2018"},{"publication_status":"published","OA_place":"publisher","oa_version":"Published Version","fulldoi":"https://doi.org/10.15479/AT:ISTA:th1064","oa":1,"article_processing_charge":"No","title":"Transcriptional regulation of macrophage migration in the Drosophila melanogaster embryo ","_id":"9","department":[{"_id":"DaSi"},{"_id":"GradSch"}],"degree_awarded":"PhD","date_created":"2018-12-11T11:44:08Z","publication_identifier":{"issn":["2663-337X"]},"page":"96","pubrep_id":"1064","abstract":[{"lang":"eng","text":"Immune cells migrating to the sites of infection navigate through diverse tissue architectures and switch their migratory mechanisms upon demand. However, little is known about systemic regulators that could allow the acquisition of these mechanisms. We performed a genetic screen in Drosophila melanogaster to identify regulators of germband invasion by embryonic macrophages into the confined space between the ectoderm and mesoderm. We have found that bZIP circadian transcription factors (TFs) Kayak (dFos) and Vrille (dNFIL3) have opposite effects on macrophage germband infiltration: Kayak facilitated and Vrille inhibited it. These TFs are enriched in the macrophages during migration and genetically interact to control it. Kayak sets a less coordinated mode of migration of the macrophage group and increases the probability and length of Levy walks. Intriguingly, the motility of kayak mutant macrophages was also strongly affected during initial germband invasion but not along another less confined route. Inhibiting Rho1 signaling within the tail ectoderm partially rescued the Kayak mutant phenotype, strongly suggesting that migrating macrophages have to overcome a barrier imposed by the stiffness of the ectoderm. Also, Kayak appeared to be important for the maintenance of the round cell shape and the rear edge translocation of the macrophages invading the germband. Complementary to this, the cortical actin cytoskeleton of Kayak- deficient macrophages was strongly affected. RNA sequencing revealed the filamin Cheerio and tetraspanin TM4SF to be downstream of Kayak. Chromatin immunoprecipitation and immunostaining revealed that the formin Diaphanous is another downstream target of Kayak. Immunostaining revealed that the formin Diaphanous is another downstream target of Kayak. Indeed, Cheerio, TM4SF and Diaphanous are required within macrophages for germband invasion, and expression of constitutively active Diaphanous in macrophages was able to rescue the kayak mutant phenotype. Moreover, Cher and Diaphanous are also reduced in the macrophages overexpressing Vrille. We hypothesize that Kayak, through its targets, increases actin polymerization and cortical tension in macrophages and thus allows extra force generation necessary for macrophage dissemination and migration through confined stiff tissues, while Vrille counterbalances it."}],"file":[{"access_level":"closed","file_name":"2018_Thesis_Belyaeva_source.docx","relation":"source_file","date_updated":"2020-07-14T12:48:14Z","embargo_to":"open_access","creator":"dernst","content_type":"application/vnd.openxmlformats-officedocument.wordprocessingml.document","checksum":"d27b2465cb70d0c9678a0381b9b6ced1","file_id":"6243","file_size":102737483,"date_created":"2019-04-08T14:13:12Z"},{"embargo":"2019-11-19","file_size":88077843,"date_created":"2019-04-08T14:14:08Z","creator":"dernst","file_id":"6244","content_type":"application/pdf","checksum":"a2939b61bde2de7b8ced77bbae0eaaed","date_updated":"2021-02-11T11:17:16Z","relation":"main_file","access_level":"open_access","file_name":"2018_Thesis_Belyaeva.pdf"}],"date_updated":"2026-09-02T08:54:56Z","doi_confirm":"1","publist_id":"8047","year":"2018","language":[{"iso":"eng"}],"publisher":"Institute of Science and Technology Austria","type":"dissertation","supervisor":[{"last_name":"Siekhaus","first_name":"Daria E","id":"3D224B9E-F248-11E8-B48F-1D18A9856A87","full_name":"Siekhaus, Daria E","orcid":"0000-0001-8323-8353"}],"day":"01","user_id":"8b945eb4-e2f2-11eb-945a-df72226e66a9","doi":"10.15479/AT:ISTA:th1064","alternative_title":["ISTA Thesis"],"status":"public","month":"07","ddc":["570"],"author":[{"last_name":"Belyaeva","id":"47F080FE-F248-11E8-B48F-1D18A9856A87","full_name":"Belyaeva, Vera","first_name":"Vera"}],"citation":{"chicago":"Belyaeva, Vera. “Transcriptional Regulation of Macrophage Migration in the Drosophila Melanogaster Embryo .” Institute of Science and Technology Austria, 2018. <a href=\"https://doi.org/10.15479/AT:ISTA:th1064\">https://doi.org/10.15479/AT:ISTA:th1064</a>.","mla":"Belyaeva, Vera. <i>Transcriptional Regulation of Macrophage Migration in the Drosophila Melanogaster Embryo </i>. Institute of Science and Technology Austria, 2018, doi:<a href=\"https://doi.org/10.15479/AT:ISTA:th1064\">10.15479/AT:ISTA:th1064</a>.","short":"V. Belyaeva, Transcriptional Regulation of Macrophage Migration in the Drosophila Melanogaster Embryo , Institute of Science and Technology Austria, 2018.","apa":"Belyaeva, V. (2018). <i>Transcriptional regulation of macrophage migration in the Drosophila melanogaster embryo </i>. Institute of Science and Technology Austria. <a href=\"https://doi.org/10.15479/AT:ISTA:th1064\">https://doi.org/10.15479/AT:ISTA:th1064</a>","ista":"Belyaeva V. 2018. Transcriptional regulation of macrophage migration in the Drosophila melanogaster embryo . Institute of Science and Technology Austria.","ama":"Belyaeva V. Transcriptional regulation of macrophage migration in the Drosophila melanogaster embryo . 2018. doi:<a href=\"https://doi.org/10.15479/AT:ISTA:th1064\">10.15479/AT:ISTA:th1064</a>","ieee":"V. Belyaeva, “Transcriptional regulation of macrophage migration in the Drosophila melanogaster embryo ,” Institute of Science and Technology Austria, 2018."},"corr_author":"1","file_date_updated":"2021-02-11T11:17:16Z","has_accepted_license":"1","date_published":"2018-07-01T00:00:00Z"},{"article_processing_charge":"No","oa":1,"fulldoi":"https://doi.org/10.15479/at:ista:th_1055","oa_version":"Published Version","OA_place":"publisher","publication_status":"published","publication_identifier":{"issn":["2663-337X"]},"date_created":"2019-04-09T14:13:39Z","degree_awarded":"PhD","department":[{"_id":"HaJa"},{"_id":"GradSch"}],"_id":"6266","title":"Design and characterization of methods and biological components to realize synthetic neurotransmission ","date_updated":"2026-09-03T06:34:46Z","file":[{"file_id":"6267","content_type":"application/pdf","checksum":"9d2c2dca04b00e485470c28b262af59a","creator":"dernst","relation":"main_file","date_updated":"2021-02-11T11:17:16Z","file_name":"2018_Thesis_McKenzie.pdf","access_level":"open_access","embargo":"2019-11-24","date_created":"2019-04-09T14:12:40Z","file_size":4906420},{"date_updated":"2020-07-14T12:47:25Z","relation":"source_file","file_name":"2018_Thesis_McKenzie_source.docx","access_level":"closed","file_id":"6268","checksum":"50b58c272899601bc6fd9642c4dc97f1","content_type":"application/vnd.openxmlformats-officedocument.wordprocessingml.document","creator":"dernst","embargo_to":"open_access","date_created":"2019-04-09T14:12:40Z","file_size":5053545}],"pubrep_id":"1055","abstract":[{"lang":"eng","text":"A major challenge in neuroscience research is to dissect the circuits that orchestrate behavior in health and disease. Proteins from a wide range of non-mammalian species, such as microbial opsins, have been successfully transplanted to specific neuronal targets to override their natural communication patterns. The goal of our work is to manipulate synaptic communication in a manner that closely incorporates the functional intricacies of synapses by preserving temporal encoding (i.e. the firing pattern of the presynaptic neuron) and connectivity (i.e. target specific synapses rather than specific neurons). Our strategy to achieve this goal builds on the use of non-mammalian transplants to create a synthetic synapse. The mode of modulation comes from pre-synaptic uptake of a synthetic neurotransmitter (SN) into synaptic vesicles by means of a genetically targeted transporter selective for the SN. Upon natural vesicular release, exposure of the SN to the synaptic cleft will modify the post-synaptic potential through an orthogonal ligand gated ion channel. To achieve this goal we have functionally characterized a mixed cationic methionine-gated ion channel from Arabidopsis thaliana, designed a method to functionally characterize a synthetic transporter in isolated synaptic vesicles without the need for transgenic animals, identified and extracted multiple prokaryotic uptake systems that are substrate specific for methionine (Met), and established a primary/cell line co-culture system that would allow future combinatorial testing of this orthogonal transmitter-transporter-channel trifecta. Synthetic synapses will provide a unique opportunity to manipulate synaptic communication while maintaining the electrophysiological integrity of the pre-synaptic cell. In this way, information may be preserved that was generated in upstream circuits and that could be essential for concerted function and information processing. "}],"page":"95","type":"dissertation","publisher":"Institute of Science and Technology Austria","language":[{"iso":"eng"}],"year":"2018","doi_confirm":"1","alternative_title":["ISTA Thesis"],"user_id":"8b945eb4-e2f2-11eb-945a-df72226e66a9","doi":"10.15479/at:ista:th_1055","day":"31","supervisor":[{"last_name":"Janovjak","first_name":"Harald L","id":"33BA6C30-F248-11E8-B48F-1D18A9856A87","full_name":"Janovjak, Harald L","orcid":"0000-0002-8023-9315"}],"author":[{"first_name":"Catherine","full_name":"Mckenzie, Catherine","id":"3EEDE19A-F248-11E8-B48F-1D18A9856A87","last_name":"Mckenzie"}],"ddc":["571","573"],"status":"public","month":"10","related_material":{"record":[{"relation":"new_edition","status":"public","id":"7132"}]},"citation":{"chicago":"Mckenzie, Catherine. “Design and Characterization of Methods and Biological Components to Realize Synthetic Neurotransmission .” Institute of Science and Technology Austria, 2018. <a href=\"https://doi.org/10.15479/at:ista:th_1055\">https://doi.org/10.15479/at:ista:th_1055</a>.","apa":"Mckenzie, C. (2018). <i>Design and characterization of methods and biological components to realize synthetic neurotransmission </i>. Institute of Science and Technology Austria. <a href=\"https://doi.org/10.15479/at:ista:th_1055\">https://doi.org/10.15479/at:ista:th_1055</a>","ista":"Mckenzie C. 2018. Design and characterization of methods and biological components to realize synthetic neurotransmission . Institute of Science and Technology Austria.","short":"C. Mckenzie, Design and Characterization of Methods and Biological Components to Realize Synthetic Neurotransmission , Institute of Science and Technology Austria, 2018.","mla":"Mckenzie, Catherine. <i>Design and Characterization of Methods and Biological Components to Realize Synthetic Neurotransmission </i>. Institute of Science and Technology Austria, 2018, doi:<a href=\"https://doi.org/10.15479/at:ista:th_1055\">10.15479/at:ista:th_1055</a>.","ama":"Mckenzie C. Design and characterization of methods and biological components to realize synthetic neurotransmission . 2018. doi:<a href=\"https://doi.org/10.15479/at:ista:th_1055\">10.15479/at:ista:th_1055</a>","ieee":"C. Mckenzie, “Design and characterization of methods and biological components to realize synthetic neurotransmission ,” Institute of Science and Technology Austria, 2018."},"date_published":"2018-10-31T00:00:00Z","file_date_updated":"2021-02-11T11:17:16Z","has_accepted_license":"1","corr_author":"1"},{"publisher":"Society for Neuroscience","type":"journal_article","year":"2018","project":[{"_id":"25681D80-B435-11E9-9278-68D0E5697425","name":"International IST Postdoc Fellowship Programme","call_identifier":"FP7","grant_number":"291734"},{"call_identifier":"FWF","_id":"257D4372-B435-11E9-9278-68D0E5697425","name":"Interneuron plasticity during spatial learning","grant_number":"I2072-B27"}],"language":[{"iso":"eng"}],"abstract":[{"lang":"eng","text":"With the advent of optogenetics, it became possible to change the activity of a targeted population of neurons in a temporally controlled manner. To combine the advantages of 60-channel in vivo tetrode recording and laser-based optogenetics, we have developed a closed-loop recording system that allows for the actual electrophysiological signal to be used as a trigger for the laser light mediating the optogenetic intervention. We have optimized the weight, size, and shape of the corresponding implant to make it compatible with the size, force, and movements of a behaving mouse, and we have shown that the system can efficiently block sharp wave ripple (SWR) events using those events themselves as a trigger. To demonstrate the full potential of the optogenetic recording system we present a pilot study addressing the contribution of SWR events to learning in a complex behavioral task."}],"volume":5,"article_number":"e0087","date_updated":"2026-10-05T22:31:09Z","intvolume":"         5","file":[{"file_size":3746884,"date_created":"2019-02-05T12:48:36Z","date_updated":"2020-07-14T12:47:13Z","relation":"main_file","file_name":"2018_ENeuro_Guerrero.pdf","access_level":"open_access","creator":"dernst","file_id":"5921","content_type":"application/pdf","checksum":"f4915d45fc7ad4648b7b7a13fdecca01"}],"department":[{"_id":"JoCs"}],"title":"Tetrode recording from the hippocampus of behaving mice coupled with four-point-irradiation closed-loop optogenetics: A technique to study the contribution of Hippocampal SWR events to learning","_id":"5914","date_created":"2019-02-03T22:59:16Z","oa_version":"Published Version","fulldoi":"https://doi.org/10.1523/ENEURO.0087-18.2018","publication_status":"published","article_processing_charge":"No","oa":1,"external_id":{"isi":["000443994700007"]},"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)"},"date_published":"2018-07-27T00:00:00Z","file_date_updated":"2020-07-14T12:47:13Z","has_accepted_license":"1","citation":{"ama":"Rangel Guerrero DK, Donnett JG, Csicsvari JL, Kovács K. Tetrode recording from the hippocampus of behaving mice coupled with four-point-irradiation closed-loop optogenetics: A technique to study the contribution of Hippocampal SWR events to learning. <i>eNeuro</i>. 2018;5(4). doi:<a href=\"https://doi.org/10.1523/ENEURO.0087-18.2018\">10.1523/ENEURO.0087-18.2018</a>","ieee":"D. K. Rangel Guerrero, J. G. Donnett, J. L. Csicsvari, and K. Kovács, “Tetrode recording from the hippocampus of behaving mice coupled with four-point-irradiation closed-loop optogenetics: A technique to study the contribution of Hippocampal SWR events to learning,” <i>eNeuro</i>, vol. 5, no. 4. Society for Neuroscience, 2018.","chicago":"Rangel Guerrero, Dámaris K, James G. Donnett, Jozsef L Csicsvari, and Krisztián Kovács. “Tetrode Recording from the Hippocampus of Behaving Mice Coupled with Four-Point-Irradiation Closed-Loop Optogenetics: A Technique to Study the Contribution of Hippocampal SWR Events to Learning.” <i>ENeuro</i>. Society for Neuroscience, 2018. <a href=\"https://doi.org/10.1523/ENEURO.0087-18.2018\">https://doi.org/10.1523/ENEURO.0087-18.2018</a>.","apa":"Rangel Guerrero, D. K., Donnett, J. G., Csicsvari, J. L., &#38; Kovács, K. (2018). Tetrode recording from the hippocampus of behaving mice coupled with four-point-irradiation closed-loop optogenetics: A technique to study the contribution of Hippocampal SWR events to learning. <i>ENeuro</i>. Society for Neuroscience. <a href=\"https://doi.org/10.1523/ENEURO.0087-18.2018\">https://doi.org/10.1523/ENEURO.0087-18.2018</a>","short":"D.K. Rangel Guerrero, J.G. Donnett, J.L. Csicsvari, K. Kovács, ENeuro 5 (2018).","ista":"Rangel Guerrero DK, Donnett JG, Csicsvari JL, Kovács K. 2018. Tetrode recording from the hippocampus of behaving mice coupled with four-point-irradiation closed-loop optogenetics: A technique to study the contribution of Hippocampal SWR events to learning. eNeuro. 5(4), e0087.","mla":"Rangel Guerrero, Dámaris K., et al. “Tetrode Recording from the Hippocampus of Behaving Mice Coupled with Four-Point-Irradiation Closed-Loop Optogenetics: A Technique to Study the Contribution of Hippocampal SWR Events to Learning.” <i>ENeuro</i>, vol. 5, no. 4, e0087, Society for Neuroscience, 2018, doi:<a href=\"https://doi.org/10.1523/ENEURO.0087-18.2018\">10.1523/ENEURO.0087-18.2018</a>."},"ec_funded":1,"scopus_import":"1","publication":"eNeuro","quality_controlled":"1","related_material":{"record":[{"relation":"dissertation_contains","status":"public","id":"6849"}]},"month":"07","status":"public","isi":1,"ddc":["570"],"author":[{"last_name":"Rangel Guerrero","first_name":"Dámaris K","orcid":"0000-0002-8602-4374","full_name":"Rangel Guerrero, Dámaris K","id":"4871BCE6-F248-11E8-B48F-1D18A9856A87"},{"full_name":"Donnett, James G.","first_name":"James G.","last_name":"Donnett"},{"last_name":"Csicsvari","first_name":"Jozsef L","id":"3FA14672-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-5193-4036","full_name":"Csicsvari, Jozsef L"},{"full_name":"Kovács, Krisztián","orcid":"0000-0001-6251-1007","id":"2AB5821E-F248-11E8-B48F-1D18A9856A87","first_name":"Krisztián","last_name":"Kovács"}],"issue":"4","day":"27","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","doi":"10.1523/ENEURO.0087-18.2018"},{"publist_id":"7274","language":[{"iso":"eng"}],"year":"2018","project":[{"name":"Prevalence and Influence of Sexual Antagonism on Genome Evolution","_id":"250BDE62-B435-11E9-9278-68D0E5697425","call_identifier":"H2020","grant_number":"715257"}],"type":"journal_article","publisher":"Genetics Society of America","page":"365 - 375","volume":208,"abstract":[{"lang":"eng","text":"The t-haplotype, a mouse meiotic driver found on chromosome 17, has been a model for autosomal segregation distortion for close to a century, but several questions remain regarding its biology and evolutionary history. A recently published set of population genomics resources for wild mice includes several individuals heterozygous for the t-haplotype, which we use to characterize this selfish element at the genomic and transcriptomic level. Our results show that large sections of the t-haplotype have been replaced by standard homologous sequences, possibly due to occasional events of recombination, and that this complicates the inference of its history. As expected for a long genomic segment of very low recombination, the t-haplotype carries an excess of fixed nonsynonymous mutations compared to the standard chromosome. This excess is stronger for regions that have not undergone recent recombination, suggesting that occasional gene flow between the t and the standard chromosome may provide a mechanism to regenerate coding sequences that have accumulated deleterious mutations. Finally, we find that t-complex genes with altered expression largely overlap with deleted or amplified regions, and that carrying a t-haplotype alters the testis expression of genes outside of the t-complex, providing new leads into the pathways involved in the biology of this segregation distorter."}],"pubrep_id":"1058","file":[{"file_size":1311661,"date_created":"2018-12-12T10:15:14Z","relation":"main_file","date_updated":"2020-07-14T12:46:50Z","file_name":"IST-2018-1058-v1+1_365.full__1_.pdf","access_level":"open_access","creator":"system","file_id":"5132","checksum":"2123845e7031a0cf043905be160f9e69","content_type":"application/pdf"}],"date_updated":"2026-10-05T22:31:17Z","intvolume":"       208","_id":"542","title":"Complex history and differentiation patterns of the t-haplotype, a mouse meiotic driver","department":[{"_id":"BeVi"}],"date_created":"2018-12-11T11:47:04Z","publication_status":"published","fulldoi":"https://doi.org/10.1534/genetics.117.300513","oa_version":"Published Version","oa":1,"article_processing_charge":"No","external_id":{"isi":["000419356300024"]},"corr_author":"1","has_accepted_license":"1","file_date_updated":"2020-07-14T12:46:50Z","date_published":"2018-01-01T00:00:00Z","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)"},"citation":{"mla":"Kelemen, Réka K., and Beatriz Vicoso. “Complex History and Differentiation Patterns of the T-Haplotype, a Mouse Meiotic Driver.” <i>Genetics</i>, vol. 208, no. 1, Genetics Society of America, 2018, pp. 365–75, doi:<a href=\"https://doi.org/10.1534/genetics.117.300513\">10.1534/genetics.117.300513</a>.","short":"R.K. Kelemen, B. Vicoso, Genetics 208 (2018) 365–375.","apa":"Kelemen, R. K., &#38; Vicoso, B. (2018). Complex history and differentiation patterns of the t-haplotype, a mouse meiotic driver. <i>Genetics</i>. Genetics Society of America. <a href=\"https://doi.org/10.1534/genetics.117.300513\">https://doi.org/10.1534/genetics.117.300513</a>","ista":"Kelemen RK, Vicoso B. 2018. Complex history and differentiation patterns of the t-haplotype, a mouse meiotic driver. Genetics. 208(1), 365–375.","chicago":"Kelemen, Réka K, and Beatriz Vicoso. “Complex History and Differentiation Patterns of the T-Haplotype, a Mouse Meiotic Driver.” <i>Genetics</i>. Genetics Society of America, 2018. <a href=\"https://doi.org/10.1534/genetics.117.300513\">https://doi.org/10.1534/genetics.117.300513</a>.","ieee":"R. K. Kelemen and B. Vicoso, “Complex history and differentiation patterns of the t-haplotype, a mouse meiotic driver,” <i>Genetics</i>, vol. 208, no. 1. Genetics Society of America, pp. 365–375, 2018.","ama":"Kelemen RK, Vicoso B. Complex history and differentiation patterns of the t-haplotype, a mouse meiotic driver. <i>Genetics</i>. 2018;208(1):365-375. doi:<a href=\"https://doi.org/10.1534/genetics.117.300513\">10.1534/genetics.117.300513</a>"},"scopus_import":"1","ec_funded":1,"related_material":{"record":[{"status":"public","relation":"popular_science","id":"5571"},{"id":"5572","status":"public","relation":"popular_science"},{"status":"public","relation":"dissertation_contains","id":"17119"}]},"quality_controlled":"1","publication":"Genetics","issue":"1","author":[{"last_name":"Kelemen","first_name":"Réka K","id":"48D3F8DE-F248-11E8-B48F-1D18A9856A87","full_name":"Kelemen, Réka K","orcid":"0000-0002-8489-9281"},{"first_name":"Beatriz","orcid":"0000-0002-4579-8306","full_name":"Vicoso, Beatriz","id":"49E1C5C6-F248-11E8-B48F-1D18A9856A87","last_name":"Vicoso"}],"month":"01","status":"public","ddc":["576"],"isi":1,"article_type":"original","day":"01","user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","doi":"10.1534/genetics.117.300513"},{"date_published":"2017-04-01T00:00:00Z","external_id":{"isi":["000398059200002"]},"scopus_import":"1","citation":{"chicago":"Fang, Chong, Anna A Nagy-Staron, Martin Grafe, Ralf Heermann, Kirsten Jung, Susanne Gebhard, and Thorsten Mascher. “Insulation and Wiring Specificity of BceR like Response Regulators and Their Target Promoters in Bacillus Subtilis.” <i>Molecular Microbiology</i>. Wiley-Blackwell, 2017. <a href=\"https://doi.org/10.1111/mmi.13597\">https://doi.org/10.1111/mmi.13597</a>.","short":"C. Fang, A.A. Nagy-Staron, M. Grafe, R. Heermann, K. Jung, S. Gebhard, T. Mascher, Molecular Microbiology 104 (2017) 16–31.","apa":"Fang, C., Nagy-Staron, A. A., Grafe, M., Heermann, R., Jung, K., Gebhard, S., &#38; Mascher, T. (2017). Insulation and wiring specificity of BceR like response regulators and their target promoters in Bacillus subtilis. <i>Molecular Microbiology</i>. Wiley-Blackwell. <a href=\"https://doi.org/10.1111/mmi.13597\">https://doi.org/10.1111/mmi.13597</a>","ista":"Fang C, Nagy-Staron AA, Grafe M, Heermann R, Jung K, Gebhard S, Mascher T. 2017. Insulation and wiring specificity of BceR like response regulators and their target promoters in Bacillus subtilis. Molecular Microbiology. 104(1), 16–31.","mla":"Fang, Chong, et al. “Insulation and Wiring Specificity of BceR like Response Regulators and Their Target Promoters in Bacillus Subtilis.” <i>Molecular Microbiology</i>, vol. 104, no. 1, Wiley-Blackwell, 2017, pp. 16–31, doi:<a href=\"https://doi.org/10.1111/mmi.13597\">10.1111/mmi.13597</a>.","ieee":"C. Fang <i>et al.</i>, “Insulation and wiring specificity of BceR like response regulators and their target promoters in Bacillus subtilis,” <i>Molecular Microbiology</i>, vol. 104, no. 1. Wiley-Blackwell, pp. 16–31, 2017.","ama":"Fang C, Nagy-Staron AA, Grafe M, et al. Insulation and wiring specificity of BceR like response regulators and their target promoters in Bacillus subtilis. <i>Molecular Microbiology</i>. 2017;104(1):16-31. doi:<a href=\"https://doi.org/10.1111/mmi.13597\">10.1111/mmi.13597</a>"},"issue":"1","isi":1,"status":"public","month":"04","author":[{"last_name":"Fang","first_name":"Chong","full_name":"Fang, Chong"},{"id":"3ABC5BA6-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-1391-8377","full_name":"Nagy-Staron, Anna A","first_name":"Anna A","last_name":"Nagy-Staron"},{"last_name":"Grafe","first_name":"Martin","full_name":"Grafe, Martin"},{"last_name":"Heermann","full_name":"Heermann, Ralf","first_name":"Ralf"},{"first_name":"Kirsten","full_name":"Jung, Kirsten","last_name":"Jung"},{"last_name":"Gebhard","first_name":"Susanne","full_name":"Gebhard, Susanne"},{"full_name":"Mascher, Thorsten","first_name":"Thorsten","last_name":"Mascher"}],"quality_controlled":"1","publication":"Molecular Microbiology","user_id":"ba8df636-2132-11f1-aed0-ed93e2281fdd","doi":"10.1111/mmi.13597","day":"01","year":"2017","language":[{"iso":"eng"}],"publisher":"Wiley-Blackwell","type":"journal_article","publist_id":"6294","intvolume":"       104","date_updated":"2026-04-16T09:56:09Z","volume":104,"page":"16 - 31","abstract":[{"text":"BceRS and PsdRS are paralogous two-component systems in Bacillus subtilis controlling the response to antimicrobial peptides. In the presence of extracellular bacitracin and nisin, respectively, the two response regulators (RRs) bind their target promoters, PbceA or PpsdA, resulting in a strong up-regulation of target gene expression and ultimately antibiotic resistance. Despite high sequence similarity between the RRs BceR and PsdR and their known binding sites, no cross-regulation has been observed between them. We therefore investigated the specificity determinants of PbceA and PpsdA that ensure the insulation of these two paralogous pathways at the RR–promoter interface. In vivo and in vitro analyses demonstrate that the regulatory regions within these two promoters contain three important elements: in addition to the known (main) binding site, we identified a linker region and a secondary binding site that are crucial for functionality. Initial binding to the high-affinity, low-specificity main binding site is a prerequisite for the subsequent highly specific binding of a second RR dimer to the low-affinity secondary binding site. In addition to this hierarchical cooperative binding, discrimination requires a competition of the two RRs for their respective binding site mediated by only slight differences in binding affinities.","lang":"eng"}],"date_created":"2018-12-11T11:50:03Z","publication_identifier":{"issn":[" 0950-382X"]},"title":"Insulation and wiring specificity of BceR like response regulators and their target promoters in Bacillus subtilis","_id":"1084","department":[{"_id":"CaGu"}],"article_processing_charge":"No","publication_status":"published","oa_version":"None","fulldoi":"https://doi.org/10.1111/mmi.13597"},{"fulldoi":"https://doi.org/10.1038/ncomms14251","oa_version":"Published Version","publication_status":"published","article_processing_charge":"No","oa":1,"department":[{"_id":"BeVi"}],"_id":"1085","title":"Convergent recombination suppression suggests role of sexual selection in guppy sex chromosome formation","publication_identifier":{"issn":["2041-1723"]},"date_created":"2018-12-11T11:50:04Z","pubrep_id":"791","abstract":[{"text":"Sex chromosomes evolve once recombination is halted between a homologous pair of chromosomes. The dominant model of sex chromosome evolution posits that recombination is suppressed between emerging X and Y chromosomes in order to resolve sexual conflict. Here we test this model using whole genome and transcriptome resequencing data in the guppy, a model for sexual selection with many Y-linked colour traits. We show that although the nascent Y chromosome encompasses nearly half of the linkage group, there has been no perceptible degradation of Y chromosome gene content or activity. Using replicate wild populations with differing levels of sexually antagonistic selection for colour, we also show that sexual selection leads to greater expansion of the non-recombining region and increased Y chromosome divergence. These results provide empirical support for longstanding models of sex chromosome catalysis, and suggest an important role for sexual selection and sexual conflict in genome evolution.","lang":"eng"}],"article_number":"14251","volume":8,"intvolume":"         8","date_updated":"2025-07-10T11:50:01Z","file":[{"file_id":"5141","content_type":"application/pdf","creator":"system","date_updated":"2018-12-12T10:15:22Z","relation":"main_file","file_name":"IST-2017-791-v1+1_ncomms14251.pdf","access_level":"open_access","date_created":"2018-12-12T10:15:22Z","file_size":955256}],"publist_id":"6292","type":"journal_article","publisher":"Nature Publishing Group","language":[{"iso":"eng"}],"year":"2017","day":"31","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","doi":"10.1038/ncomms14251","publication":"Nature Communications","quality_controlled":"1","author":[{"full_name":"Wright, Alison","first_name":"Alison","last_name":"Wright"},{"last_name":"Darolti","full_name":"Darolti, Iulia","first_name":"Iulia"},{"first_name":"Natasha","full_name":"Bloch, Natasha","last_name":"Bloch"},{"last_name":"Oostra","first_name":"Vicencio","full_name":"Oostra, Vicencio"},{"full_name":"Sandkam, Benjamin","first_name":"Benjamin","last_name":"Sandkam"},{"first_name":"Séverine","full_name":"Buechel, Séverine","last_name":"Buechel"},{"last_name":"Kolm","full_name":"Kolm, Niclas","first_name":"Niclas"},{"last_name":"Breden","full_name":"Breden, Felix","first_name":"Felix"},{"last_name":"Vicoso","id":"49E1C5C6-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-4579-8306","full_name":"Vicoso, Beatriz","first_name":"Beatriz"},{"last_name":"Mank","first_name":"Judith","full_name":"Mank, Judith"}],"isi":1,"month":"01","ddc":["570","576"],"status":"public","citation":{"mla":"Wright, Alison, et al. “Convergent Recombination Suppression Suggests Role of Sexual Selection in Guppy Sex Chromosome Formation.” <i>Nature Communications</i>, vol. 8, 14251, Nature Publishing Group, 2017, doi:<a href=\"https://doi.org/10.1038/ncomms14251\">10.1038/ncomms14251</a>.","apa":"Wright, A., Darolti, I., Bloch, N., Oostra, V., Sandkam, B., Buechel, S., … Mank, J. (2017). Convergent recombination suppression suggests role of sexual selection in guppy sex chromosome formation. <i>Nature Communications</i>. Nature Publishing Group. <a href=\"https://doi.org/10.1038/ncomms14251\">https://doi.org/10.1038/ncomms14251</a>","ista":"Wright A, Darolti I, Bloch N, Oostra V, Sandkam B, Buechel S, Kolm N, Breden F, Vicoso B, Mank J. 2017. Convergent recombination suppression suggests role of sexual selection in guppy sex chromosome formation. Nature Communications. 8, 14251.","short":"A. Wright, I. Darolti, N. Bloch, V. Oostra, B. Sandkam, S. Buechel, N. Kolm, F. Breden, B. Vicoso, J. Mank, Nature Communications 8 (2017).","chicago":"Wright, Alison, Iulia Darolti, Natasha Bloch, Vicencio Oostra, Benjamin Sandkam, Séverine Buechel, Niclas Kolm, Felix Breden, Beatriz Vicoso, and Judith Mank. “Convergent Recombination Suppression Suggests Role of Sexual Selection in Guppy Sex Chromosome Formation.” <i>Nature Communications</i>. Nature Publishing Group, 2017. <a href=\"https://doi.org/10.1038/ncomms14251\">https://doi.org/10.1038/ncomms14251</a>.","ama":"Wright A, Darolti I, Bloch N, et al. Convergent recombination suppression suggests role of sexual selection in guppy sex chromosome formation. <i>Nature Communications</i>. 2017;8. doi:<a href=\"https://doi.org/10.1038/ncomms14251\">10.1038/ncomms14251</a>","ieee":"A. Wright <i>et al.</i>, “Convergent recombination suppression suggests role of sexual selection in guppy sex chromosome formation,” <i>Nature Communications</i>, vol. 8. Nature Publishing Group, 2017."},"scopus_import":"1","external_id":{"isi":["000392953700001"]},"date_published":"2017-01-31T00:00:00Z","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)"},"has_accepted_license":"1","file_date_updated":"2018-12-12T10:15:22Z"},{"doi":"10.1038/srep41002","user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","day":"01","author":[{"last_name":"Di Giglio","full_name":"Di Giglio, Maria","first_name":"Maria"},{"last_name":"Muttenthaler","first_name":"Markus","full_name":"Muttenthaler, Markus"},{"last_name":"Harpsøe","full_name":"Harpsøe, Kasper","first_name":"Kasper"},{"last_name":"Liutkeviciute","first_name":"Zita","full_name":"Liutkeviciute, Zita"},{"last_name":"Keov","full_name":"Keov, Peter","first_name":"Peter"},{"full_name":"Eder, Thomas","first_name":"Thomas","last_name":"Eder"},{"last_name":"Rattei","full_name":"Rattei, Thomas","first_name":"Thomas"},{"last_name":"Arrowsmith","full_name":"Arrowsmith, Sarah","first_name":"Sarah"},{"last_name":"Wray","full_name":"Wray, Susan","first_name":"Susan"},{"last_name":"Marek","first_name":"Ales","full_name":"Marek, Ales"},{"first_name":"Tomas","full_name":"Elbert, Tomas","last_name":"Elbert"},{"full_name":"Alewood, Paul","first_name":"Paul","last_name":"Alewood"},{"last_name":"Gloriam","full_name":"Gloriam, David","first_name":"David"},{"first_name":"Christian","full_name":"Gruber, Christian","last_name":"Gruber"}],"ddc":["570","590"],"month":"02","status":"public","isi":1,"publication":"Scientific Reports","quality_controlled":"1","scopus_import":"1","citation":{"ama":"Di Giglio M, Muttenthaler M, Harpsøe K, et al. Development of a human vasopressin V1a-receptor antagonist from an evolutionary-related insect neuropeptide. <i>Scientific Reports</i>. 2017;7:41002. doi:<a href=\"https://doi.org/10.1038/srep41002\">10.1038/srep41002</a>","ieee":"M. Di Giglio <i>et al.</i>, “Development of a human vasopressin V1a-receptor antagonist from an evolutionary-related insect neuropeptide,” <i>Scientific Reports</i>, vol. 7. Nature Publishing Group, p. 41002, 2017.","mla":"Di Giglio, Maria, et al. “Development of a Human Vasopressin V1a-Receptor Antagonist from an Evolutionary-Related Insect Neuropeptide.” <i>Scientific Reports</i>, vol. 7, Nature Publishing Group, 2017, p. 41002, doi:<a href=\"https://doi.org/10.1038/srep41002\">10.1038/srep41002</a>.","ista":"Di Giglio M, Muttenthaler M, Harpsøe K, Liutkeviciute Z, Keov P, Eder T, Rattei T, Arrowsmith S, Wray S, Marek A, Elbert T, Alewood P, Gloriam D, Gruber C. 2017. Development of a human vasopressin V1a-receptor antagonist from an evolutionary-related insect neuropeptide. Scientific Reports. 7, 41002.","short":"M. Di Giglio, M. Muttenthaler, K. Harpsøe, Z. Liutkeviciute, P. Keov, T. Eder, T. Rattei, S. Arrowsmith, S. Wray, A. Marek, T. Elbert, P. Alewood, D. Gloriam, C. Gruber, Scientific Reports 7 (2017) 41002.","apa":"Di Giglio, M., Muttenthaler, M., Harpsøe, K., Liutkeviciute, Z., Keov, P., Eder, T., … Gruber, C. (2017). Development of a human vasopressin V1a-receptor antagonist from an evolutionary-related insect neuropeptide. <i>Scientific Reports</i>. Nature Publishing Group. <a href=\"https://doi.org/10.1038/srep41002\">https://doi.org/10.1038/srep41002</a>","chicago":"Di Giglio, Maria, Markus Muttenthaler, Kasper Harpsøe, Zita Liutkeviciute, Peter Keov, Thomas Eder, Thomas Rattei, et al. “Development of a Human Vasopressin V1a-Receptor Antagonist from an Evolutionary-Related Insect Neuropeptide.” <i>Scientific Reports</i>. Nature Publishing Group, 2017. <a href=\"https://doi.org/10.1038/srep41002\">https://doi.org/10.1038/srep41002</a>."},"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)"},"date_published":"2017-02-01T00:00:00Z","has_accepted_license":"1","file_date_updated":"2018-12-12T10:14:59Z","external_id":{"isi":["000393163800001"]},"article_processing_charge":"No","oa":1,"fulldoi":"https://doi.org/10.1038/srep41002","oa_version":"Published Version","publication_status":"published","date_created":"2018-12-11T11:50:04Z","_id":"1086","title":"Development of a human vasopressin V1a-receptor antagonist from an evolutionary-related insect neuropeptide","date_updated":"2023-09-20T11:47:47Z","intvolume":"         7","file":[{"creator":"system","content_type":"application/pdf","file_id":"5115","file_name":"IST-2017-790-v1+1_srep41002_1_.pdf","access_level":"open_access","relation":"main_file","date_updated":"2018-12-12T10:14:59Z","file_size":1994139,"date_created":"2018-12-12T10:14:59Z"}],"abstract":[{"text":"Characterisation of G protein-coupled receptors (GPCR) relies on the availability of a toolbox of ligands that selectively modulate different functional states of the receptors. To uncover such molecules, we explored a unique strategy for ligand discovery that takes advantage of the evolutionary conservation of the 600-million-year-old oxytocin/vasopressin signalling system. We isolated the insect oxytocin/vasopressin orthologue inotocin from the black garden ant (Lasius niger), identified and cloned its cognate receptor and determined its pharmacological properties on the insect and human oxytocin/vasopressin receptors. Subsequently, we identified a functional dichotomy: inotocin activated the insect inotocin and the human vasopressin V1b receptors, but inhibited the human V1aR. Replacement of Arg8 of inotocin by D-Arg8 led to a potent, stable and competitive V1aR-antagonist ([D-Arg8]-inotocin) with a 3,000-fold binding selectivity for the human V1aR over the other three subtypes, OTR, V1bR and V2R. The Arg8/D-Arg8 ligand-pair was further investigated to gain novel insights into the oxytocin/vasopressin peptide-receptor interaction, which led to the identification of key residues of the receptors that are important for ligand functionality and selectivity. These observations could play an important role for development of oxytocin/vasopressin receptor modulators that would enable clear distinction of the physiological and pathological responses of the individual receptor subtypes.","lang":"eng"}],"pubrep_id":"790","page":"41002","volume":7,"type":"journal_article","publisher":"Nature Publishing Group","language":[{"iso":"eng"}],"year":"2017","publist_id":"6291"},{"article_processing_charge":"No","oa":1,"oa_version":"Submitted Version","fulldoi":"https://doi.org/10.1017/jfm.2017.14","publication_status":"published","publication_identifier":{"issn":["0022-1120"]},"date_created":"2018-12-11T11:50:04Z","department":[{"_id":"BjHo"}],"title":"Speed and structure of turbulent fronts in pipe flow","_id":"1087","intvolume":"       813","date_updated":"2025-06-04T08:35:11Z","acknowledged_ssus":[{"_id":"ScienComp"}],"arxiv":1,"abstract":[{"text":"Using extensive direct numerical simulations, the dynamics of laminar-turbulent fronts in pipe flow is investigated for Reynolds numbers between and 5500. We here investigate the physical distinction between the fronts of weak and strong slugs both by analysing the turbulent kinetic energy budget and by comparing the downstream front motion to the advection speed of bulk turbulent structures. Our study shows that weak downstream fronts travel slower than turbulent structures in the bulk and correspond to decaying turbulence at the front. At the downstream front speed becomes faster than the advection speed, marking the onset of strong fronts. In contrast to weak fronts, turbulent eddies are generated at strong fronts by feeding on the downstream laminar flow. Our study also suggests that temporal fluctuations of production and dissipation at the downstream laminar-turbulent front drive the dynamical switches between the two types of front observed up to.","lang":"eng"}],"volume":813,"page":"1045 - 1059","publisher":"Cambridge University Press","type":"journal_article","project":[{"grant_number":"306589","_id":"25152F3A-B435-11E9-9278-68D0E5697425","name":"Decoding the complexity of turbulence at its origin","call_identifier":"FP7"}],"year":"2017","language":[{"iso":"eng"}],"publist_id":"6290","doi":"10.1017/jfm.2017.14","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","day":"25","isi":1,"month":"02","status":"public","author":[{"full_name":"Song, Baofang","first_name":"Baofang","last_name":"Song"},{"full_name":"Barkley, Dwight","first_name":"Dwight","last_name":"Barkley"},{"last_name":"Hof","first_name":"Björn","orcid":"0000-0003-2057-2754","full_name":"Hof, Björn","id":"3A374330-F248-11E8-B48F-1D18A9856A87"},{"full_name":"Avila, Marc","first_name":"Marc","last_name":"Avila"}],"main_file_link":[{"url":"https://arxiv.org/abs/1603.04077","open_access":"1"}],"publication":"Journal of Fluid Mechanics","quality_controlled":"1","ec_funded":1,"scopus_import":"1","citation":{"ama":"Song B, Barkley D, Hof B, Avila M. Speed and structure of turbulent fronts in pipe flow. <i>Journal of Fluid Mechanics</i>. 2017;813:1045-1059. doi:<a href=\"https://doi.org/10.1017/jfm.2017.14\">10.1017/jfm.2017.14</a>","ieee":"B. Song, D. Barkley, B. Hof, and M. Avila, “Speed and structure of turbulent fronts in pipe flow,” <i>Journal of Fluid Mechanics</i>, vol. 813. Cambridge University Press, pp. 1045–1059, 2017.","mla":"Song, Baofang, et al. “Speed and Structure of Turbulent Fronts in Pipe Flow.” <i>Journal of Fluid Mechanics</i>, vol. 813, Cambridge University Press, 2017, pp. 1045–59, doi:<a href=\"https://doi.org/10.1017/jfm.2017.14\">10.1017/jfm.2017.14</a>.","ista":"Song B, Barkley D, Hof B, Avila M. 2017. Speed and structure of turbulent fronts in pipe flow. Journal of Fluid Mechanics. 813, 1045–1059.","apa":"Song, B., Barkley, D., Hof, B., &#38; Avila, M. (2017). Speed and structure of turbulent fronts in pipe flow. <i>Journal of Fluid Mechanics</i>. Cambridge University Press. <a href=\"https://doi.org/10.1017/jfm.2017.14\">https://doi.org/10.1017/jfm.2017.14</a>","short":"B. Song, D. Barkley, B. Hof, M. Avila, Journal of Fluid Mechanics 813 (2017) 1045–1059.","chicago":"Song, Baofang, Dwight Barkley, Björn Hof, and Marc Avila. “Speed and Structure of Turbulent Fronts in Pipe Flow.” <i>Journal of Fluid Mechanics</i>. Cambridge University Press, 2017. <a href=\"https://doi.org/10.1017/jfm.2017.14\">https://doi.org/10.1017/jfm.2017.14</a>."},"date_published":"2017-02-25T00:00:00Z","external_id":{"arxiv":["1603.04077"],"isi":["000394376400044"]}},{"publist_id":"6288","publisher":"Institute of Mathematical Statistics","type":"journal_article","project":[{"grant_number":"Y 903-N35","call_identifier":"FWF","_id":"2530CA10-B435-11E9-9278-68D0E5697425","name":"Gaussian Graphical Models: Theory and Applications"}],"year":"2017","language":[{"iso":"eng"}],"arxiv":1,"abstract":[{"text":"We discuss properties of distributions that are multivariate totally positive of order two (MTP2) related to conditional independence. In particular, we show that any independence model generated by an MTP2 distribution is a compositional semigraphoid which is upward-stable and singleton-transitive. In addition, we prove that any MTP2 distribution satisfying an appropriate support condition is faithful to its concentration graph. Finally, we analyze factorization properties of MTP2 distributions and discuss ways of constructing MTP2 distributions; in particular we give conditions on the log-linear parameters of a discrete distribution which ensure MTP2 and characterize conditional Gaussian distributions which satisfy MTP2.","lang":"eng"}],"volume":45,"page":"1152 - 1184","date_updated":"2025-06-04T08:35:37Z","intvolume":"        45","department":[{"_id":"CaUh"}],"title":"Total positivity in Markov structures","_id":"1089","publication_identifier":{"issn":["0090-5364"]},"date_created":"2018-12-11T11:50:05Z","oa_version":"Submitted Version","fulldoi":"https://doi.org/10.1214/16-AOS1478","publication_status":"published","article_processing_charge":"No","oa":1,"corr_author":"1","external_id":{"isi":["000404395900008"],"arxiv":["1510.01290"]},"date_published":"2017-06-01T00:00:00Z","citation":{"ieee":"S. Fallat, S. Lauritzen, K. Sadeghi, C. Uhler, N. Wermuth, and P. Zwiernik, “Total positivity in Markov structures,” <i>Annals of Statistics</i>, vol. 45, no. 3. Institute of Mathematical Statistics, pp. 1152–1184, 2017.","ama":"Fallat S, Lauritzen S, Sadeghi K, Uhler C, Wermuth N, Zwiernik P. Total positivity in Markov structures. <i>Annals of Statistics</i>. 2017;45(3):1152-1184. doi:<a href=\"https://doi.org/10.1214/16-AOS1478\">10.1214/16-AOS1478</a>","short":"S. Fallat, S. Lauritzen, K. Sadeghi, C. Uhler, N. Wermuth, P. Zwiernik, Annals of Statistics 45 (2017) 1152–1184.","ista":"Fallat S, Lauritzen S, Sadeghi K, Uhler C, Wermuth N, Zwiernik P. 2017. Total positivity in Markov structures. Annals of Statistics. 45(3), 1152–1184.","apa":"Fallat, S., Lauritzen, S., Sadeghi, K., Uhler, C., Wermuth, N., &#38; Zwiernik, P. (2017). Total positivity in Markov structures. <i>Annals of Statistics</i>. Institute of Mathematical Statistics. <a href=\"https://doi.org/10.1214/16-AOS1478\">https://doi.org/10.1214/16-AOS1478</a>","mla":"Fallat, Shaun, et al. “Total Positivity in Markov Structures.” <i>Annals of Statistics</i>, vol. 45, no. 3, Institute of Mathematical Statistics, 2017, pp. 1152–84, doi:<a href=\"https://doi.org/10.1214/16-AOS1478\">10.1214/16-AOS1478</a>.","chicago":"Fallat, Shaun, Steffen Lauritzen, Kayvan Sadeghi, Caroline Uhler, Nanny Wermuth, and Piotr Zwiernik. “Total Positivity in Markov Structures.” <i>Annals of Statistics</i>. Institute of Mathematical Statistics, 2017. <a href=\"https://doi.org/10.1214/16-AOS1478\">https://doi.org/10.1214/16-AOS1478</a>."},"scopus_import":"1","publication":"Annals of Statistics","quality_controlled":"1","month":"06","status":"public","isi":1,"author":[{"last_name":"Fallat","full_name":"Fallat, Shaun","first_name":"Shaun"},{"last_name":"Lauritzen","full_name":"Lauritzen, Steffen","first_name":"Steffen"},{"last_name":"Sadeghi","full_name":"Sadeghi, Kayvan","first_name":"Kayvan"},{"last_name":"Uhler","full_name":"Uhler, Caroline","orcid":"0000-0002-7008-0216","id":"49ADD78E-F248-11E8-B48F-1D18A9856A87","first_name":"Caroline"},{"last_name":"Wermuth","first_name":"Nanny","full_name":"Wermuth, Nanny"},{"first_name":"Piotr","full_name":"Zwiernik, Piotr","last_name":"Zwiernik"}],"main_file_link":[{"open_access":"1","url":"https://arxiv.org/abs/1510.01290"}],"issue":"3","day":"01","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","doi":"10.1214/16-AOS1478"},{"publist_id":"6266","type":"journal_article","publisher":"Nature Publishing Group","language":[{"iso":"eng"}],"project":[{"grant_number":"604102","name":"Localization of ion channels and receptors by two and three-dimensional immunoelectron microscopic approaches","_id":"25CD3DD2-B435-11E9-9278-68D0E5697425","call_identifier":"FP7"},{"name":"Sensitivity to higher-order statistics in natural scenes","_id":"254D1A94-B435-11E9-9278-68D0E5697425","call_identifier":"FWF","grant_number":"P 25651-N26"}],"year":"2017","pubrep_id":"921","abstract":[{"lang":"eng","text":"In the early visual system, cells of the same type perform the same computation in different places of the visual field. How these cells code together a complex visual scene is unclear. A common assumption is that cells of a single-type extract a single-stimulus feature to form a feature map, but this has rarely been observed directly. Using large-scale recordings in the rat retina, we show that a homogeneous population of fast OFF ganglion cells simultaneously encodes two radically different features of a visual scene. Cells close to a moving object code quasilinearly for its position, while distant cells remain largely invariant to the object's position and, instead, respond nonlinearly to changes in the object's speed. We develop a quantitative model that accounts for this effect and identify a disinhibitory circuit that mediates it. Ganglion cells of a single type thus do not code for one, but two features simultaneously. This richer, flexible neural map might also be present in other sensory systems."}],"article_number":"1964","volume":8,"date_updated":"2025-07-10T11:50:05Z","intvolume":"         8","file":[{"date_updated":"2018-12-12T10:16:06Z","relation":"main_file","file_name":"IST-2018-921-v1+1_s41467-017-02159-y.pdf","access_level":"open_access","creator":"system","file_id":"5191","content_type":"application/pdf","file_size":2872887,"date_created":"2018-12-12T10:16:06Z"}],"department":[{"_id":"GaTk"}],"_id":"1104","title":"Multiplexed computations in retinal ganglion cells of a single type","publication_identifier":{"issn":["2041-1723"]},"date_created":"2018-12-11T11:50:10Z","fulldoi":"https://doi.org/10.1038/s41467-017-02159-y","oa_version":"Published Version","publication_status":"published","article_processing_charge":"No","oa":1,"external_id":{"isi":["000417241200004"]},"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)"},"date_published":"2017-12-06T00:00:00Z","has_accepted_license":"1","file_date_updated":"2018-12-12T10:16:06Z","citation":{"mla":"Deny, Stephane, et al. “Multiplexed Computations in Retinal Ganglion Cells of a Single Type.” <i>Nature Communications</i>, vol. 8, no. 1, 1964, Nature Publishing Group, 2017, doi:<a href=\"https://doi.org/10.1038/s41467-017-02159-y\">10.1038/s41467-017-02159-y</a>.","short":"S. Deny, U. Ferrari, E. Mace, P. Yger, R. Caplette, S. Picaud, G. Tkačik, O. Marre, Nature Communications 8 (2017).","apa":"Deny, S., Ferrari, U., Mace, E., Yger, P., Caplette, R., Picaud, S., … Marre, O. (2017). Multiplexed computations in retinal ganglion cells of a single type. <i>Nature Communications</i>. Nature Publishing Group. <a href=\"https://doi.org/10.1038/s41467-017-02159-y\">https://doi.org/10.1038/s41467-017-02159-y</a>","ista":"Deny S, Ferrari U, Mace E, Yger P, Caplette R, Picaud S, Tkačik G, Marre O. 2017. Multiplexed computations in retinal ganglion cells of a single type. Nature Communications. 8(1), 1964.","chicago":"Deny, Stephane, Ulisse Ferrari, Emilie Mace, Pierre Yger, Romain Caplette, Serge Picaud, Gašper Tkačik, and Olivier Marre. “Multiplexed Computations in Retinal Ganglion Cells of a Single Type.” <i>Nature Communications</i>. Nature Publishing Group, 2017. <a href=\"https://doi.org/10.1038/s41467-017-02159-y\">https://doi.org/10.1038/s41467-017-02159-y</a>.","ama":"Deny S, Ferrari U, Mace E, et al. Multiplexed computations in retinal ganglion cells of a single type. <i>Nature Communications</i>. 2017;8(1). doi:<a href=\"https://doi.org/10.1038/s41467-017-02159-y\">10.1038/s41467-017-02159-y</a>","ieee":"S. Deny <i>et al.</i>, “Multiplexed computations in retinal ganglion cells of a single type,” <i>Nature Communications</i>, vol. 8, no. 1. Nature Publishing Group, 2017."},"ec_funded":1,"scopus_import":"1","publication":"Nature Communications","quality_controlled":"1","author":[{"full_name":"Deny, Stephane","first_name":"Stephane","last_name":"Deny"},{"last_name":"Ferrari","first_name":"Ulisse","full_name":"Ferrari, Ulisse"},{"last_name":"Mace","first_name":"Emilie","full_name":"Mace, Emilie"},{"last_name":"Yger","full_name":"Yger, Pierre","first_name":"Pierre"},{"first_name":"Romain","full_name":"Caplette, Romain","last_name":"Caplette"},{"first_name":"Serge","full_name":"Picaud, Serge","last_name":"Picaud"},{"first_name":"Gasper","id":"3D494DCA-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-6699-1455","full_name":"Tkacik, Gasper","last_name":"Tkacik"},{"full_name":"Marre, Olivier","first_name":"Olivier","last_name":"Marre"}],"month":"12","isi":1,"ddc":["571"],"status":"public","issue":"1","day":"06","doi":"10.1038/s41467-017-02159-y","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87"},{"abstract":[{"lang":"eng","text":"Premature aging disorders provide an opportunity to study the mechanisms that drive aging. In Hutchinson-Gilford progeria syndrome (HGPS), a mutant form of the nuclear scaffold protein lamin A distorts nuclei and sequesters nuclear proteins. We sought to investigate protein homeostasis in this disease. Here, we report a widespread increase in protein turnover in HGPS-derived cells compared to normal cells. We determine that global protein synthesis is elevated as a consequence of activated nucleoli and enhanced ribosome biogenesis in HGPS-derived fibroblasts. Depleting normal lamin A or inducing mutant lamin A expression are each sufficient to drive nucleolar expansion. We further show that nucleolar size correlates with donor age in primary fibroblasts derived from healthy individuals and that ribosomal RNA production increases with age, indicating that nucleolar size and activity can serve as aging biomarkers. While limiting ribosome biogenesis extends lifespan in several systems, we show that increased ribosome biogenesis and activity are a hallmark of premature aging."}],"volume":8,"article_number":"328","date_updated":"2024-10-14T11:20:12Z","intvolume":"         8","extern":"1","publisher":"Springer Nature","type":"journal_article","year":"2017","language":[{"iso":"eng"}],"oa_version":"Published Version","fulldoi":"https://doi.org/10.1038/s41467-017-00322-z","pmid":1,"publication_status":"published","article_processing_charge":"No","oa":1,"title":"Nucleolar expansion and elevated protein translation in premature aging","_id":"11065","publication_identifier":{"issn":["2041-1723"]},"date_created":"2022-04-07T07:45:50Z","citation":{"ieee":"A. Buchwalter and M. Hetzer, “Nucleolar expansion and elevated protein translation in premature aging,” <i>Nature Communications</i>, vol. 8. Springer Nature, 2017.","ama":"Buchwalter A, Hetzer M. Nucleolar expansion and elevated protein translation in premature aging. <i>Nature Communications</i>. 2017;8. doi:<a href=\"https://doi.org/10.1038/s41467-017-00322-z\">10.1038/s41467-017-00322-z</a>","chicago":"Buchwalter, Abigail, and Martin Hetzer. “Nucleolar Expansion and Elevated Protein Translation in Premature Aging.” <i>Nature Communications</i>. Springer Nature, 2017. <a href=\"https://doi.org/10.1038/s41467-017-00322-z\">https://doi.org/10.1038/s41467-017-00322-z</a>.","ista":"Buchwalter A, Hetzer M. 2017. Nucleolar expansion and elevated protein translation in premature aging. Nature Communications. 8, 328.","short":"A. Buchwalter, M. Hetzer, Nature Communications 8 (2017).","apa":"Buchwalter, A., &#38; Hetzer, M. (2017). Nucleolar expansion and elevated protein translation in premature aging. <i>Nature Communications</i>. Springer Nature. <a href=\"https://doi.org/10.1038/s41467-017-00322-z\">https://doi.org/10.1038/s41467-017-00322-z</a>","mla":"Buchwalter, Abigail, and Martin Hetzer. “Nucleolar Expansion and Elevated Protein Translation in Premature Aging.” <i>Nature Communications</i>, vol. 8, 328, Springer Nature, 2017, doi:<a href=\"https://doi.org/10.1038/s41467-017-00322-z\">10.1038/s41467-017-00322-z</a>."},"scopus_import":"1","external_id":{"pmid":["28855503"]},"date_published":"2017-08-30T00:00:00Z","day":"30","article_type":"original","keyword":["General Physics and Astronomy","General Biochemistry","Genetics and Molecular Biology","General Chemistry"],"doi":"10.1038/s41467-017-00322-z","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","publication":"Nature Communications","quality_controlled":"1","month":"08","status":"public","author":[{"full_name":"Buchwalter, Abigail","first_name":"Abigail","last_name":"Buchwalter"},{"first_name":"Martin W","id":"86c0d31b-b4eb-11ec-ac5a-eae7b2e135ed","orcid":"0000-0002-2111-992X","full_name":"HETZER, Martin W","last_name":"HETZER"}],"main_file_link":[{"url":"https://doi.org/10.1038/s41467-017-00322-z","open_access":"1"}]},{"scopus_import":"1","citation":{"mla":"Franks, Tobias M., et al. “Nup98 Recruits the Wdr82–Set1A/COMPASS Complex to Promoters to Regulate H3K4 Trimethylation in Hematopoietic Progenitor Cells.” <i>Genes &#38; Development</i>, vol. 31, no. 22, Cold Spring Harbor Laboratory, 2017, pp. 2222–34, doi:<a href=\"https://doi.org/10.1101/gad.306753.117\">10.1101/gad.306753.117</a>.","apa":"Franks, T. M., McCloskey, A., Shokhirev, M. N., Benner, C., Rathore, A., &#38; Hetzer, M. (2017). Nup98 recruits the Wdr82–Set1A/COMPASS complex to promoters to regulate H3K4 trimethylation in hematopoietic progenitor cells. <i>Genes &#38; Development</i>. Cold Spring Harbor Laboratory. <a href=\"https://doi.org/10.1101/gad.306753.117\">https://doi.org/10.1101/gad.306753.117</a>","short":"T.M. Franks, A. McCloskey, M.N. Shokhirev, C. Benner, A. Rathore, M. Hetzer, Genes &#38; Development 31 (2017) 2222–2234.","ista":"Franks TM, McCloskey A, Shokhirev MN, Benner C, Rathore A, Hetzer M. 2017. Nup98 recruits the Wdr82–Set1A/COMPASS complex to promoters to regulate H3K4 trimethylation in hematopoietic progenitor cells. Genes &#38; Development. 31(22), 2222–2234.","chicago":"Franks, Tobias M., Asako McCloskey, Maxim Nikolaievich Shokhirev, Chris Benner, Annie Rathore, and Martin Hetzer. “Nup98 Recruits the Wdr82–Set1A/COMPASS Complex to Promoters to Regulate H3K4 Trimethylation in Hematopoietic Progenitor Cells.” <i>Genes &#38; Development</i>. Cold Spring Harbor Laboratory, 2017. <a href=\"https://doi.org/10.1101/gad.306753.117\">https://doi.org/10.1101/gad.306753.117</a>.","ama":"Franks TM, McCloskey A, Shokhirev MN, Benner C, Rathore A, Hetzer M. Nup98 recruits the Wdr82–Set1A/COMPASS complex to promoters to regulate H3K4 trimethylation in hematopoietic progenitor cells. <i>Genes &#38; Development</i>. 2017;31(22):2222-2234. doi:<a href=\"https://doi.org/10.1101/gad.306753.117\">10.1101/gad.306753.117</a>","ieee":"T. M. Franks, A. McCloskey, M. N. Shokhirev, C. Benner, A. Rathore, and M. Hetzer, “Nup98 recruits the Wdr82–Set1A/COMPASS complex to promoters to regulate H3K4 trimethylation in hematopoietic progenitor cells,” <i>Genes &#38; Development</i>, vol. 31, no. 22. Cold Spring Harbor Laboratory, pp. 2222–2234, 2017."},"date_published":"2017-12-21T00:00:00Z","external_id":{"pmid":["29269482"]},"keyword":["Developmental Biology","Genetics"],"doi":"10.1101/gad.306753.117","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","day":"21","article_type":"original","month":"12","status":"public","author":[{"last_name":"Franks","full_name":"Franks, Tobias M.","first_name":"Tobias M."},{"last_name":"McCloskey","full_name":"McCloskey, Asako","first_name":"Asako"},{"last_name":"Shokhirev","first_name":"Maxim Nikolaievich","full_name":"Shokhirev, Maxim Nikolaievich"},{"last_name":"Benner","first_name":"Chris","full_name":"Benner, Chris"},{"last_name":"Rathore","first_name":"Annie","full_name":"Rathore, Annie"},{"last_name":"HETZER","first_name":"Martin W","full_name":"HETZER, Martin W","orcid":"0000-0002-2111-992X","id":"86c0d31b-b4eb-11ec-ac5a-eae7b2e135ed"}],"issue":"22","main_file_link":[{"url":"https://doi.org/10.1101/gad.306753.117","open_access":"1"}],"publication":"Genes & Development","quality_controlled":"1","intvolume":"        31","date_updated":"2024-10-14T11:20:24Z","extern":"1","abstract":[{"lang":"eng","text":"Recent studies have shown that a subset of nucleoporins (Nups) can detach from the nuclear pore complex and move into the nuclear interior to regulate transcription. One such dynamic Nup, called Nup98, has been implicated in gene activation in healthy cells and has been shown to drive leukemogenesis when mutated in patients with acute myeloid leukemia (AML). Here we show that in hematopoietic cells, Nup98 binds predominantly to transcription start sites to recruit the Wdr82–Set1A/COMPASS (complex of proteins associated with Set1) complex, which is required for deposition of the histone 3 Lys4 trimethyl (H3K4me3)-activating mark. Depletion of Nup98 or Wdr82 abolishes Set1A recruitment to chromatin and subsequently ablates H3K4me3 at adjacent promoters. Furthermore, expression of a Nup98 fusion protein implicated in aggressive AML causes mislocalization of H3K4me3 at abnormal regions and up-regulation of associated genes. Our findings establish a function of Nup98 in hematopoietic gene activation and provide mechanistic insight into which Nup98 leukemic fusion proteins promote AML."}],"volume":31,"page":"2222-2234","publisher":"Cold Spring Harbor Laboratory","type":"journal_article","year":"2017","language":[{"iso":"eng"}],"article_processing_charge":"No","oa":1,"oa_version":"Published Version","fulldoi":"https://doi.org/10.1101/gad.306753.117","pmid":1,"publication_status":"published","publication_identifier":{"issn":["0890-9369","1549-5477"]},"date_created":"2022-04-07T07:45:59Z","title":"Nup98 recruits the Wdr82–Set1A/COMPASS complex to promoters to regulate H3K4 trimethylation in hematopoietic progenitor cells","_id":"11066"},{"language":[{"iso":"eng"}],"year":"2017","type":"journal_article","publisher":"Elsevier","page":"618-634.e7","volume":21,"abstract":[{"lang":"eng","text":"Neural progenitor cells (NeuPCs) possess a unique nuclear architecture that changes during differentiation. Nucleoporins are linked with cell-type-specific gene regulation, coupling physical changes in nuclear structure to transcriptional output; but, whether and how they coordinate with key fate-determining transcription factors is unclear. Here we show that the nucleoporin Nup153 interacts with Sox2 in adult NeuPCs, where it is indispensable for their maintenance and controls neuronal differentiation. Genome-wide analyses show that Nup153 and Sox2 bind and co-regulate hundreds of genes. Binding of Nup153 to gene promoters or transcriptional end sites correlates with increased or decreased gene expression, respectively, and inhibiting Nup153 expression alters open chromatin configurations at its target genes, disrupts genomic localization of Sox2, and promotes differentiation in vitro and a gliogenic fate switch in vivo. Together, these findings reveal that nuclear structural proteins may exert bimodal transcriptional effects to control cell fate."}],"extern":"1","intvolume":"        21","date_updated":"2022-07-18T08:33:07Z","_id":"11067","title":"Nup153 interacts with Sox2 to enable bimodal gene regulation and maintenance of neural progenitor cells","date_created":"2022-04-07T07:46:12Z","publication_identifier":{"issn":["1934-5909"]},"publication_status":"published","pmid":1,"fulldoi":"https://doi.org/10.1016/j.stem.2017.08.012","oa_version":"Published Version","oa":1,"article_processing_charge":"No","external_id":{"pmid":["28919367"]},"date_published":"2017-11-02T00:00:00Z","citation":{"short":"T. Toda, J.Y. Hsu, S.B. Linker, L. Hu, S.T. Schafer, J. Mertens, F.V. Jacinto, M. Hetzer, F.H. Gage, Cell Stem Cell 21 (2017) 618–634.e7.","ista":"Toda T, Hsu JY, Linker SB, Hu L, Schafer ST, Mertens J, Jacinto FV, Hetzer M, Gage FH. 2017. Nup153 interacts with Sox2 to enable bimodal gene regulation and maintenance of neural progenitor cells. Cell Stem Cell. 21(5), 618–634.e7.","apa":"Toda, T., Hsu, J. Y., Linker, S. B., Hu, L., Schafer, S. T., Mertens, J., … Gage, F. H. (2017). Nup153 interacts with Sox2 to enable bimodal gene regulation and maintenance of neural progenitor cells. <i>Cell Stem Cell</i>. Elsevier. <a href=\"https://doi.org/10.1016/j.stem.2017.08.012\">https://doi.org/10.1016/j.stem.2017.08.012</a>","mla":"Toda, Tomohisa, et al. “Nup153 Interacts with Sox2 to Enable Bimodal Gene Regulation and Maintenance of Neural Progenitor Cells.” <i>Cell Stem Cell</i>, vol. 21, no. 5, Elsevier, 2017, p. 618–634.e7, doi:<a href=\"https://doi.org/10.1016/j.stem.2017.08.012\">10.1016/j.stem.2017.08.012</a>.","chicago":"Toda, Tomohisa, Jonathan Y. Hsu, Sara B. Linker, Lauren Hu, Simon T. Schafer, Jerome Mertens, Filipe V. Jacinto, Martin Hetzer, and Fred H. Gage. “Nup153 Interacts with Sox2 to Enable Bimodal Gene Regulation and Maintenance of Neural Progenitor Cells.” <i>Cell Stem Cell</i>. Elsevier, 2017. <a href=\"https://doi.org/10.1016/j.stem.2017.08.012\">https://doi.org/10.1016/j.stem.2017.08.012</a>.","ama":"Toda T, Hsu JY, Linker SB, et al. Nup153 interacts with Sox2 to enable bimodal gene regulation and maintenance of neural progenitor cells. <i>Cell Stem Cell</i>. 2017;21(5):618-634.e7. doi:<a href=\"https://doi.org/10.1016/j.stem.2017.08.012\">10.1016/j.stem.2017.08.012</a>","ieee":"T. Toda <i>et al.</i>, “Nup153 interacts with Sox2 to enable bimodal gene regulation and maintenance of neural progenitor cells,” <i>Cell Stem Cell</i>, vol. 21, no. 5. Elsevier, p. 618–634.e7, 2017."},"scopus_import":"1","quality_controlled":"1","publication":"Cell Stem Cell","main_file_link":[{"url":"https://doi.org/10.1016/j.stem.2017.08.012","open_access":"1"}],"issue":"5","author":[{"last_name":"Toda","full_name":"Toda, Tomohisa","first_name":"Tomohisa"},{"last_name":"Hsu","first_name":"Jonathan Y.","full_name":"Hsu, Jonathan Y."},{"first_name":"Sara B.","full_name":"Linker, Sara B.","last_name":"Linker"},{"full_name":"Hu, Lauren","first_name":"Lauren","last_name":"Hu"},{"first_name":"Simon T.","full_name":"Schafer, Simon T.","last_name":"Schafer"},{"full_name":"Mertens, Jerome","first_name":"Jerome","last_name":"Mertens"},{"first_name":"Filipe V.","full_name":"Jacinto, Filipe V.","last_name":"Jacinto"},{"last_name":"HETZER","orcid":"0000-0002-2111-992X","full_name":"HETZER, Martin W","id":"86c0d31b-b4eb-11ec-ac5a-eae7b2e135ed","first_name":"Martin W"},{"first_name":"Fred H.","full_name":"Gage, Fred H.","last_name":"Gage"}],"status":"public","month":"11","article_type":"original","day":"02","user_id":"72615eeb-f1f3-11ec-aa25-d4573ddc34fd","doi":"10.1016/j.stem.2017.08.012","keyword":["Cell Biology","Genetics","Molecular Medicine"]},{"author":[{"last_name":"Breuss","full_name":"Breuss, Martin","first_name":"Martin"},{"first_name":"Andi H","id":"38853E16-F248-11E8-B48F-1D18A9856A87","full_name":"Hansen, Andi H","last_name":"Hansen"},{"full_name":"Landler, Lukas","first_name":"Lukas","last_name":"Landler"},{"full_name":"Keays, David","first_name":"David","last_name":"Keays"}],"isi":1,"month":"04","ddc":["570","571"],"status":"public","quality_controlled":"1","publication":"Behavioural Brain Research","user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","doi":"10.1016/j.bbr.2017.01.029","license":"https://creativecommons.org/licenses/by-nc-nd/4.0/","day":"14","acknowledgement":"Austrian Science Fund (FWF) for funding this research [I914,P21092]","has_accepted_license":"1","file_date_updated":"2018-12-12T10:12:03Z","date_published":"2017-04-14T00:00:00Z","tmp":{"legal_code_url":"https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode","name":"Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0)","image":"/images/cc_by_nc_nd.png","short":"CC BY-NC-ND (4.0)"},"external_id":{"isi":["000397369100007"]},"citation":{"mla":"Breuss, Martin, et al. “Brain Specific Knockin of the Pathogenic Tubb5 E401K Allele Causes Defects in Motor Coordination and Prepulse Inhibition.” <i>Behavioural Brain Research</i>, vol. 323, Elsevier, 2017, pp. 47–55, doi:<a href=\"https://doi.org/10.1016/j.bbr.2017.01.029\">10.1016/j.bbr.2017.01.029</a>.","short":"M. Breuss, A.H. Hansen, L. Landler, D. Keays, Behavioural Brain Research 323 (2017) 47–55.","apa":"Breuss, M., Hansen, A. H., Landler, L., &#38; Keays, D. (2017). Brain specific knockin of the pathogenic Tubb5 E401K allele causes defects in motor coordination and prepulse inhibition. <i>Behavioural Brain Research</i>. Elsevier. <a href=\"https://doi.org/10.1016/j.bbr.2017.01.029\">https://doi.org/10.1016/j.bbr.2017.01.029</a>","ista":"Breuss M, Hansen AH, Landler L, Keays D. 2017. Brain specific knockin of the pathogenic Tubb5 E401K allele causes defects in motor coordination and prepulse inhibition. Behavioural Brain Research. 323, 47–55.","chicago":"Breuss, Martin, Andi H Hansen, Lukas Landler, and David Keays. “Brain Specific Knockin of the Pathogenic Tubb5 E401K Allele Causes Defects in Motor Coordination and Prepulse Inhibition.” <i>Behavioural Brain Research</i>. Elsevier, 2017. <a href=\"https://doi.org/10.1016/j.bbr.2017.01.029\">https://doi.org/10.1016/j.bbr.2017.01.029</a>.","ama":"Breuss M, Hansen AH, Landler L, Keays D. Brain specific knockin of the pathogenic Tubb5 E401K allele causes defects in motor coordination and prepulse inhibition. <i>Behavioural Brain Research</i>. 2017;323:47-55. doi:<a href=\"https://doi.org/10.1016/j.bbr.2017.01.029\">10.1016/j.bbr.2017.01.029</a>","ieee":"M. Breuss, A. H. Hansen, L. Landler, and D. Keays, “Brain specific knockin of the pathogenic Tubb5 E401K allele causes defects in motor coordination and prepulse inhibition,” <i>Behavioural Brain Research</i>, vol. 323. Elsevier, pp. 47–55, 2017."},"date_created":"2018-12-11T11:50:11Z","publication_identifier":{"issn":["01664328"]},"_id":"1107","title":"Brain specific knockin of the pathogenic Tubb5 E401K allele causes defects in motor coordination and prepulse inhibition","oa":1,"article_processing_charge":"No","publication_status":"published","fulldoi":"https://doi.org/10.1016/j.bbr.2017.01.029","oa_version":"Published Version","language":[{"iso":"eng"}],"year":"2017","type":"journal_article","publisher":"Elsevier","publist_id":"6262","file":[{"date_created":"2018-12-12T10:12:03Z","file_size":2291511,"content_type":"application/pdf","file_id":"4921","creator":"system","access_level":"open_access","file_name":"IST-2017-868-v1+1_1-s2.0-S0166432816309160-main.pdf","date_updated":"2018-12-12T10:12:03Z","relation":"main_file"}],"extern":"1","date_updated":"2023-09-20T11:37:25Z","intvolume":"       323","page":"47 - 55","volume":323,"pubrep_id":"868","abstract":[{"lang":"eng","text":"The generation, migration, and differentiation of neurons requires the functional integrity of the microtubule cytoskeleton. Mutations in the tubulin gene family are known to cause various neurological diseases including lissencephaly, ocular motor disorders, polymicrogyria and amyotrophic lateral sclerosis. We have previously reported that mutations in TUBB5 cause microcephaly that is accompanied by severe intellectual impairment and motor delay. Here we present the characterization of a Tubb5 mouse model that allows for the conditional expression of the pathogenic E401K mutation. Homozygous knockin animals exhibit a severe reduction in brain size and in body weight. These animals do not show any significant impairment in general activity, anxiety, or in the acoustic startle response, however, present with notable defects in motor coordination. When assessed on the static rod apparatus mice took longer to orient and often lost their balance completely. Interestingly, mutant animals also showed defects in prepulse inhibition, a phenotype associated with sensorimotor gating and considered an endophenotype for schizophrenia. This study provides insight into the behavioral consequences of tubulin gene mutations."}]},{"ec_funded":1,"citation":{"chicago":"Zimin, Alexander, and Christoph Lampert. “Learning Theory for Conditional Risk Minimization,” 54:213–22. ML Research Press, 2017.","mla":"Zimin, Alexander, and Christoph Lampert. <i>Learning Theory for Conditional Risk Minimization</i>. Vol. 54, ML Research Press, 2017, pp. 213–22.","apa":"Zimin, A., &#38; Lampert, C. (2017). Learning theory for conditional risk minimization (Vol. 54, pp. 213–222). Presented at the AISTATS: Artificial Intelligence and Statistics, Fort Lauderdale, FL, United States: ML Research Press.","short":"A. Zimin, C. Lampert, in:, ML Research Press, 2017, pp. 213–222.","ista":"Zimin A, Lampert C. 2017. Learning theory for conditional risk minimization. AISTATS: Artificial Intelligence and Statistics, PMLR, vol. 54, 213–222.","ieee":"A. Zimin and C. Lampert, “Learning theory for conditional risk minimization,” presented at the AISTATS: Artificial Intelligence and Statistics, Fort Lauderdale, FL, United States, 2017, vol. 54, pp. 213–222.","ama":"Zimin A, Lampert C. Learning theory for conditional risk minimization. In: Vol 54. ML Research Press; 2017:213-222."},"date_published":"2017-04-01T00:00:00Z","external_id":{"isi":["000509368500024"]},"user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","alternative_title":["PMLR"],"day":"01","main_file_link":[{"open_access":"1","url":"http://proceedings.mlr.press/v54/zimin17a/zimin17a.pdf"}],"author":[{"last_name":"Zimin","first_name":"Alexander","full_name":"Zimin, Alexander","id":"37099E9C-F248-11E8-B48F-1D18A9856A87"},{"first_name":"Christoph","full_name":"Lampert, Christoph","orcid":"0000-0001-8622-7887","id":"40C20FD2-F248-11E8-B48F-1D18A9856A87","last_name":"Lampert"}],"month":"04","isi":1,"status":"public","quality_controlled":"1","conference":{"end_date":"2017-04-22","location":"Fort Lauderdale, FL, United States","start_date":"2017-04-20","name":"AISTATS: Artificial Intelligence and Statistics"},"date_updated":"2025-04-15T07:10:22Z","intvolume":"        54","page":"213 - 222","volume":54,"abstract":[{"lang":"eng","text":"In this work we study the learnability of stochastic processes with respect to the conditional risk, i.e. the existence of a learning algorithm that improves its next-step performance with the amount of observed data. We introduce a notion of pairwise discrepancy between conditional distributions at different times steps and show how certain properties of these discrepancies can be used to construct a successful learning algorithm. Our main results are two theorems that establish criteria for learnability for many classes of stochastic processes, including all special cases studied previously in the literature."}],"language":[{"iso":"eng"}],"project":[{"grant_number":"308036","_id":"2532554C-B435-11E9-9278-68D0E5697425","name":"Lifelong Learning of Visual Scene Understanding","call_identifier":"FP7"}],"year":"2017","type":"conference","publisher":"ML Research Press","publist_id":"6261","oa":1,"article_processing_charge":"No","publication_status":"published","oa_version":"Submitted Version","date_created":"2018-12-11T11:50:11Z","_id":"1108","title":"Learning theory for conditional risk minimization","department":[{"_id":"ChLa"}]},{"volume":118,"article_number":"203203","arxiv":1,"abstract":[{"text":"Rotation of molecules embedded in He nanodroplets is explored by a combination of fs laser-induced alignment experiments and angulon quasiparticle theory. We demonstrate that at low fluence of the fs alignment pulse, the molecule and its solvation shell can be set into coherent collective rotation lasting long enough to form revivals. With increasing fluence, however, the revivals disappear -- instead, rotational dynamics as rapid as for an isolated molecule is observed during the first few picoseconds. Classical calculations trace this phenomenon to transient decoupling of the molecule from its He shell. Our results open novel opportunities for studying non-equilibrium solute-solvent dynamics and quantum thermalization. ","lang":"eng"}],"intvolume":"       118","date_updated":"2025-06-04T08:36:27Z","publist_id":"6260","project":[{"call_identifier":"FWF","name":"Quantum rotations in the presence of a many-body environment","_id":"26031614-B435-11E9-9278-68D0E5697425","grant_number":"P29902"}],"year":"2017","language":[{"iso":"eng"}],"publisher":"American Physical Society","type":"journal_article","publication_status":"published","oa_version":"Preprint","fulldoi":"https://doi.org/10.1103/PhysRevLett.118.203203","oa":1,"article_processing_charge":"No","title":"Laser-induced rotation of iodine molecules in helium nanodroplets: Revivals and breaking-free","_id":"1109","department":[{"_id":"MiLe"}],"date_created":"2018-12-11T11:50:12Z","citation":{"mla":"Shepperson, Benjamin, et al. “Laser-Induced Rotation of Iodine Molecules in Helium Nanodroplets: Revivals and Breaking-Free.” <i>Physical Review Letters</i>, vol. 118, no. 20, 203203, American Physical Society, 2017, doi:<a href=\"https://doi.org/10.1103/PhysRevLett.118.203203\">10.1103/PhysRevLett.118.203203</a>.","ista":"Shepperson B, Søndergaard A, Christiansen L, Kaczmarczyk J, Zillich R, Lemeshko M, Stapelfeldt H. 2017. Laser-induced rotation of iodine molecules in helium nanodroplets: Revivals and breaking-free. Physical Review Letters. 118(20), 203203.","apa":"Shepperson, B., Søndergaard, A., Christiansen, L., Kaczmarczyk, J., Zillich, R., Lemeshko, M., &#38; Stapelfeldt, H. (2017). Laser-induced rotation of iodine molecules in helium nanodroplets: Revivals and breaking-free. <i>Physical Review Letters</i>. American Physical Society. <a href=\"https://doi.org/10.1103/PhysRevLett.118.203203\">https://doi.org/10.1103/PhysRevLett.118.203203</a>","short":"B. Shepperson, A. Søndergaard, L. Christiansen, J. Kaczmarczyk, R. Zillich, M. Lemeshko, H. Stapelfeldt, Physical Review Letters 118 (2017).","chicago":"Shepperson, Benjamin, Anders Søndergaard, Lars Christiansen, Jan Kaczmarczyk, Robert Zillich, Mikhail Lemeshko, and Henrik Stapelfeldt. “Laser-Induced Rotation of Iodine Molecules in Helium Nanodroplets: Revivals and Breaking-Free.” <i>Physical Review Letters</i>. American Physical Society, 2017. <a href=\"https://doi.org/10.1103/PhysRevLett.118.203203\">https://doi.org/10.1103/PhysRevLett.118.203203</a>.","ieee":"B. Shepperson <i>et al.</i>, “Laser-induced rotation of iodine molecules in helium nanodroplets: Revivals and breaking-free,” <i>Physical Review Letters</i>, vol. 118, no. 20. American Physical Society, 2017.","ama":"Shepperson B, Søndergaard A, Christiansen L, et al. Laser-induced rotation of iodine molecules in helium nanodroplets: Revivals and breaking-free. <i>Physical Review Letters</i>. 2017;118(20). doi:<a href=\"https://doi.org/10.1103/PhysRevLett.118.203203\">10.1103/PhysRevLett.118.203203</a>"},"scopus_import":"1","external_id":{"arxiv":["1702.01977"],"isi":["000401664000005"]},"date_published":"2017-05-19T00:00:00Z","day":"19","doi":"10.1103/PhysRevLett.118.203203","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","quality_controlled":"1","publication":"Physical Review Letters","main_file_link":[{"url":"https://arxiv.org/abs/1702.01977","open_access":"1"}],"issue":"20","status":"public","isi":1,"month":"05","author":[{"last_name":"Shepperson","first_name":"Benjamin","full_name":"Shepperson, Benjamin"},{"last_name":"Søndergaard","full_name":"Søndergaard, Anders","first_name":"Anders"},{"full_name":"Christiansen, Lars","first_name":"Lars","last_name":"Christiansen"},{"first_name":"Jan","full_name":"Kaczmarczyk, Jan","orcid":"0000-0002-1629-3675","id":"46C405DE-F248-11E8-B48F-1D18A9856A87","last_name":"Kaczmarczyk"},{"first_name":"Robert","full_name":"Zillich, Robert","last_name":"Zillich"},{"last_name":"Lemeshko","first_name":"Mikhail","id":"37CB05FA-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-6990-7802","full_name":"Lemeshko, Mikhail"},{"full_name":"Stapelfeldt, Henrik","first_name":"Henrik","last_name":"Stapelfeldt"}]}]