[{"tmp":{"name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","short":"CC BY (4.0)","image":"/images/cc_by.png"},"oa":1,"project":[{"grant_number":"F03523","_id":"25473368-B435-11E9-9278-68D0E5697425","call_identifier":"FWF","name":"Transmembrane Transporters in Health and Disease"}],"doi":"10.15479/AT:ISTA:th_992","language":[{"iso":"eng"}],"supervisor":[{"full_name":"Novarino, Gaia","id":"3E57A680-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-7673-7178","first_name":"Gaia","last_name":"Novarino"}],"degree_awarded":"PhD","acknowledged_ssus":[{"_id":"PreCl"},{"_id":"EM-Fac"},{"_id":"Bio"}],"publication_identifier":{"issn":["2663-337X"]},"month":"03","year":"2018","department":[{"_id":"GaNo"}],"publisher":"Institute of Science and Technology Austria","publication_status":"published","related_material":{"record":[{"id":"1183","status":"public","relation":"part_of_dissertation"}]},"author":[{"full_name":"Tarlungeanu, Dora-Clara","last_name":"Tarlungeanu","first_name":"Dora-Clara","id":"2ABCE612-F248-11E8-B48F-1D18A9856A87"}],"date_updated":"2023-09-07T12:38:59Z","date_created":"2018-12-11T11:46:14Z","publist_id":"7434","file_date_updated":"2021-02-11T23:30:15Z","license":"https://creativecommons.org/licenses/by/4.0/","citation":{"ieee":"D.-C. Tarlungeanu, “The branched chain amino acids in autism spectrum disorders ,” Institute of Science and Technology Austria, 2018.","apa":"Tarlungeanu, D.-C. (2018). The branched chain amino acids in autism spectrum disorders . Institute of Science and Technology Austria. https://doi.org/10.15479/AT:ISTA:th_992","ista":"Tarlungeanu D-C. 2018. The branched chain amino acids in autism spectrum disorders . Institute of Science and Technology Austria.","ama":"Tarlungeanu D-C. The branched chain amino acids in autism spectrum disorders . 2018. doi:10.15479/AT:ISTA:th_992","chicago":"Tarlungeanu, Dora-Clara. “The Branched Chain Amino Acids in Autism Spectrum Disorders .” Institute of Science and Technology Austria, 2018. https://doi.org/10.15479/AT:ISTA:th_992.","short":"D.-C. Tarlungeanu, The Branched Chain Amino Acids in Autism Spectrum Disorders , Institute of Science and Technology Austria, 2018.","mla":"Tarlungeanu, Dora-Clara. The Branched Chain Amino Acids in Autism Spectrum Disorders . Institute of Science and Technology Austria, 2018, doi:10.15479/AT:ISTA:th_992."},"page":"88","date_published":"2018-03-01T00:00:00Z","article_processing_charge":"No","has_accepted_license":"1","day":"01","user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","_id":"395","status":"public","title":"The branched chain amino acids in autism spectrum disorders ","ddc":["570","616"],"pubrep_id":"992","file":[{"access_level":"closed","embargo_to":"open_access","file_name":"2018_Thesis_Tarlungeanu_source.docx","content_type":"application/vnd.openxmlformats-officedocument.wordprocessingml.document","file_size":43684035,"creator":"dernst","relation":"source_file","file_id":"6217","checksum":"9f5231c96e0ad945040841a8630232da","date_created":"2019-04-05T09:19:17Z","date_updated":"2021-02-11T23:30:15Z"},{"checksum":"0c33c370aa2010df5c552db57a6d01e9","date_created":"2019-04-05T09:19:17Z","date_updated":"2021-02-11T11:17:16Z","relation":"main_file","file_id":"6218","embargo":"2018-03-15","content_type":"application/pdf","file_size":30511532,"creator":"dernst","access_level":"open_access","file_name":"2018_Thesis_Tarlungeanu.pdf"}],"oa_version":"Published Version","type":"dissertation","alternative_title":["ISTA Thesis"],"abstract":[{"text":"Autism spectrum disorders (ASD) are a group of genetic disorders often overlapping with other neurological conditions. Despite the remarkable number of scientific breakthroughs of the last 100 years, the treatment of neurodevelopmental disorders (e.g. autism spectrum disorder, intellectual disability, epilepsy) remains a great challenge. Recent advancements in geno mics, like whole-exome or whole-genome sequencing, have enabled scientists to identify numerous mutations underlying neurodevelopmental disorders. Given the few hundred risk genes that were discovered, the etiological variability and the heterogeneous phenotypic outcomes, the need for genotype -along with phenotype- based diagnosis of individual patients becomes a requisite. Driven by this rationale, in a previous study our group described mutations, identified via whole - exome sequencing, in the gene BCKDK – encoding for a key regulator of branched chain amin o acid (BCAA) catabolism - as a cause of ASD. Following up on the role of BCAAs, in the study described here we show that the solute carrier transporter 7a5 (SLC7A5), a large neutral amino acid transporter localized mainly at the blood brain barrier (BBB), has an essential role in maintaining normal levels of brain BCAAs. In mice, deletion of Slc7a5 from the endothelial cells of the BBB leads to atypical brain amino acid profile, abnormal mRNA translation and severe neurolo gical abnormalities. Additionally, deletion of Slc7a5 from the neural progenitor cell population leads to microcephaly. Interestingly, we demonstrate that BCAA intracerebroventricular administration ameliorates abnormal behaviors in adult mutant mice. Furthermore, whole - exome sequencing of patients diagnosed with neurological dis o r ders helped us identify several patients with autistic traits, microcephaly and motor delay carrying deleterious homozygous mutations in the SLC7A5 gene. In conclusion, our data elucidate a neurological syndrome defined by SLC7A5 mutations and support an essential role for t he BCAA s in human bra in function. Together with r ecent studies (described in chapter two) that have successfully made the transition into clinical practice, our findings on the role of B CAAs might have a crucial impact on the development of novel individualized therapeutic strategies for ASD. ","lang":"eng"}]},{"status":"public","ddc":["571","576"],"title":"From the left to the right: A tale of asymmetries, environments, and hippocampal development","_id":"51","user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","oa_version":"Published Version","file":[{"date_updated":"2021-02-11T23:30:13Z","date_created":"2019-04-09T07:16:26Z","checksum":"dcc7b55619d8509dd62b8e99d6cdee44","file_id":"6251","relation":"source_file","creator":"dernst","content_type":"application/msword","file_size":141270528,"file_name":"2018_Thesis_Case_Source.doc","embargo_to":"open_access","access_level":"closed"},{"access_level":"open_access","file_name":"2018_Thesis_Case.pdf","creator":"dernst","file_size":15193621,"content_type":"application/pdf","embargo":"2019-07-05","file_id":"6252","relation":"main_file","checksum":"f69fdd5c8709c4e618aa8c1a1221153d","date_created":"2019-04-09T07:16:23Z","date_updated":"2021-02-11T11:17:14Z"}],"pubrep_id":"1032","alternative_title":["ISTA Thesis"],"type":"dissertation","abstract":[{"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.","lang":"eng"}],"page":"186","citation":{"ama":"Case MJ. From the left to the right: A tale of asymmetries, environments, and hippocampal development. 2018. doi:10.15479/AT:ISTA:th_1032","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.","apa":"Case, M. J. (2018). From the left to the right: A tale of asymmetries, environments, and hippocampal development. Institute of Science and Technology Austria. https://doi.org/10.15479/AT:ISTA:th_1032","ista":"Case MJ. 2018. From the left to the right: A tale of asymmetries, environments, and hippocampal development. Institute of Science and Technology Austria.","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.","mla":"Case, Matthew J. From the Left to the Right: A Tale of Asymmetries, Environments, and Hippocampal Development. Institute of Science and Technology Austria, 2018, doi:10.15479/AT:ISTA:th_1032.","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. https://doi.org/10.15479/AT:ISTA:th_1032."},"date_published":"2018-06-27T00:00:00Z","day":"27","article_processing_charge":"No","has_accepted_license":"1","publication_status":"published","department":[{"_id":"RySh"}],"publisher":"Institute of Science and Technology Austria","year":"2018","date_updated":"2023-09-07T12:39:22Z","date_created":"2018-12-11T11:44:22Z","author":[{"last_name":"Case","first_name":"Matthew J","id":"44B7CA5A-F248-11E8-B48F-1D18A9856A87","full_name":"Case, Matthew J"}],"related_material":{"record":[{"status":"public","relation":"part_of_dissertation","id":"682"}]},"file_date_updated":"2021-02-11T23:30:13Z","publist_id":"8003","oa":1,"supervisor":[{"first_name":"Ryuichi","last_name":"Shigemoto","id":"499F3ABC-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0001-8761-9444","full_name":"Shigemoto, Ryuichi"}],"degree_awarded":"PhD","language":[{"iso":"eng"}],"doi":"10.15479/AT:ISTA:th_1032","month":"06","publication_identifier":{"issn":["2663-337X"]}},{"month":"11","publication_identifier":{"issn":["2663-337X"]},"degree_awarded":"PhD","supervisor":[{"orcid":"0000-0002-4579-8306","id":"49E1C5C6-F248-11E8-B48F-1D18A9856A87","last_name":"Vicoso","first_name":"Beatriz","full_name":"Vicoso, Beatriz"}],"language":[{"iso":"eng"}],"doi":"10.15479/AT:ISTA:th1057","oa":1,"file_date_updated":"2021-02-11T11:17:16Z","publist_id":"8046","date_created":"2018-12-11T11:44:08Z","date_updated":"2023-09-07T12:40:44Z","author":[{"orcid":"0000-0002-7903-3010","id":"2D6B7A9A-F248-11E8-B48F-1D18A9856A87","last_name":"Laukoter","first_name":"Susanne","full_name":"Laukoter, Susanne"}],"publication_status":"published","publisher":"Institute of Science and Technology Austria","department":[{"_id":"SiHi"}],"year":"2018","day":"21","has_accepted_license":"1","article_processing_charge":"No","date_published":"2018-11-21T00:00:00Z","page":"1 - 139","citation":{"ista":"Laukoter S. 2018. Role of genomic imprinting in cerebral cortex development. Institute of Science and Technology Austria.","ieee":"S. Laukoter, “Role of genomic imprinting in cerebral cortex development,” Institute of Science and Technology Austria, 2018.","apa":"Laukoter, S. (2018). Role of genomic imprinting in cerebral cortex development. Institute of Science and Technology Austria. https://doi.org/10.15479/AT:ISTA:th1057","ama":"Laukoter S. Role of genomic imprinting in cerebral cortex development. 2018:1-139. doi:10.15479/AT:ISTA:th1057","chicago":"Laukoter, Susanne. “Role of Genomic Imprinting in Cerebral Cortex Development.” Institute of Science and Technology Austria, 2018. https://doi.org/10.15479/AT:ISTA:th1057.","mla":"Laukoter, Susanne. Role of Genomic Imprinting in Cerebral Cortex Development. Institute of Science and Technology Austria, 2018, pp. 1–139, doi:10.15479/AT:ISTA:th1057.","short":"S. Laukoter, Role of Genomic Imprinting in Cerebral Cortex Development, Institute of Science and Technology Austria, 2018."},"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."}],"alternative_title":["ISTA Thesis"],"type":"dissertation","oa_version":"Published Version","file":[{"date_created":"2019-05-10T07:47:04Z","date_updated":"2019-11-23T23:30:03Z","checksum":"41fdbf5fdce312802935d88a8ad9932c","relation":"source_file","file_id":"6396","content_type":"application/vnd.openxmlformats-officedocument.wordprocessingml.document","file_size":17949175,"creator":"dernst","embargo_to":"open_access","file_name":"Thesis_LaukoterSusanne_FINAL.docx","access_level":"closed"},{"file_name":"Thesis_LaukoterSusanne_FINAL.pdf","access_level":"open_access","creator":"dernst","file_size":21187245,"content_type":"application/pdf","embargo":"2019-11-21","file_id":"6397","relation":"main_file","date_created":"2019-05-10T07:47:04Z","date_updated":"2021-02-11T11:17:16Z","checksum":"53001a9a0c9e570e598d861bb0af28aa"}],"pubrep_id":"1057","status":"public","ddc":["570"],"title":"Role of genomic imprinting in cerebral cortex development","_id":"10","user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1"},{"publication_identifier":{"issn":["2663-337X"]},"month":"04","tmp":{"name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","short":"CC BY (4.0)","image":"/images/cc_by.png"},"oa":1,"language":[{"iso":"eng"}],"degree_awarded":"PhD","acknowledged_ssus":[{"_id":"NanoFab"},{"_id":"Bio"},{"_id":"PreCl"},{"_id":"EM-Fac"}],"supervisor":[{"id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-6620-9179","first_name":"Michael K","last_name":"Sixt","full_name":"Sixt, Michael K"}],"doi":"10.15479/AT:ISTA:th_998","publist_id":"7542","file_date_updated":"2021-02-11T23:30:17Z","publisher":"Institute of Science and Technology Austria","department":[{"_id":"MiSi"}],"publication_status":"published","acknowledgement":"First of all I would like to thank Michael Sixt for giving me the opportunity to work in \r\nhis group and for his support throughout the years. He is a truly inspiring person and \r\nthe best boss one can imagine. I would also like to thank all current and past \r\nmembers of the Sixt group for their help and the great working atmosphere in the lab. \r\nIt is a true privilege to work with such a bright, funny and friendly group of people and \r\nI’m proud that I could be part of it. Furthermore, I would like to say ‘thank you’ to Daria Siekhaus for all the meetings and discussion we had throughout the years \r\nand to Federica Benvenuti for being part of my committee. I am also grateful to Jack \r\nMerrin in the nanofabrication facility and all the people working in the bioimaging-\r\n, the electron microscopy- and the preclinical facilities.","year":"2018","date_updated":"2023-09-07T12:39:44Z","date_created":"2018-12-11T11:45:49Z","related_material":{"record":[{"status":"public","relation":"part_of_dissertation","id":"1321"}]},"author":[{"orcid":"0000-0002-1073-744X","id":"3B1B77E4-F248-11E8-B48F-1D18A9856A87","last_name":"Leithner","first_name":"Alexander F","full_name":"Leithner, Alexander F"}],"has_accepted_license":"1","article_processing_charge":"No","day":"12","page":"99","citation":{"ista":"Leithner AF. 2018. Branched actin networks in dendritic cell biology. Institute of Science and Technology Austria.","ieee":"A. F. Leithner, “Branched actin networks in dendritic cell biology,” Institute of Science and Technology Austria, 2018.","apa":"Leithner, A. F. (2018). Branched actin networks in dendritic cell biology. Institute of Science and Technology Austria. https://doi.org/10.15479/AT:ISTA:th_998","ama":"Leithner AF. Branched actin networks in dendritic cell biology. 2018. doi:10.15479/AT:ISTA:th_998","chicago":"Leithner, Alexander F. “Branched Actin Networks in Dendritic Cell Biology.” Institute of Science and Technology Austria, 2018. https://doi.org/10.15479/AT:ISTA:th_998.","mla":"Leithner, Alexander F. Branched Actin Networks in Dendritic Cell Biology. Institute of Science and Technology Austria, 2018, doi:10.15479/AT:ISTA:th_998.","short":"A.F. Leithner, Branched Actin Networks in Dendritic Cell Biology, Institute of Science and Technology Austria, 2018."},"date_published":"2018-04-12T00:00:00Z","alternative_title":["ISTA Thesis"],"type":"dissertation","abstract":[{"lang":"eng","text":"In the here presented thesis, we explore the role of branched actin networks in cell migration and antigen presentation, the two most relevant processes in dendritic cell biology. Branched actin networks construct lamellipodial protrusions at the leading edge of migrating cells. These are typically seen as adhesive structures, which mediate force transduction to the extracellular matrix that leads to forward locomotion. We ablated Arp2/3 nucleation promoting factor WAVE in DCs and found that the resulting cells lack lamellipodial protrusions. Instead, depending on the maturation state, one or multiple filopodia were formed. By challenging these cells in a variety of migration assays we found that lamellipodial protrusions are dispensable for the locomotion of leukocytes and actually dampen the speed of migration. However, lamellipodia are critically required to negotiate complex environments that DCs experience while they travel to the next draining lymph node. Taken together our results suggest that leukocyte lamellipodia have rather a sensory- than a force transducing function. Furthermore, we show for the first time structure and dynamics of dendritic cell F-actin at the immunological synapse with naïve T cells. Dendritic cell F-actin appears as dynamic foci that are nucleated by the Arp2/3 complex. WAVE ablated dendritic cells show increased membrane tension, leading to an altered ultrastructure of the immunological synapse and severe T cell priming defects. These results point towards a previously unappreciated role of the cellular mechanics of dendritic cells in T cell activation. Additionally, we present a novel cell culture based system for the differentiation of dendritic cells from conditionally immortalized hematopoietic precursors. These precursor cells are genetically tractable via the CRISPR/Cas9 system while they retain their ability to differentiate into highly migratory dendritic cells and other immune cells. This will foster the study of all aspects of dendritic cell biology and beyond. "}],"status":"public","ddc":["571","599","610"],"title":"Branched actin networks in dendritic cell biology","_id":"323","user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","file":[{"content_type":"application/vnd.openxmlformats-officedocument.wordprocessingml.document","file_size":29027671,"creator":"dernst","access_level":"closed","embargo_to":"open_access","file_name":"PhD_thesis_AlexLeithner_final_version.docx","checksum":"d5e3edbac548c26c1fa43a4b37a54a4c","date_updated":"2021-02-11T23:30:17Z","date_created":"2019-04-05T09:23:11Z","relation":"source_file","file_id":"6219"},{"file_size":66045341,"content_type":"application/pdf","creator":"dernst","file_name":"PhD_thesis_AlexLeithner.pdf","access_level":"open_access","date_updated":"2021-02-11T11:17:16Z","date_created":"2019-04-05T09:23:11Z","checksum":"071f7476db29e41146824ebd0697cb10","relation":"main_file","embargo":"2019-04-15","file_id":"6220"}],"oa_version":"Published Version","pubrep_id":"998"},{"day":"01","article_processing_charge":"No","has_accepted_license":"1","page":"147","citation":{"mla":"Hurny, Andrej. Identification and Characterization of Novel Auxin-Cytokinin Cross-Talk Components. Institute of Science and Technology Austria, 2018, doi:10.15479/AT:ISTA:th_930.","short":"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. https://doi.org/10.15479/AT:ISTA:th_930.","ama":"Hurny A. Identification and characterization of novel auxin-cytokinin cross-talk components. 2018. doi:10.15479/AT:ISTA:th_930","ista":"Hurny A. 2018. Identification and characterization of novel auxin-cytokinin cross-talk components. Institute of Science and Technology Austria.","ieee":"A. Hurny, “Identification and characterization of novel auxin-cytokinin cross-talk components,” Institute of Science and Technology Austria, 2018.","apa":"Hurny, A. (2018). Identification and characterization of novel auxin-cytokinin cross-talk components. Institute of Science and Technology Austria. https://doi.org/10.15479/AT:ISTA:th_930"},"date_published":"2018-01-01T00:00:00Z","alternative_title":["ISTA Thesis"],"type":"dissertation","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."}],"title":"Identification and characterization of novel auxin-cytokinin cross-talk components","status":"public","ddc":["570"],"user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","_id":"539","oa_version":"Published Version","file":[{"relation":"source_file","file_id":"6226","checksum":"0c9d6d1c80d9857e6e545213467bbcb2","date_updated":"2020-12-02T23:30:08Z","date_created":"2019-04-05T09:37:56Z","access_level":"closed","embargo_to":"open_access","file_name":"2018_Hurny_thesis_source.docx","file_size":28112114,"content_type":"application/vnd.openxmlformats-officedocument.wordprocessingml.document","creator":"dernst"},{"date_created":"2019-04-05T09:37:55Z","date_updated":"2020-12-02T09:52:16Z","checksum":"ecbe481a1413d270bd501b872c7ed54f","relation":"main_file","file_id":"6227","embargo":"2019-07-10","file_size":12524427,"content_type":"application/pdf","creator":"dernst","file_name":"2018_Hurny_thesis.pdf","access_level":"open_access"}],"pubrep_id":"930","month":"01","publication_identifier":{"issn":["2663-337X"]},"oa":1,"tmp":{"name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","short":"CC BY (4.0)","image":"/images/cc_by.png"},"supervisor":[{"last_name":"Benková","first_name":"Eva","orcid":"0000-0002-8510-9739","id":"38F4F166-F248-11E8-B48F-1D18A9856A87","full_name":"Benková, Eva"}],"degree_awarded":"PhD","language":[{"iso":"eng"}],"doi":"10.15479/AT:ISTA:th_930","file_date_updated":"2020-12-02T23:30:08Z","publist_id":"7277","publication_status":"published","department":[{"_id":"EvBe"}],"publisher":"Institute of Science and Technology Austria","year":"2018","date_updated":"2023-09-07T12:41:06Z","date_created":"2018-12-11T11:47:03Z","author":[{"full_name":"Hurny, Andrej","first_name":"Andrej","last_name":"Hurny","id":"4DC4AF46-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0003-3638-1426"}],"related_material":{"record":[{"status":"public","relation":"part_of_dissertation","id":"1024"}]}}]