[{"title":"Functional deficiency of MHC class i enhances LTP and abolishes LTD in the nucleus accumbens of mice","abstract":[{"lang":"eng","text":"Major histocompatibility complex class I (MHCI) molecules were recently identified as novel regulators of synaptic plasticity. These molecules are expressed in various brain areas, especially in regions undergoing activity-dependent synaptic plasticity, but their role in the nucleus accumbens (NAc) is unknown. In this study, we investigated the effects of genetic disruption of MHCI function, through deletion of β2-microblobulin, which causes lack of cell surface expression of MHCI. First, we confirmed that MHCI molecules are expressed in the NAc core in wild-type mice. Second, we performed electrophysiological recordings with NAc core slices from wild-type and β2-microglobulin knock-out mice lacking cell surface expression of MHCI. We found that low frequency stimulation induced long-term depression in wild-type but not knock-out mice, whereas high frequency stimulation induced long-term potentiation in both genotypes, with a larger magnitude in knock-out mice. Furthermore, we demonstrated that knock-out mice showed more persistent behavioral sensitization to cocaine, which is a NAc-related behavior. Using this model, we analyzed the density of total AMPA receptors and their subunits GluR1 and GluR2 in the NAc core, by SDS-digested freeze-fracture replica labeling. After repeated cocaine exposure, the density of GluR1 was increased, but there was no change in total AMPA receptors and GluR2 levels in wildtype mice. In contrast, following repeated cocaine exposure, increased densities of total AMPA receptors, GluR1 and GluR2 were observed in knock-out mice. These results indicate that functional deficiency of MHCI enhances synaptic potentiation, induced by electrical and pharmacological stimulation."}],"publisher":"Public Library of Science","file":[{"date_created":"2018-12-12T10:09:01Z","relation":"main_file","file_size":6262085,"access_level":"open_access","creator":"system","file_name":"IST-2016-439-v1+1_journal.pone.0107099.pdf","date_updated":"2020-07-14T12:45:20Z","checksum":"1f3be936be93114596d61ba44cacee69","content_type":"application/pdf","file_id":"4724"}],"date_updated":"2025-09-29T13:04:38Z","doi":"10.1371/journal.pone.0107099","status":"public","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)"},"oa":1,"date_created":"2018-12-11T11:54:35Z","_id":"1895","external_id":{"isi":["000343671700028"]},"date_published":"2014-09-30T00:00:00Z","publist_id":"5200","year":"2014","file_date_updated":"2020-07-14T12:45:20Z","day":"30","article_processing_charge":"No","type":"journal_article","user_id":"317138e5-6ab7-11ef-aa6d-ffef3953e345","publication":"PLoS One","has_accepted_license":"1","citation":{"ama":"Edamura M, Murakami G, Meng H, et al. Functional deficiency of MHC class i enhances LTP and abolishes LTD in the nucleus accumbens of mice. <i>PLoS One</i>. 2014;9(9). doi:<a href=\"https://doi.org/10.1371/journal.pone.0107099\">10.1371/journal.pone.0107099</a>","apa":"Edamura, M., Murakami, G., Meng, H., Itakura, M., Shigemoto, R., Fukuda, A., &#38; Nakahara, D. (2014). Functional deficiency of MHC class i enhances LTP and abolishes LTD in the nucleus accumbens of mice. <i>PLoS One</i>. Public Library of Science. <a href=\"https://doi.org/10.1371/journal.pone.0107099\">https://doi.org/10.1371/journal.pone.0107099</a>","short":"M. Edamura, G. Murakami, H. Meng, M. Itakura, R. Shigemoto, A. Fukuda, D. Nakahara, PLoS One 9 (2014).","ieee":"M. Edamura <i>et al.</i>, “Functional deficiency of MHC class i enhances LTP and abolishes LTD in the nucleus accumbens of mice,” <i>PLoS One</i>, vol. 9, no. 9. Public Library of Science, 2014.","chicago":"Edamura, Mitsuhiro, Gen Murakami, Hongrui Meng, Makoto Itakura, Ryuichi Shigemoto, Atsuo Fukuda, and Daiichiro Nakahara. “Functional Deficiency of MHC Class i Enhances LTP and Abolishes LTD in the Nucleus Accumbens of Mice.” <i>PLoS One</i>. Public Library of Science, 2014. <a href=\"https://doi.org/10.1371/journal.pone.0107099\">https://doi.org/10.1371/journal.pone.0107099</a>.","mla":"Edamura, Mitsuhiro, et al. “Functional Deficiency of MHC Class i Enhances LTP and Abolishes LTD in the Nucleus Accumbens of Mice.” <i>PLoS One</i>, vol. 9, no. 9, e107099, Public Library of Science, 2014, doi:<a href=\"https://doi.org/10.1371/journal.pone.0107099\">10.1371/journal.pone.0107099</a>.","ista":"Edamura M, Murakami G, Meng H, Itakura M, Shigemoto R, Fukuda A, Nakahara D. 2014. Functional deficiency of MHC class i enhances LTP and abolishes LTD in the nucleus accumbens of mice. PLoS One. 9(9), e107099."},"article_number":"e107099","issue":"9","pubrep_id":"439","language":[{"iso":"eng"}],"oa_version":"Published Version","scopus_import":"1","intvolume":"         9","ddc":["570"],"acknowledgement":"This work was supported in part by a Grant-in-Aid for Scientific Research on Innovative Areas (Comprehensive Brain Science Network) and (B) 17330153, from the Ministry of Education, Culture, Sports, Science and Technology of Japan.","department":[{"_id":"RySh"}],"author":[{"full_name":"Edamura, Mitsuhiro","last_name":"Edamura","first_name":"Mitsuhiro"},{"first_name":"Gen","last_name":"Murakami","full_name":"Murakami, Gen"},{"full_name":"Meng, Hongrui","last_name":"Meng","first_name":"Hongrui"},{"last_name":"Itakura","full_name":"Itakura, Makoto","first_name":"Makoto"},{"orcid":"0000-0001-8761-9444","full_name":"Shigemoto, Ryuichi","last_name":"Shigemoto","first_name":"Ryuichi","id":"499F3ABC-F248-11E8-B48F-1D18A9856A87"},{"first_name":"Atsuo","last_name":"Fukuda","full_name":"Fukuda, Atsuo"},{"first_name":"Daiichiro","last_name":"Nakahara","full_name":"Nakahara, Daiichiro"}],"isi":1,"publication_status":"published","month":"09","volume":9},{"main_file_link":[{"open_access":"1","url":"http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4145132/"}],"publisher":"American Society of Plant Biologists","abstract":[{"lang":"eng","text":"GNOM is one of the most characterized membrane trafficking regulators in plants, with crucial roles in development. GNOM encodes an ARF-guanine nucleotide exchange factor (ARF-GEF) that activates small GTPases of the ARF (ADP ribosylation factor) class to mediate vesicle budding at endomembranes. The crucial role of GNOM in recycling of PIN auxin transporters and other proteins to the plasma membrane was identified in studies using the ARF-GEF inhibitor brefeldin A (BFA). GNOM, the most prominent regulator of recycling in plants, has been proposed to act and localize at so far elusive recycling endosomes. Here, we report the GNOM localization in context of its cellular function in Arabidopsis thaliana. State-of-the-art imaging, pharmacological interference, and ultrastructure analysis show that GNOM predominantly localizes to Golgi apparatus. Super-resolution confocal live imaging microscopy identified GNOM and its closest homolog GNOM-like 1 at distinct subdomains on Golgi cisternae. Short-term BFA treatment stabilizes GNOM at the Golgi apparatus, whereas prolonged exposures results in GNOM translocation to trans-Golgi network (TGN)/early endosomes (EEs). Malformed TGN/EE in gnom mutants suggests a role for GNOM in maintaining TGN/EE function. Our results redefine the subcellular action of GNOM and reevaluate the identity and function of recycling endosomes in plants."}],"title":"Insights into the localization and function of the membrane trafficking regulator GNOM ARF-GEF at the Golgi apparatus in Arabidopsis","oa":1,"status":"public","date_updated":"2025-09-29T13:04:06Z","doi":"10.1105/tpc.114.125880","year":"2014","publist_id":"5199","date_published":"2014-07-01T00:00:00Z","_id":"1897","external_id":{"isi":["000342076200027"]},"date_created":"2018-12-11T11:54:36Z","publication":"Plant Cell","type":"journal_article","user_id":"317138e5-6ab7-11ef-aa6d-ffef3953e345","article_processing_charge":"No","day":"01","issue":"7","citation":{"ista":"Naramoto S, Otegui M, Kutsuna N, De Rycke R, Dainobu T, Karampelias M, Fujimoto M, Feraru E, Miki D, Fukuda H, Nakano A, Friml J. 2014. Insights into the localization and function of the membrane trafficking regulator GNOM ARF-GEF at the Golgi apparatus in Arabidopsis. Plant Cell. 26(7), 3062–3076.","mla":"Naramoto, Satoshi, et al. “Insights into the Localization and Function of the Membrane Trafficking Regulator GNOM ARF-GEF at the Golgi Apparatus in Arabidopsis.” <i>Plant Cell</i>, vol. 26, no. 7, American Society of Plant Biologists, 2014, pp. 3062–76, doi:<a href=\"https://doi.org/10.1105/tpc.114.125880\">10.1105/tpc.114.125880</a>.","ieee":"S. Naramoto <i>et al.</i>, “Insights into the localization and function of the membrane trafficking regulator GNOM ARF-GEF at the Golgi apparatus in Arabidopsis,” <i>Plant Cell</i>, vol. 26, no. 7. American Society of Plant Biologists, pp. 3062–3076, 2014.","chicago":"Naramoto, Satoshi, Marisa Otegui, Natsumaro Kutsuna, Riet De Rycke, Tomoko Dainobu, Michael Karampelias, Masaru Fujimoto, et al. “Insights into the Localization and Function of the Membrane Trafficking Regulator GNOM ARF-GEF at the Golgi Apparatus in Arabidopsis.” <i>Plant Cell</i>. American Society of Plant Biologists, 2014. <a href=\"https://doi.org/10.1105/tpc.114.125880\">https://doi.org/10.1105/tpc.114.125880</a>.","short":"S. Naramoto, M. Otegui, N. Kutsuna, R. De Rycke, T. Dainobu, M. Karampelias, M. Fujimoto, E. Feraru, D. Miki, H. Fukuda, A. Nakano, J. Friml, Plant Cell 26 (2014) 3062–3076.","apa":"Naramoto, S., Otegui, M., Kutsuna, N., De Rycke, R., Dainobu, T., Karampelias, M., … Friml, J. (2014). Insights into the localization and function of the membrane trafficking regulator GNOM ARF-GEF at the Golgi apparatus in Arabidopsis. <i>Plant Cell</i>. American Society of Plant Biologists. <a href=\"https://doi.org/10.1105/tpc.114.125880\">https://doi.org/10.1105/tpc.114.125880</a>","ama":"Naramoto S, Otegui M, Kutsuna N, et al. Insights into the localization and function of the membrane trafficking regulator GNOM ARF-GEF at the Golgi apparatus in Arabidopsis. <i>Plant Cell</i>. 2014;26(7):3062-3076. doi:<a href=\"https://doi.org/10.1105/tpc.114.125880\">10.1105/tpc.114.125880</a>"},"page":"3062 - 3076","oa_version":"Submitted Version","language":[{"iso":"eng"}],"month":"07","volume":26,"isi":1,"publication_status":"published","author":[{"first_name":"Satoshi","last_name":"Naramoto","full_name":"Naramoto, Satoshi"},{"last_name":"Otegui","full_name":"Otegui, Marisa","first_name":"Marisa"},{"first_name":"Natsumaro","full_name":"Kutsuna, Natsumaro","last_name":"Kutsuna"},{"first_name":"Riet","full_name":"De Rycke, Riet","last_name":"De Rycke"},{"last_name":"Dainobu","full_name":"Dainobu, Tomoko","first_name":"Tomoko"},{"last_name":"Karampelias","full_name":"Karampelias, Michael","first_name":"Michael"},{"last_name":"Fujimoto","full_name":"Fujimoto, Masaru","first_name":"Masaru"},{"last_name":"Feraru","full_name":"Feraru, Elena","first_name":"Elena"},{"last_name":"Miki","full_name":"Miki, Daisuke","first_name":"Daisuke"},{"last_name":"Fukuda","full_name":"Fukuda, Hiroo","first_name":"Hiroo"},{"first_name":"Akihiko","full_name":"Nakano, Akihiko","last_name":"Nakano"},{"orcid":"0000-0002-8302-7596","last_name":"Friml","full_name":"Friml, Jirí","id":"4159519E-F248-11E8-B48F-1D18A9856A87","first_name":"Jirí"}],"department":[{"_id":"JiFr"}],"acknowledgement":"This work was supported by the Odysseus Program of the Research Foundation-Flanders (J.F.).","intvolume":"        26","scopus_import":"1"},{"oa_version":"None","page":"152 - 163","language":[{"iso":"eng"}],"month":"10","volume":84,"author":[{"first_name":"Andreas","full_name":"Ritzau Jost, Andreas","last_name":"Ritzau Jost"},{"last_name":"Delvendahl","full_name":"Delvendahl, Igor","first_name":"Igor"},{"last_name":"Rings","full_name":"Rings, Annika","first_name":"Annika"},{"full_name":"Byczkowicz, Niklas","last_name":"Byczkowicz","first_name":"Niklas"},{"first_name":"Harumi","id":"2E55CDF2-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0001-7429-7896","full_name":"Harada, Harumi","last_name":"Harada"},{"id":"499F3ABC-F248-11E8-B48F-1D18A9856A87","first_name":"Ryuichi","full_name":"Shigemoto, Ryuichi","last_name":"Shigemoto","orcid":"0000-0001-8761-9444"},{"first_name":"Johannes","last_name":"Hirrlinger","full_name":"Hirrlinger, Johannes"},{"first_name":"Jens","last_name":"Eilers","full_name":"Eilers, Jens"},{"first_name":"Stefan","last_name":"Hallermann","full_name":"Hallermann, Stefan"}],"department":[{"_id":"RySh"}],"isi":1,"publication_status":"published","scopus_import":"1","intvolume":"        84","issue":"1","citation":{"chicago":"Ritzau Jost, Andreas, Igor Delvendahl, Annika Rings, Niklas Byczkowicz, Harumi Harada, Ryuichi Shigemoto, Johannes Hirrlinger, Jens Eilers, and Stefan Hallermann. “Ultrafast Action Potentials Mediate Kilohertz Signaling at a Central Synapse.” <i>Neuron</i>. Elsevier, 2014. <a href=\"https://doi.org/10.1016/j.neuron.2014.08.036\">https://doi.org/10.1016/j.neuron.2014.08.036</a>.","ieee":"A. Ritzau Jost <i>et al.</i>, “Ultrafast action potentials mediate kilohertz signaling at a central synapse,” <i>Neuron</i>, vol. 84, no. 1. Elsevier, pp. 152–163, 2014.","mla":"Ritzau Jost, Andreas, et al. “Ultrafast Action Potentials Mediate Kilohertz Signaling at a Central Synapse.” <i>Neuron</i>, vol. 84, no. 1, Elsevier, 2014, pp. 152–63, doi:<a href=\"https://doi.org/10.1016/j.neuron.2014.08.036\">10.1016/j.neuron.2014.08.036</a>.","ista":"Ritzau Jost A, Delvendahl I, Rings A, Byczkowicz N, Harada H, Shigemoto R, Hirrlinger J, Eilers J, Hallermann S. 2014. Ultrafast action potentials mediate kilohertz signaling at a central synapse. Neuron. 84(1), 152–163.","ama":"Ritzau Jost A, Delvendahl I, Rings A, et al. Ultrafast action potentials mediate kilohertz signaling at a central synapse. <i>Neuron</i>. 2014;84(1):152-163. doi:<a href=\"https://doi.org/10.1016/j.neuron.2014.08.036\">10.1016/j.neuron.2014.08.036</a>","apa":"Ritzau Jost, A., Delvendahl, I., Rings, A., Byczkowicz, N., Harada, H., Shigemoto, R., … Hallermann, S. (2014). Ultrafast action potentials mediate kilohertz signaling at a central synapse. <i>Neuron</i>. Elsevier. <a href=\"https://doi.org/10.1016/j.neuron.2014.08.036\">https://doi.org/10.1016/j.neuron.2014.08.036</a>","short":"A. Ritzau Jost, I. Delvendahl, A. Rings, N. Byczkowicz, H. Harada, R. Shigemoto, J. Hirrlinger, J. Eilers, S. Hallermann, Neuron 84 (2014) 152–163."},"publist_id":"5197","year":"2014","_id":"1898","external_id":{"isi":["000342502800017"]},"date_published":"2014-10-01T00:00:00Z","date_created":"2018-12-11T11:54:36Z","publication":"Neuron","user_id":"317138e5-6ab7-11ef-aa6d-ffef3953e345","type":"journal_article","day":"01","article_processing_charge":"No","abstract":[{"lang":"eng","text":"Fast synaptic transmission is important for rapid information processing. To explore the maximal rate of neuronal signaling and to analyze the presynaptic mechanisms, we focused on the input layer of the cerebellar cortex, where exceptionally high action potential (AP) frequencies have been reported invivo. With paired recordings between presynaptic cerebellar mossy fiber boutons and postsynaptic granule cells, we demonstrate reliable neurotransmission upto ~1 kHz. Presynaptic APs are ultrafast, with ~100μs half-duration. Both Kv1 and Kv3 potassium channels mediate the fast repolarization, rapidly inactivating sodium channels ensure metabolic efficiency, and little AP broadening occurs during bursts of up to 1.5 kHz. Presynaptic Cav2.1 (P/Q-type) calcium channels open efficiently during ultrafast APs. Furthermore, a subset of synaptic vesicles is tightly coupled to Ca2+ channels, and vesicles are rapidly recruited to the release site. These data reveal mechanisms of presynaptic AP generation and transmitter release underlying neuronal kHz signaling."}],"title":"Ultrafast action potentials mediate kilohertz signaling at a central synapse","quality_controlled":"1","publisher":"Elsevier","doi":"10.1016/j.neuron.2014.08.036","status":"public","date_updated":"2025-09-29T13:03:03Z"},{"oa":1,"article_type":"original","date_updated":"2025-09-29T12:32:05Z","status":"public","doi":"10.1038/ncb3001","main_file_link":[{"url":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4159251/","open_access":"1"}],"abstract":[{"lang":"eng","text":"Asymmetric cell divisions allow stem cells to balance proliferation and differentiation. During embryogenesis, murine epidermis expands rapidly from a single layer of unspecified basal layer progenitors to a stratified, differentiated epithelium. Morphogenesis involves perpendicular (asymmetric) divisions and the spindle orientation protein LGN, but little is known about how the apical localization of LGN is regulated. Here, we combine conventional genetics and lentiviral-mediated in vivo RNAi to explore the functions of the LGN-interacting proteins Par3, mInsc and Gα i3. Whereas loss of each gene alone leads to randomized division angles, combined loss of Gnai3 and mInsc causes a phenotype of mostly planar divisions, akin to loss of LGN. These findings lend experimental support for the hitherto untested model that Par3-mInsc and Gα i3 act cooperatively to polarize LGN and promote perpendicular divisions. Finally, we uncover a developmental switch between delamination-driven early stratification and spindle-orientation-dependent differentiation that occurs around E15, revealing a two-step mechanism underlying epidermal maturation."}],"title":"Par3-mInsc and Gα i3 cooperate to promote oriented epidermal cell divisions through LGN","quality_controlled":"1","publisher":"Nature Publishing Group","publication":"Nature Cell Biology","user_id":"317138e5-6ab7-11ef-aa6d-ffef3953e345","type":"journal_article","day":"13","article_processing_charge":"No","publist_id":"5196","year":"2014","_id":"1899","external_id":{"pmid":["25016959"],"isi":["000339904900008"]},"date_published":"2014-07-13T00:00:00Z","date_created":"2018-12-11T11:54:36Z","pmid":1,"issue":"8","citation":{"chicago":"Williams, Scott, Lyndsay Ratliff, Maria P Postiglione, Juergen Knoblich, and Elaine Fuchs. “Par3-MInsc and Gα I3 Cooperate to Promote Oriented Epidermal Cell Divisions through LGN.” <i>Nature Cell Biology</i>. Nature Publishing Group, 2014. <a href=\"https://doi.org/10.1038/ncb3001\">https://doi.org/10.1038/ncb3001</a>.","ieee":"S. Williams, L. Ratliff, M. P. Postiglione, J. Knoblich, and E. Fuchs, “Par3-mInsc and Gα i3 cooperate to promote oriented epidermal cell divisions through LGN,” <i>Nature Cell Biology</i>, vol. 16, no. 8. Nature Publishing Group, pp. 758–769, 2014.","mla":"Williams, Scott, et al. “Par3-MInsc and Gα I3 Cooperate to Promote Oriented Epidermal Cell Divisions through LGN.” <i>Nature Cell Biology</i>, vol. 16, no. 8, Nature Publishing Group, 2014, pp. 758–69, doi:<a href=\"https://doi.org/10.1038/ncb3001\">10.1038/ncb3001</a>.","ista":"Williams S, Ratliff L, Postiglione MP, Knoblich J, Fuchs E. 2014. Par3-mInsc and Gα i3 cooperate to promote oriented epidermal cell divisions through LGN. Nature Cell Biology. 16(8), 758–769.","ama":"Williams S, Ratliff L, Postiglione MP, Knoblich J, Fuchs E. Par3-mInsc and Gα i3 cooperate to promote oriented epidermal cell divisions through LGN. <i>Nature Cell Biology</i>. 2014;16(8):758-769. doi:<a href=\"https://doi.org/10.1038/ncb3001\">10.1038/ncb3001</a>","apa":"Williams, S., Ratliff, L., Postiglione, M. P., Knoblich, J., &#38; Fuchs, E. (2014). Par3-mInsc and Gα i3 cooperate to promote oriented epidermal cell divisions through LGN. <i>Nature Cell Biology</i>. Nature Publishing Group. <a href=\"https://doi.org/10.1038/ncb3001\">https://doi.org/10.1038/ncb3001</a>","short":"S. Williams, L. Ratliff, M.P. Postiglione, J. Knoblich, E. Fuchs, Nature Cell Biology 16 (2014) 758–769."},"volume":16,"month":"07","author":[{"last_name":"Williams","full_name":"Williams, Scott","first_name":"Scott"},{"first_name":"Lyndsay","last_name":"Ratliff","full_name":"Ratliff, Lyndsay"},{"last_name":"Postiglione","full_name":"Postiglione, Maria P","first_name":"Maria P","id":"2C67902A-F248-11E8-B48F-1D18A9856A87"},{"full_name":"Knoblich, Juergen","last_name":"Knoblich","first_name":"Juergen"},{"full_name":"Fuchs, Elaine","last_name":"Fuchs","first_name":"Elaine"}],"department":[{"_id":"SiHi"}],"isi":1,"publication_status":"published","scopus_import":"1","intvolume":"        16","oa_version":"Submitted Version","page":"758 - 769","language":[{"iso":"eng"}]},{"oa_version":"None","page":"127 - 129","language":[{"iso":"eng"}],"month":"01","volume":16,"department":[{"_id":"CaHe"}],"author":[{"id":"3ECECA3A-F248-11E8-B48F-1D18A9856A87","first_name":"Martin","last_name":"Behrndt","full_name":"Behrndt, Martin"},{"id":"39427864-F248-11E8-B48F-1D18A9856A87","first_name":"Carl-Philipp J","orcid":"0000-0002-0912-4566","full_name":"Heisenberg, Carl-Philipp J","last_name":"Heisenberg"}],"isi":1,"publication_status":"published","scopus_import":"1","intvolume":"        16","issue":"2","citation":{"ista":"Behrndt M, Heisenberg C-PJ. 2014. Lateral junction dynamics lead the way out. Nature Cell Biology. 16(2), 127–129.","mla":"Behrndt, Martin, and Carl-Philipp J. Heisenberg. “Lateral Junction Dynamics Lead the Way Out.” <i>Nature Cell Biology</i>, vol. 16, no. 2, Nature Publishing Group, 2014, pp. 127–29, doi:<a href=\"https://doi.org/10.1038/ncb2913\">10.1038/ncb2913</a>.","ieee":"M. Behrndt and C.-P. J. Heisenberg, “Lateral junction dynamics lead the way out,” <i>Nature Cell Biology</i>, vol. 16, no. 2. Nature Publishing Group, pp. 127–129, 2014.","chicago":"Behrndt, Martin, and Carl-Philipp J Heisenberg. “Lateral Junction Dynamics Lead the Way Out.” <i>Nature Cell Biology</i>. Nature Publishing Group, 2014. <a href=\"https://doi.org/10.1038/ncb2913\">https://doi.org/10.1038/ncb2913</a>.","short":"M. Behrndt, C.-P.J. Heisenberg, Nature Cell Biology 16 (2014) 127–129.","apa":"Behrndt, M., &#38; Heisenberg, C.-P. J. (2014). Lateral junction dynamics lead the way out. <i>Nature Cell Biology</i>. Nature Publishing Group. <a href=\"https://doi.org/10.1038/ncb2913\">https://doi.org/10.1038/ncb2913</a>","ama":"Behrndt M, Heisenberg C-PJ. Lateral junction dynamics lead the way out. <i>Nature Cell Biology</i>. 2014;16(2):127-129. doi:<a href=\"https://doi.org/10.1038/ncb2913\">10.1038/ncb2913</a>"},"corr_author":"1","publist_id":"5195","year":"2014","_id":"1900","external_id":{"isi":["000331161400001"]},"date_published":"2014-01-31T00:00:00Z","date_created":"2018-12-11T11:54:37Z","publication":"Nature Cell Biology","type":"journal_article","user_id":"317138e5-6ab7-11ef-aa6d-ffef3953e345","day":"31","article_processing_charge":"No","title":"Lateral junction dynamics lead the way out","abstract":[{"lang":"eng","text":"Epithelial cell layers need to be tightly regulated to maintain their integrity and correct function. Cell integration into epithelial sheets is now shown to depend on the N-WASP-regulated stabilization of cortical F-actin, which generates distinct patterns of apical-lateral contractility at E-cadherin-based cell-cell junctions."}],"quality_controlled":"1","publisher":"Nature Publishing Group","date_updated":"2025-09-29T12:31:29Z","doi":"10.1038/ncb2913","status":"public"},{"acknowledgement":"This work was supported by funding from the projects CZ.1.07/2.3.00/20.0043 and CZ.1.05/1.1.00/02.0068 (to CEITEC, Central European Institute of Technology) and the Odysseus program of the Research Foundation-Flanders to J.F\r\n","intvolume":"         7","scopus_import":"1","volume":7,"month":"02","publication_status":"published","isi":1,"department":[{"_id":"JiFr"}],"author":[{"last_name":"Tian","full_name":"Tian, Huiyu","first_name":"Huiyu"},{"first_name":"Krzysztof T","full_name":"Wabnik, Krzysztof T","last_name":"Wabnik"},{"first_name":"Tiantian","full_name":"Niu, Tiantian","last_name":"Niu"},{"first_name":"Hongjiang","last_name":"Li","full_name":"Li, Hongjiang"},{"full_name":"Yu, Qianqian","last_name":"Yu","first_name":"Qianqian"},{"last_name":"Pollmann","full_name":"Pollmann, Stephan","first_name":"Stephan"},{"full_name":"Vanneste, Steffen","last_name":"Vanneste","first_name":"Steffen"},{"first_name":"Willy","full_name":"Govaerts, Willy","last_name":"Govaerts"},{"full_name":"Rolčík, Jakub","last_name":"Rolčík","first_name":"Jakub"},{"first_name":"Markus","full_name":"Geisler, Markus","last_name":"Geisler"},{"last_name":"Friml","full_name":"Friml, Jirí","orcid":"0000-0002-8302-7596","id":"4159519E-F248-11E8-B48F-1D18A9856A87","first_name":"Jirí"},{"first_name":"Zhaojun","full_name":"Ding, Zhaojun","last_name":"Ding"}],"page":"277 - 289","oa_version":"None","language":[{"iso":"eng"}],"issue":"2","citation":{"apa":"Tian, H., Wabnik, K. T., Niu, T., Li, H., Yu, Q., Pollmann, S., … Ding, Z. (2014). WOX5-IAA17 feedback circuit-mediated cellular auxin response is crucial for the patterning of root stem cell niches in arabidopsis. <i>Molecular Plant</i>. Oxford University Press. <a href=\"https://doi.org/10.1093/mp/sst118\">https://doi.org/10.1093/mp/sst118</a>","ama":"Tian H, Wabnik KT, Niu T, et al. WOX5-IAA17 feedback circuit-mediated cellular auxin response is crucial for the patterning of root stem cell niches in arabidopsis. <i>Molecular Plant</i>. 2014;7(2):277-289. doi:<a href=\"https://doi.org/10.1093/mp/sst118\">10.1093/mp/sst118</a>","short":"H. Tian, K.T. Wabnik, T. Niu, H. Li, Q. Yu, S. Pollmann, S. Vanneste, W. Govaerts, J. Rolčík, M. Geisler, J. Friml, Z. Ding, Molecular Plant 7 (2014) 277–289.","mla":"Tian, Huiyu, et al. “WOX5-IAA17 Feedback Circuit-Mediated Cellular Auxin Response Is Crucial for the Patterning of Root Stem Cell Niches in Arabidopsis.” <i>Molecular Plant</i>, vol. 7, no. 2, Oxford University Press, 2014, pp. 277–89, doi:<a href=\"https://doi.org/10.1093/mp/sst118\">10.1093/mp/sst118</a>.","chicago":"Tian, Huiyu, Krzysztof T Wabnik, Tiantian Niu, Hongjiang Li, Qianqian Yu, Stephan Pollmann, Steffen Vanneste, et al. “WOX5-IAA17 Feedback Circuit-Mediated Cellular Auxin Response Is Crucial for the Patterning of Root Stem Cell Niches in Arabidopsis.” <i>Molecular Plant</i>. Oxford University Press, 2014. <a href=\"https://doi.org/10.1093/mp/sst118\">https://doi.org/10.1093/mp/sst118</a>.","ieee":"H. Tian <i>et al.</i>, “WOX5-IAA17 feedback circuit-mediated cellular auxin response is crucial for the patterning of root stem cell niches in arabidopsis,” <i>Molecular Plant</i>, vol. 7, no. 2. Oxford University Press, pp. 277–289, 2014.","ista":"Tian H, Wabnik KT, Niu T, Li H, Yu Q, Pollmann S, Vanneste S, Govaerts W, Rolčík J, Geisler M, Friml J, Ding Z. 2014. WOX5-IAA17 feedback circuit-mediated cellular auxin response is crucial for the patterning of root stem cell niches in arabidopsis. Molecular Plant. 7(2), 277–289."},"article_processing_charge":"No","day":"01","publication":"Molecular Plant","type":"journal_article","user_id":"317138e5-6ab7-11ef-aa6d-ffef3953e345","date_published":"2014-02-01T00:00:00Z","external_id":{"isi":["000330841400003"]},"_id":"1901","date_created":"2018-12-11T11:54:37Z","year":"2014","publist_id":"5194","doi":"10.1093/mp/sst118","status":"public","date_updated":"2025-09-29T12:30:56Z","publisher":"Oxford University Press","abstract":[{"lang":"eng","text":"In plants, the patterning of stem cell-enriched meristems requires a graded auxin response maximum that emerges from the concerted action of polar auxin transport, auxin biosynthesis, auxin metabolism, and cellular auxin response machinery. However, mechanisms underlying this auxin response maximum-mediated root stem cell maintenance are not fully understood. Here, we present unexpected evidence that WUSCHEL-RELATED HOMEOBOX 5 (WOX5) transcription factor modulates expression of auxin biosynthetic genes in the quiescent center (QC) of the root and thus provides a robust mechanism for the maintenance of auxin response maximum in the root tip. This WOX5 action is balanced through the activity of indole-3-acetic acid 17 (IAA17) auxin response repressor. Our combined genetic, cell biology, and computational modeling studies revealed a previously uncharacterized feedback loop linking WOX5-mediated auxin production to IAA17-dependent repression of auxin responses. This WOX5-IAA17 feedback circuit further assures the maintenance of auxin response maximum in the root tip and thereby contributes to the maintenance of distal stem cell (DSC) populations. Our experimental studies and in silico computer simulations both demonstrate that the WOX5-IAA17 feedback circuit is essential for the maintenance of auxin gradient in the root tip and the auxin-mediated root DSC differentiation."}],"title":"WOX5-IAA17 feedback circuit-mediated cellular auxin response is crucial for the patterning of root stem cell niches in arabidopsis"},{"date_updated":"2026-06-18T18:03:30Z","status":"public","doi":"10.1093/molbev/mst187","oa":1,"article_type":"original","publisher":"Oxford University Press","quality_controlled":"1","title":"Growth rates made easy","abstract":[{"text":"In the 1960s-1980s, determination of bacterial growth rates was an important tool in microbial genetics, biochemistry, molecular biology, and microbial physiology. The exciting technical developments of the 1990s and the 2000s eclipsed that tool; as a result, many investigators today lack experience with growth rate measurements. Recently, investigators in a number of areas have started to use measurements of bacterial growth rates for a variety of purposes. Those measurements have been greatly facilitated by the availability of microwell plate readers that permit the simultaneous measurements on up to 384 different cultures. Only the exponential (logarithmic) portions of the resulting growth curves are useful for determining growth rates, and manual determination of that portion and calculation of growth rates can be tedious for high-throughput purposes. Here, we introduce the program GrowthRates that uses plate reader output files to automatically determine the exponential portion of the curve and to automatically calculate the growth rate, the maximum culture density, and the duration of the growth lag phase. GrowthRates is freely available for Macintosh, Windows, and Linux.We discuss the effects of culture volume, the classical bacterial growth curve, and the differences between determinations in rich media and minimal (mineral salts) media. This protocol covers calibration of the plate reader, growth of culture inocula for both rich and minimal media, and experimental setup. As a guide to reliability, we report typical day-to-day variation in growth rates and variation within experiments with respect to position of wells within the plates.","lang":"eng"}],"main_file_link":[{"open_access":"1","url":"https://doi.org/10.1093/molbev/mst187"}],"publication_identifier":{"eissn":["1537-1719"],"issn":["0737-4038"]},"article_processing_charge":"No","day":"01","publication":"Molecular Biology and Evolution","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","type":"journal_article","date_published":"2014-01-01T00:00:00Z","_id":"1902","external_id":{"pmid":["24170494"],"isi":["000329253200022"]},"pmid":1,"date_created":"2018-12-11T11:54:37Z","year":"2014","publist_id":"5193","OA_place":"publisher","issue":"1","OA_type":"free access","citation":{"short":"B. Hall, H. Acar, A. Nandipati, M. Barlow, Molecular Biology and Evolution 31 (2014) 232–238.","apa":"Hall, B., Acar, H., Nandipati, A., &#38; Barlow, M. (2014). Growth rates made easy. <i>Molecular Biology and Evolution</i>. Oxford University Press. <a href=\"https://doi.org/10.1093/molbev/mst187\">https://doi.org/10.1093/molbev/mst187</a>","ama":"Hall B, Acar H, Nandipati A, Barlow M. Growth rates made easy. <i>Molecular Biology and Evolution</i>. 2014;31(1):232-238. doi:<a href=\"https://doi.org/10.1093/molbev/mst187\">10.1093/molbev/mst187</a>","ista":"Hall B, Acar H, Nandipati A, Barlow M. 2014. Growth rates made easy. Molecular Biology and Evolution. 31(1), 232–238.","mla":"Hall, Barry, et al. “Growth Rates Made Easy.” <i>Molecular Biology and Evolution</i>, vol. 31, no. 1, Oxford University Press, 2014, pp. 232–38, doi:<a href=\"https://doi.org/10.1093/molbev/mst187\">10.1093/molbev/mst187</a>.","chicago":"Hall, Barry, Hande Acar, Anna Nandipati, and Miriam Barlow. “Growth Rates Made Easy.” <i>Molecular Biology and Evolution</i>. Oxford University Press, 2014. <a href=\"https://doi.org/10.1093/molbev/mst187\">https://doi.org/10.1093/molbev/mst187</a>.","ieee":"B. Hall, H. Acar, A. Nandipati, and M. Barlow, “Growth rates made easy,” <i>Molecular Biology and Evolution</i>, vol. 31, no. 1. Oxford University Press, pp. 232–238, 2014."},"ddc":["570"],"intvolume":"        31","scopus_import":"1","month":"01","volume":31,"isi":1,"publication_status":"published","author":[{"first_name":"Barry","last_name":"Hall","full_name":"Hall, Barry"},{"first_name":"Hande","id":"2DDF136A-F248-11E8-B48F-1D18A9856A87","full_name":"Acar, Hande","last_name":"Acar","orcid":"0000-0003-1986-9753"},{"first_name":"Anna","last_name":"Nandipati","full_name":"Nandipati, Anna"},{"full_name":"Barlow, Miriam","last_name":"Barlow","first_name":"Miriam"}],"department":[{"_id":"JoBo"}],"page":"232 - 238","oa_version":"Published Version","language":[{"iso":"eng"}]},{"oa_version":"None","page":"960 - 974","language":[{"iso":"eng"}],"volume":27,"month":"04","author":[{"last_name":"Tobler","full_name":"Tobler, Michael","first_name":"Michael"},{"full_name":"Plath, Martin","last_name":"Plath","first_name":"Martin"},{"full_name":"Riesch, Rüdiger","last_name":"Riesch","first_name":"Rüdiger"},{"first_name":"Ingo","last_name":"Schlupp","full_name":"Schlupp, Ingo"},{"id":"406F989C-F248-11E8-B48F-1D18A9856A87","first_name":"Anna V","last_name":"Grasse","full_name":"Grasse, Anna V"},{"first_name":"Gopi","full_name":"Munimanda, Gopi","last_name":"Munimanda"},{"full_name":"Setzer, C","last_name":"Setzer","first_name":"C"},{"full_name":"Penn, Dustin","last_name":"Penn","first_name":"Dustin"},{"last_name":"Moodley","full_name":"Moodley, Yoshan","first_name":"Yoshan"}],"department":[{"_id":"SyCr"}],"publication_status":"published","isi":1,"acknowledgement":"This study was funded by grants from the National Science Foundation (NSF) to MT (IOS-1121832) and IS (DEB-0743406) and from the German Science Foundation (DFG; PL 470/1-2) and ‘LOEWE − Landesoffensive zur Entwicklung wissenschaftlich-ökonomischer Exzellenz’ of Hesse's Ministry of Higher Education, Research, and the Arts, to MP.","scopus_import":"1","intvolume":"        27","OA_type":"free access","issue":"5","citation":{"mla":"Tobler, Michael, et al. “Selection from Parasites Favours Immunogenetic Diversity but Not Divergence among Locally Adapted Host Populations.” <i>Journal of Evolutionary Biology</i>, vol. 27, no. 5, Wiley, 2014, pp. 960–74, doi:<a href=\"https://doi.org/10.1111/jeb.12370\">10.1111/jeb.12370</a>.","chicago":"Tobler, Michael, Martin Plath, Rüdiger Riesch, Ingo Schlupp, Anna V Grasse, Gopi Munimanda, C Setzer, Dustin Penn, and Yoshan Moodley. “Selection from Parasites Favours Immunogenetic Diversity but Not Divergence among Locally Adapted Host Populations.” <i>Journal of Evolutionary Biology</i>. Wiley, 2014. <a href=\"https://doi.org/10.1111/jeb.12370\">https://doi.org/10.1111/jeb.12370</a>.","ieee":"M. Tobler <i>et al.</i>, “Selection from parasites favours immunogenetic diversity but not divergence among locally adapted host populations,” <i>Journal of Evolutionary Biology</i>, vol. 27, no. 5. Wiley, pp. 960–974, 2014.","ista":"Tobler M, Plath M, Riesch R, Schlupp I, Grasse AV, Munimanda G, Setzer C, Penn D, Moodley Y. 2014. Selection from parasites favours immunogenetic diversity but not divergence among locally adapted host populations. Journal of Evolutionary Biology. 27(5), 960–974.","apa":"Tobler, M., Plath, M., Riesch, R., Schlupp, I., Grasse, A. V., Munimanda, G., … Moodley, Y. (2014). Selection from parasites favours immunogenetic diversity but not divergence among locally adapted host populations. <i>Journal of Evolutionary Biology</i>. Wiley. <a href=\"https://doi.org/10.1111/jeb.12370\">https://doi.org/10.1111/jeb.12370</a>","ama":"Tobler M, Plath M, Riesch R, et al. Selection from parasites favours immunogenetic diversity but not divergence among locally adapted host populations. <i>Journal of Evolutionary Biology</i>. 2014;27(5):960-974. doi:<a href=\"https://doi.org/10.1111/jeb.12370\">10.1111/jeb.12370</a>","short":"M. Tobler, M. Plath, R. Riesch, I. Schlupp, A.V. Grasse, G. Munimanda, C. Setzer, D. Penn, Y. Moodley, Journal of Evolutionary Biology 27 (2014) 960–974."},"publist_id":"5190","year":"2014","_id":"1905","external_id":{"pmid":["24725091"],"isi":["000334966800015"]},"date_published":"2014-04-12T00:00:00Z","date_created":"2018-12-11T11:54:38Z","pmid":1,"publication":"Journal of Evolutionary Biology","user_id":"317138e5-6ab7-11ef-aa6d-ffef3953e345","type":"journal_article","day":"12","article_processing_charge":"No","main_file_link":[{"url":"https://doi.org/10.1111/jeb.12370","open_access":"1"}],"publication_identifier":{"issn":["1010-061X"],"eissn":["1420-9101"]},"abstract":[{"lang":"eng","text":"The unprecedented polymorphism in the major histocompatibility complex (MHC) genes is thought to be maintained by balancing selection from parasites. However, do parasites also drive divergence at MHC loci between host populations, or do the effects of balancing selection maintain similarities among populations? We examined MHC variation in populations of the livebearing fish Poecilia mexicana and characterized their parasite communities. Poecilia mexicana populations in the Cueva del Azufre system are locally adapted to darkness and the presence of toxic hydrogen sulphide, representing highly divergent ecotypes or incipient species. Parasite communities differed significantly across populations, and populations with higher parasite loads had higher levels of diversity at class II MHC genes. However, despite different parasite communities, marked divergence in adaptive traits and in neutral genetic markers, we found MHC alleles to be remarkably similar among host populations. Our findings indicate that balancing selection from parasites maintains immunogenetic diversity of hosts, but this process does not promote MHC divergence in this system. On the contrary, we suggest that balancing selection on immunogenetic loci may outweigh divergent selection causing divergence, thereby hindering host divergence and speciation. Our findings support the hypothesis that balancing selection maintains MHC similarities among lineages during and after speciation (trans-species evolution)."}],"title":"Selection from parasites favours immunogenetic diversity but not divergence among locally adapted host populations","quality_controlled":"1","publisher":"Wiley","oa":1,"article_type":"original","status":"public","date_updated":"2025-09-29T12:28:21Z","doi":"10.1111/jeb.12370"},{"date_published":"2014-09-09T00:00:00Z","external_id":{"isi":["000341566500006"]},"_id":"1906","date_created":"2018-12-11T11:54:39Z","file_date_updated":"2020-07-14T12:45:20Z","year":"2014","publist_id":"5189","article_processing_charge":"No","day":"09","publication":"IEEE Transactions on Visualization and Computer Graphics","user_id":"317138e5-6ab7-11ef-aa6d-ffef3953e345","type":"journal_article","file":[{"content_type":"application/pdf","file_id":"5297","checksum":"5bf58942d2eb20adf03c7f9ea2e68124","date_updated":"2020-07-14T12:45:20Z","file_name":"IST-2016-573-v1+1_arikan-2014-pcvis-draft.pdf","creator":"system","access_level":"open_access","file_size":13594598,"relation":"main_file","date_created":"2018-12-12T10:17:41Z"}],"publisher":"IEEE","abstract":[{"lang":"eng","text":"In this paper, we introduce a novel scene representation for the visualization of large-scale point clouds accompanied by a set of high-resolution photographs. Many real-world applications deal with very densely sampled point-cloud data, which are augmented with photographs that often reveal lighting variations and inaccuracies in registration. Consequently, the high-quality representation of the captured data, i.e., both point clouds and photographs together, is a challenging and time-consuming task. We propose a two-phase approach, in which the first (preprocessing) phase generates multiple overlapping surface patches and handles the problem of seamless texture generation locally for each patch. The second phase stitches these patches at render-time to produce a high-quality visualization of the data. As a result of the proposed localization of the global texturing problem, our algorithm is more than an order of magnitude faster than equivalent mesh-based texturing techniques. Furthermore, since our preprocessing phase requires only a minor fraction of the whole data set at once, we provide maximum flexibility when dealing with growing data sets."}],"title":"Large-scale point-cloud visualization through localized textured surface reconstruction","project":[{"call_identifier":"FWF","grant_number":"P 24352-N23","name":"Deep Pictures: Creating Visual and Haptic Vector Images","_id":"25357BD2-B435-11E9-9278-68D0E5697425"}],"date_updated":"2025-09-29T12:27:48Z","status":"public","doi":"10.1109/TVCG.2014.2312011","oa":1,"pubrep_id":"573","page":"1280 - 1292","oa_version":"Submitted Version","language":[{"iso":"eng"}],"acknowledgement":"This research was supported by the Austrian Research Promotion Agency (FFG) project REPLICATE (no. 835948), the EU FP7 project HARVEST4D (no. 323567).","ddc":["000"],"intvolume":"        20","scopus_import":"1","volume":20,"month":"09","publication_status":"published","isi":1,"department":[{"_id":"ChWo"}],"author":[{"first_name":"Murat","last_name":"Arikan","full_name":"Arikan, Murat"},{"first_name":"Reinhold","full_name":"Preiner, Reinhold","last_name":"Preiner"},{"first_name":"Claus","last_name":"Scheiblauer","full_name":"Scheiblauer, Claus"},{"first_name":"Stefan","id":"44D6411A-F248-11E8-B48F-1D18A9856A87","last_name":"Jeschke","full_name":"Jeschke, Stefan"},{"last_name":"Wimmer","full_name":"Wimmer, Michael","first_name":"Michael"}],"has_accepted_license":"1","issue":"9","citation":{"ista":"Arikan M, Preiner R, Scheiblauer C, Jeschke S, Wimmer M. 2014. Large-scale point-cloud visualization through localized textured surface reconstruction. IEEE Transactions on Visualization and Computer Graphics. 20(9), 1280–1292.","mla":"Arikan, Murat, et al. “Large-Scale Point-Cloud Visualization through Localized Textured Surface Reconstruction.” <i>IEEE Transactions on Visualization and Computer Graphics</i>, vol. 20, no. 9, IEEE, 2014, pp. 1280–92, doi:<a href=\"https://doi.org/10.1109/TVCG.2014.2312011\">10.1109/TVCG.2014.2312011</a>.","ieee":"M. Arikan, R. Preiner, C. Scheiblauer, S. Jeschke, and M. Wimmer, “Large-scale point-cloud visualization through localized textured surface reconstruction,” <i>IEEE Transactions on Visualization and Computer Graphics</i>, vol. 20, no. 9. IEEE, pp. 1280–1292, 2014.","chicago":"Arikan, Murat, Reinhold Preiner, Claus Scheiblauer, Stefan Jeschke, and Michael Wimmer. “Large-Scale Point-Cloud Visualization through Localized Textured Surface Reconstruction.” <i>IEEE Transactions on Visualization and Computer Graphics</i>. IEEE, 2014. <a href=\"https://doi.org/10.1109/TVCG.2014.2312011\">https://doi.org/10.1109/TVCG.2014.2312011</a>.","short":"M. Arikan, R. Preiner, C. Scheiblauer, S. Jeschke, M. Wimmer, IEEE Transactions on Visualization and Computer Graphics 20 (2014) 1280–1292.","apa":"Arikan, M., Preiner, R., Scheiblauer, C., Jeschke, S., &#38; Wimmer, M. (2014). Large-scale point-cloud visualization through localized textured surface reconstruction. <i>IEEE Transactions on Visualization and Computer Graphics</i>. IEEE. <a href=\"https://doi.org/10.1109/TVCG.2014.2312011\">https://doi.org/10.1109/TVCG.2014.2312011</a>","ama":"Arikan M, Preiner R, Scheiblauer C, Jeschke S, Wimmer M. Large-scale point-cloud visualization through localized textured surface reconstruction. <i>IEEE Transactions on Visualization and Computer Graphics</i>. 2014;20(9):1280-1292. doi:<a href=\"https://doi.org/10.1109/TVCG.2014.2312011\">10.1109/TVCG.2014.2312011</a>"}},{"main_file_link":[{"url":"https://eprint.iacr.org/2014/299","open_access":"1"}],"article_number":"6875125","citation":{"mla":"Demay, Grégory, et al. “Optimality of Non-Adaptive Strategies: The Case of Parallel Games.” <i>IEEE International Symposium on Information Theory</i>, 6875125, IEEE, 2014, doi:<a href=\"https://doi.org/10.1109/ISIT.2014.6875125\">10.1109/ISIT.2014.6875125</a>.","chicago":"Demay, Grégory, Peter Gazi, Ueli Maurer, and Björn Tackmann. “Optimality of Non-Adaptive Strategies: The Case of Parallel Games.” In <i>IEEE International Symposium on Information Theory</i>. IEEE, 2014. <a href=\"https://doi.org/10.1109/ISIT.2014.6875125\">https://doi.org/10.1109/ISIT.2014.6875125</a>.","ieee":"G. Demay, P. Gazi, U. Maurer, and B. Tackmann, “Optimality of non-adaptive strategies: The case of parallel games,” in <i>IEEE International Symposium on Information Theory</i>, Honolulu, USA, 2014.","ista":"Demay G, Gazi P, Maurer U, Tackmann B. 2014. Optimality of non-adaptive strategies: The case of parallel games. IEEE International Symposium on Information Theory. IEEE International Symposium on Information Theory Proceedings, 6875125.","apa":"Demay, G., Gazi, P., Maurer, U., &#38; Tackmann, B. (2014). Optimality of non-adaptive strategies: The case of parallel games. In <i>IEEE International Symposium on Information Theory</i>. Honolulu, USA: IEEE. <a href=\"https://doi.org/10.1109/ISIT.2014.6875125\">https://doi.org/10.1109/ISIT.2014.6875125</a>","ama":"Demay G, Gazi P, Maurer U, Tackmann B. Optimality of non-adaptive strategies: The case of parallel games. In: <i>IEEE International Symposium on Information Theory</i>. IEEE; 2014. doi:<a href=\"https://doi.org/10.1109/ISIT.2014.6875125\">10.1109/ISIT.2014.6875125</a>","short":"G. Demay, P. Gazi, U. Maurer, B. Tackmann, in:, IEEE International Symposium on Information Theory, IEEE, 2014."},"publisher":"IEEE","abstract":[{"lang":"eng","text":"Most cryptographic security proofs require showing that two systems are indistinguishable. A central tool in such proofs is that of a game, where winning the game means provoking a certain condition, and it is shown that the two systems considered cannot be distinguished unless this condition is provoked. Upper bounding the probability of winning such a game, i.e., provoking this condition, for an arbitrary strategy is usually hard, except in the special case where the best strategy for winning such a game is known to be non-adaptive. A sufficient criterion for ensuring the optimality of non-adaptive strategies is that of conditional equivalence to a system, a notion introduced in [1]. In this paper, we show that this criterion is not necessary to ensure the optimality of non-adaptive strategies by giving two results of independent interest: 1) the optimality of non-adaptive strategies is not preserved under parallel composition; 2) in contrast, conditional equivalence is preserved under parallel composition."}],"quality_controlled":"1","title":"Optimality of non-adaptive strategies: The case of parallel games","oa":1,"date_updated":"2021-01-12T06:53:59Z","doi":"10.1109/ISIT.2014.6875125","status":"public","oa_version":"Submitted Version","year":"2014","language":[{"iso":"eng"}],"publist_id":"5188","date_published":"2014-01-01T00:00:00Z","_id":"1907","date_created":"2018-12-11T11:54:39Z","month":"01","publication":"IEEE International Symposium on Information Theory","user_id":"4435EBFC-F248-11E8-B48F-1D18A9856A87","type":"conference","publication_status":"published","author":[{"first_name":"Grégory","last_name":"Demay","full_name":"Demay, Grégory"},{"full_name":"Gazi, Peter","last_name":"Gazi","id":"3E0BFE38-F248-11E8-B48F-1D18A9856A87","first_name":"Peter"},{"first_name":"Ueli","full_name":"Maurer, Ueli","last_name":"Maurer"},{"first_name":"Björn","full_name":"Tackmann, Björn","last_name":"Tackmann"}],"department":[{"_id":"KrPi"}],"conference":{"start_date":"2014-06-29","location":"Honolulu, USA","end_date":"2014-07-04","name":"IEEE International Symposium on Information Theory Proceedings"},"day":"01","scopus_import":1},{"month":"04","volume":196,"author":[{"id":"2D0CE020-F248-11E8-B48F-1D18A9856A87","first_name":"Daniel","last_name":"Weissman","full_name":"Weissman, Daniel"},{"last_name":"Hallatschek","full_name":"Hallatschek, Oskar","first_name":"Oskar"}],"department":[{"_id":"NiBa"}],"isi":1,"publication_status":"published","scopus_import":"1","intvolume":"       196","oa_version":"Submitted Version","page":"1167 - 1183","language":[{"iso":"eng"}],"issue":"4","citation":{"ista":"Weissman D, Hallatschek O. 2014. The rate of adaptation in large sexual populations with linear chromosomes. Genetics. 196(4), 1167–1183.","ieee":"D. Weissman and O. Hallatschek, “The rate of adaptation in large sexual populations with linear chromosomes,” <i>Genetics</i>, vol. 196, no. 4. Genetics Society of America, pp. 1167–1183, 2014.","chicago":"Weissman, Daniel, and Oskar Hallatschek. “The Rate of Adaptation in Large Sexual Populations with Linear Chromosomes.” <i>Genetics</i>. Genetics Society of America, 2014. <a href=\"https://doi.org/10.1534/genetics.113.160705\">https://doi.org/10.1534/genetics.113.160705</a>.","mla":"Weissman, Daniel, and Oskar Hallatschek. “The Rate of Adaptation in Large Sexual Populations with Linear Chromosomes.” <i>Genetics</i>, vol. 196, no. 4, Genetics Society of America, 2014, pp. 1167–83, doi:<a href=\"https://doi.org/10.1534/genetics.113.160705\">10.1534/genetics.113.160705</a>.","short":"D. Weissman, O. Hallatschek, Genetics 196 (2014) 1167–1183.","ama":"Weissman D, Hallatschek O. The rate of adaptation in large sexual populations with linear chromosomes. <i>Genetics</i>. 2014;196(4):1167-1183. doi:<a href=\"https://doi.org/10.1534/genetics.113.160705\">10.1534/genetics.113.160705</a>","apa":"Weissman, D., &#38; Hallatschek, O. (2014). The rate of adaptation in large sexual populations with linear chromosomes. <i>Genetics</i>. Genetics Society of America. <a href=\"https://doi.org/10.1534/genetics.113.160705\">https://doi.org/10.1534/genetics.113.160705</a>"},"corr_author":"1","ec_funded":1,"publication":"Genetics","user_id":"317138e5-6ab7-11ef-aa6d-ffef3953e345","type":"journal_article","day":"01","article_processing_charge":"No","publist_id":"5187","year":"2014","_id":"1908","external_id":{"arxiv":["1307.0737"],"isi":["000334179300022"]},"date_published":"2014-04-01T00:00:00Z","date_created":"2018-12-11T11:54:39Z","oa":1,"status":"public","doi":"10.1534/genetics.113.160705","date_updated":"2025-09-29T12:27:03Z","project":[{"name":"Limits to selection in biology and in evolutionary computation","grant_number":"250152","_id":"25B07788-B435-11E9-9278-68D0E5697425","call_identifier":"FP7"}],"arxiv":1,"main_file_link":[{"url":"http://arxiv.org/abs/1307.0737","open_access":"1"}],"abstract":[{"lang":"eng","text":"In large populations, multiple beneficial mutations may be simultaneously spreading. In asexual populations, these mutations must either arise on the same background or compete against each other. In sexual populations, recombination can bring together beneficial alleles from different backgrounds, but tightly linked alleles may still greatly interfere with each other. We show for well-mixed populations that when this interference is strong, the genome can be seen as consisting of many effectively asexual stretches linked together. The rate at which beneficial alleles fix is thus roughly proportional to the rate of recombination and depends only logarithmically on the mutation supply and the strength of selection. Our scaling arguments also allow us to predict, with reasonable accuracy, the fitness distribution of fixed mutations when the mutational effect sizes are broad. We focus on the regime in which crossovers occur more frequently than beneficial mutations, as is likely to be the case for many natural populations."}],"title":"The rate of adaptation in large sexual populations with linear chromosomes","quality_controlled":"1","publisher":"Genetics Society of America"},{"has_accepted_license":"1","citation":{"apa":"Ezard, T., Prizak, R., &#38; Hoyle, R. (2014). The fitness costs of adaptation via phenotypic plasticity and maternal effects. <i>Functional Ecology</i>. Wiley-Blackwell. <a href=\"https://doi.org/10.1111/1365-2435.12207\">https://doi.org/10.1111/1365-2435.12207</a>","ama":"Ezard T, Prizak R, Hoyle R. The fitness costs of adaptation via phenotypic plasticity and maternal effects. <i>Functional Ecology</i>. 2014;28(3):693-701. doi:<a href=\"https://doi.org/10.1111/1365-2435.12207\">10.1111/1365-2435.12207</a>","short":"T. Ezard, R. Prizak, R. Hoyle, Functional Ecology 28 (2014) 693–701.","mla":"Ezard, Thomas, et al. “The Fitness Costs of Adaptation via Phenotypic Plasticity and Maternal Effects.” <i>Functional Ecology</i>, vol. 28, no. 3, Wiley-Blackwell, 2014, pp. 693–701, doi:<a href=\"https://doi.org/10.1111/1365-2435.12207\">10.1111/1365-2435.12207</a>.","chicago":"Ezard, Thomas, Roshan Prizak, and Rebecca Hoyle. “The Fitness Costs of Adaptation via Phenotypic Plasticity and Maternal Effects.” <i>Functional Ecology</i>. Wiley-Blackwell, 2014. <a href=\"https://doi.org/10.1111/1365-2435.12207\">https://doi.org/10.1111/1365-2435.12207</a>.","ieee":"T. Ezard, R. Prizak, and R. Hoyle, “The fitness costs of adaptation via phenotypic plasticity and maternal effects,” <i>Functional Ecology</i>, vol. 28, no. 3. Wiley-Blackwell, pp. 693–701, 2014.","ista":"Ezard T, Prizak R, Hoyle R. 2014. The fitness costs of adaptation via phenotypic plasticity and maternal effects. Functional Ecology. 28(3), 693–701."},"issue":"3","pubrep_id":"419","language":[{"iso":"eng"}],"oa_version":"Published Version","page":"693 - 701","scopus_import":"1","intvolume":"        28","ddc":["570"],"acknowledgement":"Engineering and Physical Sciences Research Council. Grant Number: EP/H031928/1","department":[{"_id":"NiBa"},{"_id":"GaTk"}],"author":[{"last_name":"Ezard","full_name":"Ezard, Thomas","first_name":"Thomas"},{"id":"4456104E-F248-11E8-B48F-1D18A9856A87","first_name":"Roshan","last_name":"Prizak","full_name":"Prizak, Roshan"},{"full_name":"Hoyle, Rebecca","last_name":"Hoyle","first_name":"Rebecca"}],"publication_status":"published","isi":1,"volume":28,"month":"06","abstract":[{"text":"Summary: Phenotypes are often environmentally dependent, which requires organisms to track environmental change. The challenge for organisms is to construct phenotypes using the most accurate environmental cue. Here, we use a quantitative genetic model of adaptation by additive genetic variance, within- and transgenerational plasticity via linear reaction norms and indirect genetic effects respectively. We show how the relative influence on the eventual phenotype of these components depends on the predictability of environmental change (fast or slow, sinusoidal or stochastic) and the developmental lag τ between when the environment is perceived and when selection acts. We then decompose expected mean fitness into three components (variance load, adaptation and fluctuation load) to study the fitness costs of within- and transgenerational plasticity. A strongly negative maternal effect coefficient m minimizes the variance load, but a strongly positive m minimises the fluctuation load. The adaptation term is maximized closer to zero, with positive or negative m preferred under different environmental scenarios. Phenotypic plasticity is higher when τ is shorter and when the environment changes frequently between seasonal extremes. Expected mean population fitness is highest away from highest observed levels of phenotypic plasticity. Within- and transgenerational plasticity act in concert to deliver well-adapted phenotypes, which emphasizes the need to study both simultaneously when investigating phenotypic evolution.","lang":"eng"}],"title":"The fitness costs of adaptation via phenotypic plasticity and maternal effects","publisher":"Wiley-Blackwell","file":[{"date_updated":"2020-07-14T12:45:20Z","checksum":"3cbe8623174709a8ceec2103246f8fe0","file_id":"5167","content_type":"application/pdf","file_size":536154,"access_level":"open_access","creator":"system","relation":"main_file","date_created":"2018-12-12T10:15:45Z","file_name":"IST-2016-419-v1+1_Ezard_et_al-2014-Functional_Ecology.pdf"}],"status":"public","doi":"10.1111/1365-2435.12207","date_updated":"2025-09-29T12:26:34Z","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)"},"oa":1,"date_created":"2018-12-11T11:54:40Z","external_id":{"isi":["000335954900016"]},"_id":"1909","date_published":"2014-06-01T00:00:00Z","publist_id":"5186","year":"2014","file_date_updated":"2020-07-14T12:45:20Z","day":"01","article_processing_charge":"No","user_id":"317138e5-6ab7-11ef-aa6d-ffef3953e345","type":"journal_article","publication":"Functional Ecology"},{"author":[{"full_name":"Konradi, Sabine","last_name":"Konradi","first_name":"Sabine"},{"last_name":"Yasmin","full_name":"Yasmin, Nighat","first_name":"Nighat"},{"full_name":"Haslwanter, Denise","last_name":"Haslwanter","first_name":"Denise"},{"first_name":"Michele","id":"3A3FC708-F248-11E8-B48F-1D18A9856A87","last_name":"Weber","full_name":"Weber, Michele"},{"last_name":"Gesslbauer","full_name":"Gesslbauer, Bernd","first_name":"Bernd"},{"first_name":"Michael K","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-6620-9179","last_name":"Sixt","full_name":"Sixt, Michael K"},{"first_name":"Herbert","full_name":"Strobl, Herbert","last_name":"Strobl"}],"department":[{"_id":"MiSi"}],"publication_status":"published","isi":1,"month":"02","volume":44,"scopus_import":"1","intvolume":"        44","acknowledgement":"FWF. Grant Number: P22058-B20","language":[{"iso":"eng"}],"oa_version":"None","page":"553 - 560","citation":{"ista":"Konradi S, Yasmin N, Haslwanter D, Weber M, Gesslbauer B, Sixt MK, Strobl H. 2014. Langerhans cell maturation is accompanied by induction of N-cadherin and the transcriptional regulators of epithelial-mesenchymal transition ZEB1/2. European Journal of Immunology. 44(2), 553–560.","chicago":"Konradi, Sabine, Nighat Yasmin, Denise Haslwanter, Michele Weber, Bernd Gesslbauer, Michael K Sixt, and Herbert Strobl. “Langerhans Cell Maturation Is Accompanied by Induction of N-Cadherin and the Transcriptional Regulators of Epithelial-Mesenchymal Transition ZEB1/2.” <i>European Journal of Immunology</i>. Wiley-Blackwell, 2014. <a href=\"https://doi.org/10.1002/eji.201343681\">https://doi.org/10.1002/eji.201343681</a>.","ieee":"S. Konradi <i>et al.</i>, “Langerhans cell maturation is accompanied by induction of N-cadherin and the transcriptional regulators of epithelial-mesenchymal transition ZEB1/2,” <i>European Journal of Immunology</i>, vol. 44, no. 2. Wiley-Blackwell, pp. 553–560, 2014.","mla":"Konradi, Sabine, et al. “Langerhans Cell Maturation Is Accompanied by Induction of N-Cadherin and the Transcriptional Regulators of Epithelial-Mesenchymal Transition ZEB1/2.” <i>European Journal of Immunology</i>, vol. 44, no. 2, Wiley-Blackwell, 2014, pp. 553–60, doi:<a href=\"https://doi.org/10.1002/eji.201343681\">10.1002/eji.201343681</a>.","short":"S. Konradi, N. Yasmin, D. Haslwanter, M. Weber, B. Gesslbauer, M.K. Sixt, H. Strobl, European Journal of Immunology 44 (2014) 553–560.","ama":"Konradi S, Yasmin N, Haslwanter D, et al. Langerhans cell maturation is accompanied by induction of N-cadherin and the transcriptional regulators of epithelial-mesenchymal transition ZEB1/2. <i>European Journal of Immunology</i>. 2014;44(2):553-560. doi:<a href=\"https://doi.org/10.1002/eji.201343681\">10.1002/eji.201343681</a>","apa":"Konradi, S., Yasmin, N., Haslwanter, D., Weber, M., Gesslbauer, B., Sixt, M. K., &#38; Strobl, H. (2014). Langerhans cell maturation is accompanied by induction of N-cadherin and the transcriptional regulators of epithelial-mesenchymal transition ZEB1/2. <i>European Journal of Immunology</i>. Wiley-Blackwell. <a href=\"https://doi.org/10.1002/eji.201343681\">https://doi.org/10.1002/eji.201343681</a>"},"issue":"2","user_id":"317138e5-6ab7-11ef-aa6d-ffef3953e345","type":"journal_article","publication":"European Journal of Immunology","day":"01","article_processing_charge":"No","publist_id":"5185","year":"2014","date_created":"2018-12-11T11:54:40Z","_id":"1910","external_id":{"isi":["000331901200025"]},"date_published":"2014-02-01T00:00:00Z","date_updated":"2025-09-29T12:26:01Z","status":"public","doi":"10.1002/eji.201343681","title":"Langerhans cell maturation is accompanied by induction of N-cadherin and the transcriptional regulators of epithelial-mesenchymal transition ZEB1/2","abstract":[{"lang":"eng","text":"angerhans cells (LCs) are a unique subset of dendritic cells (DCs) that express epithelial adhesion molecules, allowing them to form contacts with epithelial cells and reside in epidermal/epithelial tissues. The dynamic regulation of epithelial adhesion plays a decisive role in the life cycle of LCs. It controls whether LCs remain immature and sessile within the epidermis or mature and egress to initiate immune responses. So far, the molecular machinery regulating epithelial adhesion molecules during LC maturation remains elusive. Here, we generated pure populations of immature human LCs in vitro to systematically probe for gene-expression changes during LC maturation. LCs down-regulate a set of epithelial genes including E-cadherin, while they upregulate the mesenchymal marker N-cadherin known to facilitate cell migration. In addition, N-cadherin is constitutively expressed by monocyte-derived DCs known to exhibit characteristics of both inflammatory-type and interstitial/dermal DCs. Moreover, the transcription factors ZEB1 and ZEB2 (ZEB is zinc-finger E-box-binding homeobox) are upregulated in migratory LCs. ZEB1 and ZEB2 have been shown to induce epithelial-to-mesenchymal transition (EMT) and invasive behavior in cancer cells undergoing metastasis. Our results provide the first hint that the molecular EMT machinery might facilitate LC mobilization. Moreover, our study suggests that N-cadherin plays a role during DC migration."}],"publisher":"Wiley-Blackwell"},{"issue":"1","citation":{"apa":"Engström, A., &#38; Noren, P. (2014). Tverberg’s Theorem and Graph Coloring. <i>Discrete &#38; Computational Geometry</i>. Springer. <a href=\"https://doi.org/10.1007/s00454-013-9556-3\">https://doi.org/10.1007/s00454-013-9556-3</a>","ama":"Engström A, Noren P. Tverberg’s Theorem and Graph Coloring. <i>Discrete &#38; Computational Geometry</i>. 2014;51(1):207-220. doi:<a href=\"https://doi.org/10.1007/s00454-013-9556-3\">10.1007/s00454-013-9556-3</a>","short":"A. Engström, P. Noren, Discrete &#38; Computational Geometry 51 (2014) 207–220.","mla":"Engström, Alexander, and Patrik Noren. “Tverberg’s Theorem and Graph Coloring.” <i>Discrete &#38; Computational Geometry</i>, vol. 51, no. 1, Springer, 2014, pp. 207–20, doi:<a href=\"https://doi.org/10.1007/s00454-013-9556-3\">10.1007/s00454-013-9556-3</a>.","ieee":"A. Engström and P. Noren, “Tverberg’s Theorem and Graph Coloring,” <i>Discrete &#38; Computational Geometry</i>, vol. 51, no. 1. Springer, pp. 207–220, 2014.","chicago":"Engström, Alexander, and Patrik Noren. “Tverberg’s Theorem and Graph Coloring.” <i>Discrete &#38; Computational Geometry</i>. Springer, 2014. <a href=\"https://doi.org/10.1007/s00454-013-9556-3\">https://doi.org/10.1007/s00454-013-9556-3</a>.","ista":"Engström A, Noren P. 2014. Tverberg’s Theorem and Graph Coloring. Discrete &#38; Computational Geometry. 51(1), 207–220."},"oa_version":"None","page":"207 - 220","language":[{"iso":"eng"}],"volume":51,"month":"01","author":[{"full_name":"Engström, Alexander","last_name":"Engström","first_name":"Alexander"},{"id":"46870C74-F248-11E8-B48F-1D18A9856A87","first_name":"Patrik","last_name":"Noren","full_name":"Noren, Patrik"}],"department":[{"_id":"CaUh"}],"isi":1,"publication_status":"published","acknowledgement":"Patrik Norén gratefully acknowledges support from the Wallenberg foundation","scopus_import":"1","intvolume":"        51","abstract":[{"text":"The topological Tverberg theorem has been generalized in several directions by setting extra restrictions on the Tverberg partitions. Restricted Tverberg partitions, defined by the idea that certain points cannot be in the same part, are encoded with graphs. When two points are adjacent in the graph, they are not in the same part. If the restrictions are too harsh, then the topological Tverberg theorem fails. The colored Tverberg theorem corresponds to graphs constructed as disjoint unions of small complete graphs. Hell studied the case of paths and cycles. In graph theory these partitions are usually viewed as graph colorings. As explored by Aharoni, Haxell, Meshulam and others there are fundamental connections between several notions of graph colorings and topological combinatorics. For ordinary graph colorings it is enough to require that the number of colors q satisfy q&gt;Δ, where Δ is the maximal degree of the graph. It was proven by the first author using equivariant topology that if q&gt;Δ 2 then the topological Tverberg theorem still works. It is conjectured that q&gt;KΔ is also enough for some constant K, and in this paper we prove a fixed-parameter version of that conjecture. The required topological connectivity results are proven with shellability, which also strengthens some previous partial results where the topological connectivity was proven with the nerve lemma.","lang":"eng"}],"title":"Tverberg's Theorem and Graph Coloring","publisher":"Springer","date_updated":"2025-09-29T12:25:31Z","doi":"10.1007/s00454-013-9556-3","status":"public","publist_id":"5183","year":"2014","_id":"1911","external_id":{"isi":["000329619100007"]},"date_published":"2014-01-01T00:00:00Z","date_created":"2018-12-11T11:54:40Z","publication":"Discrete & Computational Geometry","type":"journal_article","user_id":"317138e5-6ab7-11ef-aa6d-ffef3953e345","day":"01","article_processing_charge":"No"},{"oa_version":"Published Version","page":"774 - 783","language":[{"iso":"eng"}],"acknowledgement":"We are grateful to members of the C.-P.H. lab, M. Concha, D. Siekhaus, and J. Vermot for comments on the manuscript and to M. Furutani-Seiki for sharing reagents. This work was supported by the Institute of Science and Technology Austria and an Alexander von Humboldt Foundation fellowship to J.C.","scopus_import":"1","intvolume":"        31","ddc":["570"],"volume":31,"month":"12","author":[{"first_name":"Julien","id":"2E3E0988-F248-11E8-B48F-1D18A9856A87","last_name":"Compagnon","full_name":"Compagnon, Julien"},{"id":"419EECCC-F248-11E8-B48F-1D18A9856A87","first_name":"Vanessa","last_name":"Barone","full_name":"Barone, Vanessa","orcid":"0000-0003-2676-3367"},{"full_name":"Rajshekar, Srivarsha","last_name":"Rajshekar","first_name":"Srivarsha"},{"last_name":"Kottmeier","full_name":"Kottmeier, Rita","first_name":"Rita"},{"full_name":"Pranjic-Ferscha, Kornelija","last_name":"Pranjic-Ferscha","id":"4362B3C2-F248-11E8-B48F-1D18A9856A87","first_name":"Kornelija"},{"last_name":"Behrndt","full_name":"Behrndt, Martin","first_name":"Martin","id":"3ECECA3A-F248-11E8-B48F-1D18A9856A87"},{"last_name":"Heisenberg","full_name":"Heisenberg, Carl-Philipp J","orcid":"0000-0002-0912-4566","id":"39427864-F248-11E8-B48F-1D18A9856A87","first_name":"Carl-Philipp J"}],"department":[{"_id":"CaHe"}],"isi":1,"publication_status":"published","related_material":{"record":[{"relation":"dissertation_contains","status":"public","id":"961"}]},"issue":"6","citation":{"chicago":"Compagnon, Julien, Vanessa Barone, Srivarsha Rajshekar, Rita Kottmeier, Kornelija Pranjic-Ferscha, Martin Behrndt, and Carl-Philipp J Heisenberg. “The Notochord Breaks Bilateral Symmetry by Controlling Cell Shapes in the Zebrafish Laterality Organ.” <i>Developmental Cell</i>. Cell Press, 2014. <a href=\"https://doi.org/10.1016/j.devcel.2014.11.003\">https://doi.org/10.1016/j.devcel.2014.11.003</a>.","ieee":"J. Compagnon <i>et al.</i>, “The notochord breaks bilateral symmetry by controlling cell shapes in the Zebrafish laterality organ,” <i>Developmental Cell</i>, vol. 31, no. 6. Cell Press, pp. 774–783, 2014.","mla":"Compagnon, Julien, et al. “The Notochord Breaks Bilateral Symmetry by Controlling Cell Shapes in the Zebrafish Laterality Organ.” <i>Developmental Cell</i>, vol. 31, no. 6, Cell Press, 2014, pp. 774–83, doi:<a href=\"https://doi.org/10.1016/j.devcel.2014.11.003\">10.1016/j.devcel.2014.11.003</a>.","ista":"Compagnon J, Barone V, Rajshekar S, Kottmeier R, Pranjic-Ferscha K, Behrndt M, Heisenberg C-PJ. 2014. The notochord breaks bilateral symmetry by controlling cell shapes in the Zebrafish laterality organ. Developmental Cell. 31(6), 774–783.","ama":"Compagnon J, Barone V, Rajshekar S, et al. The notochord breaks bilateral symmetry by controlling cell shapes in the Zebrafish laterality organ. <i>Developmental Cell</i>. 2014;31(6):774-783. doi:<a href=\"https://doi.org/10.1016/j.devcel.2014.11.003\">10.1016/j.devcel.2014.11.003</a>","apa":"Compagnon, J., Barone, V., Rajshekar, S., Kottmeier, R., Pranjic-Ferscha, K., Behrndt, M., &#38; Heisenberg, C.-P. J. (2014). The notochord breaks bilateral symmetry by controlling cell shapes in the Zebrafish laterality organ. <i>Developmental Cell</i>. Cell Press. <a href=\"https://doi.org/10.1016/j.devcel.2014.11.003\">https://doi.org/10.1016/j.devcel.2014.11.003</a>","short":"J. Compagnon, V. Barone, S. Rajshekar, R. Kottmeier, K. Pranjic-Ferscha, M. Behrndt, C.-P.J. Heisenberg, Developmental Cell 31 (2014) 774–783."},"corr_author":"1","_id":"1912","external_id":{"isi":["000346742900012"],"pmid":["25535919"]},"date_published":"2014-12-22T00:00:00Z","pmid":1,"date_created":"2018-12-11T11:54:41Z","publist_id":"5182","year":"2014","day":"22","article_processing_charge":"No","publication":"Developmental Cell","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","type":"journal_article","title":"The notochord breaks bilateral symmetry by controlling cell shapes in the Zebrafish laterality organ","quality_controlled":"1","abstract":[{"text":"Kupffer's vesicle (KV) is the zebrafish organ of laterality, patterning the embryo along its left-right (LR) axis. Regional differences in cell shape within the lumen-lining KV epithelium are essential for its LR patterning function. However, the processes by which KV cells acquire their characteristic shapes are largely unknown. Here, we show that the notochord induces regional differences in cell shape within KV by triggering extracellular matrix (ECM) accumulation adjacent to anterior-dorsal (AD) regions of KV. This localized ECM deposition restricts apical expansion of lumen-lining epithelial cells in AD regions of KV during lumen growth. Our study provides mechanistic insight into the processes by which KV translates global embryonic patterning into regional cell shape differences required for its LR symmetry-breaking function.","lang":"eng"}],"publisher":"Cell Press","main_file_link":[{"open_access":"1","url":"https://www.ncbi.nlm.nih.gov/pubmed/25535919"}],"doi":"10.1016/j.devcel.2014.11.003","status":"public","date_updated":"2026-06-18T18:12:41Z","oa":1},{"issue":"5-6","citation":{"chicago":"Milenković, Ivan, Tatjana Petrov, and Gábor Kovács. “Patterns of Hippocampal Tau Pathology Differentiate Neurodegenerative Dementias.” <i>Dementia and Geriatric Cognitive Disorders</i>. Karger Publishers, 2014. <a href=\"https://doi.org/10.1159/000365548\">https://doi.org/10.1159/000365548</a>.","ieee":"I. Milenković, T. Petrov, and G. Kovács, “Patterns of hippocampal tau pathology differentiate neurodegenerative dementias,” <i>Dementia and Geriatric Cognitive Disorders</i>, vol. 38, no. 5–6. Karger Publishers, pp. 375–388, 2014.","mla":"Milenković, Ivan, et al. “Patterns of Hippocampal Tau Pathology Differentiate Neurodegenerative Dementias.” <i>Dementia and Geriatric Cognitive Disorders</i>, vol. 38, no. 5–6, Karger Publishers, 2014, pp. 375–88, doi:<a href=\"https://doi.org/10.1159/000365548\">10.1159/000365548</a>.","ista":"Milenković I, Petrov T, Kovács G. 2014. Patterns of hippocampal tau pathology differentiate neurodegenerative dementias. Dementia and Geriatric Cognitive Disorders. 38(5–6), 375–388.","ama":"Milenković I, Petrov T, Kovács G. Patterns of hippocampal tau pathology differentiate neurodegenerative dementias. <i>Dementia and Geriatric Cognitive Disorders</i>. 2014;38(5-6):375-388. doi:<a href=\"https://doi.org/10.1159/000365548\">10.1159/000365548</a>","apa":"Milenković, I., Petrov, T., &#38; Kovács, G. (2014). Patterns of hippocampal tau pathology differentiate neurodegenerative dementias. <i>Dementia and Geriatric Cognitive Disorders</i>. Karger Publishers. <a href=\"https://doi.org/10.1159/000365548\">https://doi.org/10.1159/000365548</a>","short":"I. Milenković, T. Petrov, G. Kovács, Dementia and Geriatric Cognitive Disorders 38 (2014) 375–388."},"oa_version":"Published Version","page":"375 - 388","language":[{"iso":"eng"}],"acknowledgement":"This study was supported by the European Commission’s 7th Framework Programme under GA No. 278486, ‘DEVELAGE’.","scopus_import":"1","intvolume":"        38","ddc":["570"],"volume":38,"month":"11","department":[{"_id":"CaGu"}],"author":[{"full_name":"Milenković, Ivan","last_name":"Milenković","first_name":"Ivan"},{"id":"3D5811FC-F248-11E8-B48F-1D18A9856A87","first_name":"Tatjana","orcid":"0000-0002-9041-0905","last_name":"Petrov","full_name":"Petrov, Tatjana"},{"first_name":"Gábor","last_name":"Kovács","full_name":"Kovács, Gábor"}],"publication_status":"published","isi":1,"quality_controlled":"1","title":"Patterns of hippocampal tau pathology differentiate neurodegenerative dementias","abstract":[{"lang":"eng","text":"Deposits of phosphorylated tau protein and convergence of pathology in the hippocampus are the hallmarks of neurodegenerative tauopathies. Thus we aimed to evaluate whether regional and cellular vulnerability patterns in the hippocampus distinguish tauopathies or are influenced by their concomitant presence. Methods: We created a heat map of phospho-tau (AT8) immunoreactivity patterns in 24 hippocampal subregions/layers in individuals with Alzheimer's disease (AD)-related neurofibrillary degeneration (n = 40), Pick's disease (n = 8), progressive supranuclear palsy (n = 7), corticobasal degeneration (n = 6), argyrophilic grain disease (AGD, n = 18), globular glial tauopathy (n = 5), and tau-astrogliopathy of the elderly (n = 10). AT8 immunoreactivity patterns were compared by mathematical analysis. Results: Our study reveals disease-specific hot spots and regional selective vulnerability for these disorders. The pattern of hippocampal AD-related tau pathology is strongly influenced by concomitant AGD. Mathematical analysis reveals that hippocampal involvement in primary tauopathies is distinguishable from early-stage AD-related neurofibrillary degeneration. Conclusion: Our data demonstrate disease-specific AT8 immunoreactivity patterns and hot spots in the hippocampus even in tauopathies, which primarily do not affect the hippocampus. These hot spots can be shifted to other regions by the co-occurrence of tauopathies like AGD. Our observations support the notion that globular glial tauopathies and tau-astrogliopathy of the elderly are distinct entities."}],"publisher":"Karger Publishers","main_file_link":[{"open_access":"1","url":"https://kops.uni-konstanz.de/bitstream/123456789/42127/1/Milenkovic_2-17ivylo2up0798.pdf"}],"publication_identifier":{"issn":["1420-8008"]},"doi":"10.1159/000365548","date_updated":"2026-06-18T18:13:04Z","status":"public","oa":1,"article_type":"original","_id":"1913","external_id":{"pmid":["25195847"],"isi":["000344049900011"]},"date_published":"2014-11-07T00:00:00Z","pmid":1,"date_created":"2018-12-11T11:54:41Z","publist_id":"5181","year":"2014","day":"07","article_processing_charge":"No","publication":"Dementia and Geriatric Cognitive Disorders","type":"journal_article","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87"},{"status":"public","date_updated":"2025-09-29T12:23:35Z","doi":"10.1016/j.cub.2013.11.019","abstract":[{"lang":"eng","text":"Targeting membrane proteins for degradation requires the sequential action of ESCRT sub-complexes ESCRT-0 to ESCRT-III. Although this machinery is generally conserved among kingdoms, plants lack the essential ESCRT-0 components. A new report closes this gap by identifying a novel protein family that substitutes for ESCRT-0 function in plants."}],"title":"Plant biology: Gatekeepers of the road to protein perdition","quality_controlled":"1","publisher":"Cell Press","publication":"Current Biology","type":"journal_article","user_id":"317138e5-6ab7-11ef-aa6d-ffef3953e345","day":"06","article_processing_charge":"No","publist_id":"5180","year":"2014","_id":"1914","external_id":{"isi":["000329501400011"]},"date_published":"2014-01-06T00:00:00Z","date_created":"2018-12-11T11:54:41Z","issue":"1","citation":{"chicago":"Sauer, Michael, and Jiří Friml. “Plant Biology: Gatekeepers of the Road to Protein Perdition.” <i>Current Biology</i>. Cell Press, 2014. <a href=\"https://doi.org/10.1016/j.cub.2013.11.019\">https://doi.org/10.1016/j.cub.2013.11.019</a>.","ieee":"M. Sauer and J. Friml, “Plant biology: Gatekeepers of the road to protein perdition,” <i>Current Biology</i>, vol. 24, no. 1. Cell Press, pp. R27–R29, 2014.","mla":"Sauer, Michael, and Jiří Friml. “Plant Biology: Gatekeepers of the Road to Protein Perdition.” <i>Current Biology</i>, vol. 24, no. 1, Cell Press, 2014, pp. R27–29, doi:<a href=\"https://doi.org/10.1016/j.cub.2013.11.019\">10.1016/j.cub.2013.11.019</a>.","ista":"Sauer M, Friml J. 2014. Plant biology: Gatekeepers of the road to protein perdition. Current Biology. 24(1), R27–R29.","ama":"Sauer M, Friml J. Plant biology: Gatekeepers of the road to protein perdition. <i>Current Biology</i>. 2014;24(1):R27-R29. doi:<a href=\"https://doi.org/10.1016/j.cub.2013.11.019\">10.1016/j.cub.2013.11.019</a>","apa":"Sauer, M., &#38; Friml, J. (2014). Plant biology: Gatekeepers of the road to protein perdition. <i>Current Biology</i>. Cell Press. <a href=\"https://doi.org/10.1016/j.cub.2013.11.019\">https://doi.org/10.1016/j.cub.2013.11.019</a>","short":"M. Sauer, J. Friml, Current Biology 24 (2014) R27–R29."},"corr_author":"1","volume":24,"month":"01","author":[{"first_name":"Michael","last_name":"Sauer","full_name":"Sauer, Michael"},{"orcid":"0000-0002-8302-7596","last_name":"Friml","full_name":"Friml, Jirí","id":"4159519E-F248-11E8-B48F-1D18A9856A87","first_name":"Jirí"}],"department":[{"_id":"JiFr"}],"publication_status":"published","isi":1,"scopus_import":"1","intvolume":"        24","oa_version":"None","page":"R27 - R29","language":[{"iso":"eng"}]},{"day":"01","article_processing_charge":"No","type":"journal_article","user_id":"317138e5-6ab7-11ef-aa6d-ffef3953e345","publication":"Biochemical Society Transactions","pmid":1,"date_created":"2018-12-11T11:54:41Z","_id":"1915","external_id":{"pmid":["24450654"],"isi":["000333444400034"]},"date_published":"2014-02-01T00:00:00Z","publist_id":"5179","year":"2014","doi":"10.1042/BST20130269","date_updated":"2025-09-29T12:22:54Z","status":"public","project":[{"name":"Polarity and subcellular dynamics in plants","grant_number":"282300","_id":"25716A02-B435-11E9-9278-68D0E5697425","call_identifier":"FP7"}],"article_type":"original","quality_controlled":"1","title":"Rho-GTPase-regulated vesicle trafficking in plant cell polarity","abstract":[{"lang":"eng","text":"ROPs (Rho of plants) belong to a large family of plant-specific Rho-like small GTPases that function as essential molecular switches to control diverse cellular processes including cytoskeleton organization, cell polarization, cytokinesis, cell differentiation and vesicle trafficking. Although the machineries of vesicle trafficking and cell polarity in plants have been individually well addressed, how ROPs co-ordinate those processes is still largely unclear. Recent progress has been made towards an understanding of the coordination of ROP signalling and trafficking of PIN (PINFORMED) transporters for the plant hormone auxin in both root and leaf pavement cells. PIN transporters constantly shuttle between the endosomal compartments and the polar plasma membrane domains, therefore the modulation of PIN-dependent auxin transport between cells is a main developmental output of ROP-regulated vesicle trafficking. The present review focuses on these cellular mechanisms, especially the integration of ROP-based vesicle trafficking and plant cell polarity."}],"publisher":"Portland Press","publication_identifier":{"eissn":["1470-8752"],"issn":["0300-5127"]},"scopus_import":"1","intvolume":"        42","acknowledgement":"This work was supported by the European Research Council [project ERC-2011-StG-20101109-PSDP], Central European Institute of Technology (CEITEC) [grant number CZ.1.05/1.1.00/02.0068], European Social Fund [grant number CZ.1.07/2.3.00/20.0043] and the Czec","department":[{"_id":"JiFr"}],"author":[{"full_name":"Chen, Xu","last_name":"Chen","first_name":"Xu","id":"4E5ADCAA-F248-11E8-B48F-1D18A9856A87"},{"first_name":"Jirí","id":"4159519E-F248-11E8-B48F-1D18A9856A87","full_name":"Friml, Jirí","last_name":"Friml","orcid":"0000-0002-8302-7596"}],"publication_status":"published","isi":1,"volume":42,"month":"02","language":[{"iso":"eng"}],"oa_version":"None","page":"212 - 218","ec_funded":1,"citation":{"ista":"Chen X, Friml J. 2014. Rho-GTPase-regulated vesicle trafficking in plant cell polarity. Biochemical Society Transactions. 42(1), 212–218.","mla":"Chen, Xu, and Jiří Friml. “Rho-GTPase-Regulated Vesicle Trafficking in Plant Cell Polarity.” <i>Biochemical Society Transactions</i>, vol. 42, no. 1, Portland Press, 2014, pp. 212–18, doi:<a href=\"https://doi.org/10.1042/BST20130269\">10.1042/BST20130269</a>.","chicago":"Chen, Xu, and Jiří Friml. “Rho-GTPase-Regulated Vesicle Trafficking in Plant Cell Polarity.” <i>Biochemical Society Transactions</i>. Portland Press, 2014. <a href=\"https://doi.org/10.1042/BST20130269\">https://doi.org/10.1042/BST20130269</a>.","ieee":"X. Chen and J. Friml, “Rho-GTPase-regulated vesicle trafficking in plant cell polarity,” <i>Biochemical Society Transactions</i>, vol. 42, no. 1. Portland Press, pp. 212–218, 2014.","short":"X. Chen, J. Friml, Biochemical Society Transactions 42 (2014) 212–218.","apa":"Chen, X., &#38; Friml, J. (2014). Rho-GTPase-regulated vesicle trafficking in plant cell polarity. <i>Biochemical Society Transactions</i>. Portland Press. <a href=\"https://doi.org/10.1042/BST20130269\">https://doi.org/10.1042/BST20130269</a>","ama":"Chen X, Friml J. Rho-GTPase-regulated vesicle trafficking in plant cell polarity. <i>Biochemical Society Transactions</i>. 2014;42(1):212-218. doi:<a href=\"https://doi.org/10.1042/BST20130269\">10.1042/BST20130269</a>"},"corr_author":"1","issue":"1"},{"citation":{"apa":"Novarino, G., Fenstermaker, A., Zaki, M., Hofree, M., Silhavy, J., Heiberg, A., … Gleeson, J. (2014). Exome sequencing links corticospinal motor neuron disease to common neurodegenerative disorders. <i>Science</i>. American Association for the Advancement of Science. <a href=\"https://doi.org/10.1126/science.1247363\">https://doi.org/10.1126/science.1247363</a>","ama":"Novarino G, Fenstermaker A, Zaki M, et al. Exome sequencing links corticospinal motor neuron disease to common neurodegenerative disorders. <i>Science</i>. 2014;343(6170):506-511. doi:<a href=\"https://doi.org/10.1126/science.1247363\">10.1126/science.1247363</a>","short":"G. Novarino, A. Fenstermaker, M. Zaki, M. Hofree, J. Silhavy, A. Heiberg, M. Abdellateef, B. Rosti, E. Scott, L. Mansour, A. Masri, H. Kayserili, J. Al Aama, G. Abdel Salam, A. Karminejad, M. Kara, B. Kara, B. Bozorgmehri, T. Ben Omran, F. Mojahedi, I. Mahmoud, N. Bouslam, A. Bouhouche, A. Benomar, S. Hanein, L. Raymond, S. Forlani, M. Mascaro, L. Selim, N. Shehata, N. Al Allawi, P. Bindu, M. Azam, M. Günel, A. Caglayan, K. Bilgüvar, A. Tolun, M. Issa, J. Schroth, E. Spencer, R. Rosti, N. Akizu, K. Vaux, A. Johansen, A. Koh, H. Megahed, A. Dürr, A. Brice, G. Stévanin, S. Gabriel, T. Ideker, J. Gleeson, Science 343 (2014) 506–511.","mla":"Novarino, Gaia, et al. “Exome Sequencing Links Corticospinal Motor Neuron Disease to Common Neurodegenerative Disorders.” <i>Science</i>, vol. 343, no. 6170, American Association for the Advancement of Science, 2014, pp. 506–11, doi:<a href=\"https://doi.org/10.1126/science.1247363\">10.1126/science.1247363</a>.","chicago":"Novarino, Gaia, Ali Fenstermaker, Maha Zaki, Matan Hofree, Jennifer Silhavy, Andrew Heiberg, Mostafa Abdellateef, et al. “Exome Sequencing Links Corticospinal Motor Neuron Disease to Common Neurodegenerative Disorders.” <i>Science</i>. American Association for the Advancement of Science, 2014. <a href=\"https://doi.org/10.1126/science.1247363\">https://doi.org/10.1126/science.1247363</a>.","ieee":"G. Novarino <i>et al.</i>, “Exome sequencing links corticospinal motor neuron disease to common neurodegenerative disorders,” <i>Science</i>, vol. 343, no. 6170. American Association for the Advancement of Science, pp. 506–511, 2014.","ista":"Novarino G, Fenstermaker A, Zaki M, Hofree M, Silhavy J, Heiberg A, Abdellateef M, Rosti B, Scott E, Mansour L, Masri A, Kayserili H, Al Aama J, Abdel Salam G, Karminejad A, Kara M, Kara B, Bozorgmehri B, Ben Omran T, Mojahedi F, Mahmoud I, Bouslam N, Bouhouche A, Benomar A, Hanein S, Raymond L, Forlani S, Mascaro M, Selim L, Shehata N, Al Allawi N, Bindu P, Azam M, Günel M, Caglayan A, Bilgüvar K, Tolun A, Issa M, Schroth J, Spencer E, Rosti R, Akizu N, Vaux K, Johansen A, Koh A, Megahed H, Dürr A, Brice A, Stévanin G, Gabriel S, Ideker T, Gleeson J. 2014. Exome sequencing links corticospinal motor neuron disease to common neurodegenerative disorders. Science. 343(6170), 506–511."},"issue":"6170","isi":1,"publication_status":"published","author":[{"first_name":"Gaia","id":"3E57A680-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-7673-7178","full_name":"Novarino, Gaia","last_name":"Novarino"},{"last_name":"Fenstermaker","full_name":"Fenstermaker, Ali","first_name":"Ali"},{"first_name":"Maha","last_name":"Zaki","full_name":"Zaki, Maha"},{"first_name":"Matan","last_name":"Hofree","full_name":"Hofree, Matan"},{"full_name":"Silhavy, Jennifer","last_name":"Silhavy","first_name":"Jennifer"},{"first_name":"Andrew","last_name":"Heiberg","full_name":"Heiberg, Andrew"},{"full_name":"Abdellateef, Mostafa","last_name":"Abdellateef","first_name":"Mostafa"},{"full_name":"Rosti, Başak","last_name":"Rosti","first_name":"Başak"},{"full_name":"Scott, Eric","last_name":"Scott","first_name":"Eric"},{"first_name":"Lobna","last_name":"Mansour","full_name":"Mansour, Lobna"},{"first_name":"Amira","last_name":"Masri","full_name":"Masri, Amira"},{"full_name":"Kayserili, Hülya","last_name":"Kayserili","first_name":"Hülya"},{"last_name":"Al Aama","full_name":"Al Aama, Jumana","first_name":"Jumana"},{"full_name":"Abdel Salam, Ghada","last_name":"Abdel Salam","first_name":"Ghada"},{"first_name":"Ariana","full_name":"Karminejad, Ariana","last_name":"Karminejad"},{"first_name":"Majdi","full_name":"Kara, Majdi","last_name":"Kara"},{"full_name":"Kara, Bülent","last_name":"Kara","first_name":"Bülent"},{"first_name":"Bita","full_name":"Bozorgmehri, Bita","last_name":"Bozorgmehri"},{"first_name":"Tawfeg","full_name":"Ben Omran, Tawfeg","last_name":"Ben Omran"},{"full_name":"Mojahedi, Faezeh","last_name":"Mojahedi","first_name":"Faezeh"},{"first_name":"Iman","full_name":"Mahmoud, Iman","last_name":"Mahmoud"},{"last_name":"Bouslam","full_name":"Bouslam, Naïma","first_name":"Naïma"},{"first_name":"Ahmed","last_name":"Bouhouche","full_name":"Bouhouche, Ahmed"},{"first_name":"Ali","last_name":"Benomar","full_name":"Benomar, Ali"},{"first_name":"Sylvain","last_name":"Hanein","full_name":"Hanein, Sylvain"},{"last_name":"Raymond","full_name":"Raymond, Laure","first_name":"Laure"},{"last_name":"Forlani","full_name":"Forlani, Sylvie","first_name":"Sylvie"},{"last_name":"Mascaro","full_name":"Mascaro, Massimo","first_name":"Massimo"},{"first_name":"Laila","last_name":"Selim","full_name":"Selim, Laila"},{"first_name":"Nabil","full_name":"Shehata, Nabil","last_name":"Shehata"},{"full_name":"Al Allawi, Nasir","last_name":"Al Allawi","first_name":"Nasir"},{"last_name":"Bindu","full_name":"Bindu, Parayil","first_name":"Parayil"},{"last_name":"Azam","full_name":"Azam, Matloob","first_name":"Matloob"},{"last_name":"Günel","full_name":"Günel, Murat","first_name":"Murat"},{"first_name":"Ahmet","last_name":"Caglayan","full_name":"Caglayan, Ahmet"},{"first_name":"Kaya","full_name":"Bilgüvar, Kaya","last_name":"Bilgüvar"},{"full_name":"Tolun, Aslihan","last_name":"Tolun","first_name":"Aslihan"},{"full_name":"Issa, Mahmoud","last_name":"Issa","first_name":"Mahmoud"},{"full_name":"Schroth, Jana","last_name":"Schroth","first_name":"Jana"},{"last_name":"Spencer","full_name":"Spencer, Emily","first_name":"Emily"},{"first_name":"Rasim","full_name":"Rosti, Rasim","last_name":"Rosti"},{"first_name":"Naiara","last_name":"Akizu","full_name":"Akizu, Naiara"},{"first_name":"Keith","full_name":"Vaux, Keith","last_name":"Vaux"},{"first_name":"Anide","last_name":"Johansen","full_name":"Johansen, Anide"},{"first_name":"Alice","full_name":"Koh, Alice","last_name":"Koh"},{"first_name":"Hisham","full_name":"Megahed, Hisham","last_name":"Megahed"},{"last_name":"Dürr","full_name":"Dürr, Alexandra","first_name":"Alexandra"},{"full_name":"Brice, Alexis","last_name":"Brice","first_name":"Alexis"},{"first_name":"Giovanni","last_name":"Stévanin","full_name":"Stévanin, Giovanni"},{"first_name":"Stacy","full_name":"Gabriel, Stacy","last_name":"Gabriel"},{"first_name":"Trey","full_name":"Ideker, Trey","last_name":"Ideker"},{"full_name":"Gleeson, Joseph","last_name":"Gleeson","first_name":"Joseph"}],"department":[{"_id":"GaNo"}],"month":"01","volume":343,"intvolume":"       343","scopus_import":"1","acknowledgement":"Supported by the Deutsche Forschungsgemeinschaft (G.N.)","language":[{"iso":"eng"}],"page":"506 - 511","oa_version":"Submitted Version","article_type":"original","oa":1,"status":"public","doi":"10.1126/science.1247363","date_updated":"2025-09-29T12:22:05Z","main_file_link":[{"url":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4157572/","open_access":"1"}],"publisher":"American Association for the Advancement of Science","quality_controlled":"1","abstract":[{"text":"Hereditary spastic paraplegias (HSPs) are neurodegenerative motor neuron diseases characterized by progressive age-dependent loss of corticospinal motor tract function. Although the genetic basis is partly understood, only a fraction of cases can receive a genetic diagnosis, and a global view of HSP is lacking. By using whole-exome sequencing in combination with network analysis, we identified 18 previously unknown putative HSP genes and validated nearly all of these genes functionally or genetically. The pathways highlighted by these mutations link HSP to cellular transport, nucleotide metabolism, and synapse and axon development. Network analysis revealed a host of further candidate genes, of which three were mutated in our cohort. Our analysis links HSP to other neurodegenerative disorders and can facilitate gene discovery and mechanistic understanding of disease.","lang":"eng"}],"title":"Exome sequencing links corticospinal motor neuron disease to common neurodegenerative disorders","type":"journal_article","user_id":"317138e5-6ab7-11ef-aa6d-ffef3953e345","publication":"Science","article_processing_charge":"No","day":"31","year":"2014","publist_id":"5178","date_created":"2018-12-11T11:54:42Z","pmid":1,"date_published":"2014-01-31T00:00:00Z","_id":"1916","external_id":{"pmid":["24482476"],"isi":["000330343700038"]}},{"publist_id":"5177","year":"2014","_id":"1917","external_id":{"pmid":["24578577"],"isi":["000332309600046"]},"date_published":"2014-02-28T00:00:00Z","date_created":"2018-12-11T11:54:42Z","pmid":1,"publication":"Science","user_id":"317138e5-6ab7-11ef-aa6d-ffef3953e345","type":"journal_article","day":"28","article_processing_charge":"No","main_file_link":[{"open_access":"1","url":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4166562/"}],"title":"Cell surface ABP1-TMK auxin sensing complex activates ROP GTPase signaling","abstract":[{"lang":"eng","text":"Auxin-binding protein 1 (ABP1) was discovered nearly 40 years ago and was shown to be essential for plant development and morphogenesis, but its mode of action remains unclear. Here, we report that the plasma membrane-localized transmembrane kinase (TMK) receptor-like kinases interact with ABP1 and transduce auxin signal to activate plasma membrane-associated ROPs [Rho-like guanosine triphosphatases (GTPase) from plants], leading to changes in the cytoskeleton and the shape of leaf pavement cells in Arabidopsis. The interaction between ABP1 and TMK at the cell surface is induced by auxin and requires ABP1 sensing of auxin. These findings show that TMK proteins and ABP1 form a cell surface auxin perception complex that activates ROP signaling pathways, regulating nontranscriptional cytoplasmic responses and associated fundamental processes."}],"quality_controlled":"1","publisher":"American Association for the Advancement of Science","oa":1,"article_type":"original","date_updated":"2025-09-29T12:20:10Z","status":"public","doi":"10.1126/science.1245125","oa_version":"Submitted Version","page":"1025 - 1028","language":[{"iso":"eng"}],"volume":343,"month":"02","department":[{"_id":"JiFr"}],"author":[{"first_name":"Tongda","full_name":"Xu, Tongda","last_name":"Xu"},{"first_name":"Ning","full_name":"Dai, Ning","last_name":"Dai"},{"last_name":"Chen","full_name":"Chen, Jisheng","first_name":"Jisheng"},{"full_name":"Nagawa, Shingo","last_name":"Nagawa","first_name":"Shingo"},{"first_name":"Min","last_name":"Cao","full_name":"Cao, Min"},{"first_name":"Hongjiang","id":"33CA54A6-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0001-5039-9660","last_name":"Li","full_name":"Li, Hongjiang"},{"first_name":"Zimin","full_name":"Zhou, Zimin","last_name":"Zhou"},{"id":"4E5ADCAA-F248-11E8-B48F-1D18A9856A87","first_name":"Xu","full_name":"Chen, Xu","last_name":"Chen"},{"last_name":"De Rycke","full_name":"De Rycke, Riet","first_name":"Riet"},{"first_name":"Hana","full_name":"Rakusová, Hana","last_name":"Rakusová"},{"first_name":"Wen","last_name":"Wang","full_name":"Wang, Wen"},{"first_name":"Alan","full_name":"Jones, Alan","last_name":"Jones"},{"full_name":"Friml, Jirí","last_name":"Friml","orcid":"0000-0002-8302-7596","first_name":"Jirí","id":"4159519E-F248-11E8-B48F-1D18A9856A87"},{"first_name":"Sara","full_name":"Patterson, Sara","last_name":"Patterson"},{"full_name":"Bleecker, Anthony","last_name":"Bleecker","first_name":"Anthony"},{"last_name":"Yang","full_name":"Yang, Zhenbiao","first_name":"Zhenbiao"}],"isi":1,"publication_status":"published","acknowledgement":"Supported by the intramural research program of the National Institute of Arthritis and Musculoskeletal and Skin Diseases and by its Laboratory Animal Care and Use Section and Flow Cytometry Group, Office of Science and Technology","scopus_import":"1","intvolume":"       343","issue":"6174","citation":{"short":"T. Xu, N. Dai, J. Chen, S. Nagawa, M. Cao, H. Li, Z. Zhou, X. Chen, R. De Rycke, H. Rakusová, W. Wang, A. Jones, J. Friml, S. Patterson, A. Bleecker, Z. Yang, Science 343 (2014) 1025–1028.","ama":"Xu T, Dai N, Chen J, et al. Cell surface ABP1-TMK auxin sensing complex activates ROP GTPase signaling. <i>Science</i>. 2014;343(6174):1025-1028. doi:<a href=\"https://doi.org/10.1126/science.1245125\">10.1126/science.1245125</a>","apa":"Xu, T., Dai, N., Chen, J., Nagawa, S., Cao, M., Li, H., … Yang, Z. (2014). Cell surface ABP1-TMK auxin sensing complex activates ROP GTPase signaling. <i>Science</i>. American Association for the Advancement of Science. <a href=\"https://doi.org/10.1126/science.1245125\">https://doi.org/10.1126/science.1245125</a>","ista":"Xu T, Dai N, Chen J, Nagawa S, Cao M, Li H, Zhou Z, Chen X, De Rycke R, Rakusová H, Wang W, Jones A, Friml J, Patterson S, Bleecker A, Yang Z. 2014. Cell surface ABP1-TMK auxin sensing complex activates ROP GTPase signaling. Science. 343(6174), 1025–1028.","ieee":"T. Xu <i>et al.</i>, “Cell surface ABP1-TMK auxin sensing complex activates ROP GTPase signaling,” <i>Science</i>, vol. 343, no. 6174. American Association for the Advancement of Science, pp. 1025–1028, 2014.","chicago":"Xu, Tongda, Ning Dai, Jisheng Chen, Shingo Nagawa, Min Cao, Hongjiang Li, Zimin Zhou, et al. “Cell Surface ABP1-TMK Auxin Sensing Complex Activates ROP GTPase Signaling.” <i>Science</i>. American Association for the Advancement of Science, 2014. <a href=\"https://doi.org/10.1126/science.1245125\">https://doi.org/10.1126/science.1245125</a>.","mla":"Xu, Tongda, et al. “Cell Surface ABP1-TMK Auxin Sensing Complex Activates ROP GTPase Signaling.” <i>Science</i>, vol. 343, no. 6174, American Association for the Advancement of Science, 2014, pp. 1025–28, doi:<a href=\"https://doi.org/10.1126/science.1245125\">10.1126/science.1245125</a>."}}]