--- _id: '15160' abstract: - lang: eng text: The circadian clock orchestrates global changes in transcriptional regulation on a daily basis via the bHLH-PAS transcription factor CLOCK:BMAL1. Pathways driven by other bHLH-PAS transcription factors have a homologous repressor that modulates activity on a tissue-specific basis, but none have been identified for CLOCK:BMAL1. We show here that the cancer/testis antigen PASD1 fulfills this role to suppress circadian rhythms. PASD1 is evolutionarily related to CLOCK and interacts with the CLOCK:BMAL1 complex to repress transcriptional activation. Expression of PASD1 is restricted to germline tissues in healthy individuals but can be induced in cells of somatic origin upon oncogenic transformation. Reducing PASD1 in human cancer cells significantly increases the amplitude of transcriptional oscillations to generate more robust circadian rhythms. Our results describe a function for a germline-specific protein in regulation of the circadian clock and provide a molecular link from oncogenic transformation to suppression of circadian rhythms. article_processing_charge: No article_type: original author: - first_name: Alicia Kathleen full_name: Michael, Alicia Kathleen id: 6437c950-2a03-11ee-914d-d6476dd7b75c last_name: Michael - first_name: Stacy L. full_name: Harvey, Stacy L. last_name: Harvey - first_name: Patrick J. full_name: Sammons, Patrick J. last_name: Sammons - first_name: Amanda P. full_name: Anderson, Amanda P. last_name: Anderson - first_name: Hema M. full_name: Kopalle, Hema M. last_name: Kopalle - first_name: Alison H. full_name: Banham, Alison H. last_name: Banham - first_name: Carrie L. full_name: Partch, Carrie L. last_name: Partch citation: ama: Michael AK, Harvey SL, Sammons PJ, et al. Cancer/Testis antigen PASD1 silences the circadian clock. Molecular Cell. 2015;58(5):743-754. doi:10.1016/j.molcel.2015.03.031 apa: Michael, A. K., Harvey, S. L., Sammons, P. J., Anderson, A. P., Kopalle, H. M., Banham, A. H., & Partch, C. L. (2015). Cancer/Testis antigen PASD1 silences the circadian clock. Molecular Cell. Elsevier. https://doi.org/10.1016/j.molcel.2015.03.031 chicago: Michael, Alicia K., Stacy L. Harvey, Patrick J. Sammons, Amanda P. Anderson, Hema M. Kopalle, Alison H. Banham, and Carrie L. Partch. “Cancer/Testis Antigen PASD1 Silences the Circadian Clock.” Molecular Cell. Elsevier, 2015. https://doi.org/10.1016/j.molcel.2015.03.031. ieee: A. K. Michael et al., “Cancer/Testis antigen PASD1 silences the circadian clock,” Molecular Cell, vol. 58, no. 5. Elsevier, pp. 743–754, 2015. ista: Michael AK, Harvey SL, Sammons PJ, Anderson AP, Kopalle HM, Banham AH, Partch CL. 2015. Cancer/Testis antigen PASD1 silences the circadian clock. Molecular Cell. 58(5), 743–754. mla: Michael, Alicia K., et al. “Cancer/Testis Antigen PASD1 Silences the Circadian Clock.” Molecular Cell, vol. 58, no. 5, Elsevier, 2015, pp. 743–54, doi:10.1016/j.molcel.2015.03.031. short: A.K. Michael, S.L. Harvey, P.J. Sammons, A.P. Anderson, H.M. Kopalle, A.H. Banham, C.L. Partch, Molecular Cell 58 (2015) 743–754. date_created: 2024-03-21T07:58:08Z date_published: 2015-06-04T00:00:00Z date_updated: 2024-03-25T11:52:26Z day: '04' doi: 10.1016/j.molcel.2015.03.031 extern: '1' intvolume: ' 58' issue: '5' keyword: - Cell Biology - Molecular Biology language: - iso: eng main_file_link: - open_access: '1' url: https://doi.org/10.1016/j.molcel.2015.03.031 month: '06' oa: 1 oa_version: Published Version page: 743-754 publication: Molecular Cell publication_identifier: issn: - 1097-2765 publication_status: published publisher: Elsevier quality_controlled: '1' scopus_import: '1' status: public title: Cancer/Testis antigen PASD1 silences the circadian clock type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 58 year: '2015' ... --- _id: '15159' abstract: - lang: eng text: It is widely recognized that BMAL1 is an essential subunit of the primary transcription factor that drives rhythmic circadian transcription in the nucleus. In a surprising turn, Lipton et al. now show that BMAL1 rhythmically interacts with translational machinery in the cytosol to stimulate protein synthesis in response to mTOR signaling. article_processing_charge: No article_type: original author: - first_name: Alicia Kathleen full_name: Michael, Alicia Kathleen id: 6437c950-2a03-11ee-914d-d6476dd7b75c last_name: Michael - first_name: Hande full_name: Asimgil, Hande last_name: Asimgil - first_name: Carrie L. full_name: Partch, Carrie L. last_name: Partch citation: ama: Michael AK, Asimgil H, Partch CL. Cytosolic BMAL1 moonlights as a translation factor. Trends in Biochemical Sciences. 2015;40(9):489-490. doi:10.1016/j.tibs.2015.07.006 apa: Michael, A. K., Asimgil, H., & Partch, C. L. (2015). Cytosolic BMAL1 moonlights as a translation factor. Trends in Biochemical Sciences. Elsevier. https://doi.org/10.1016/j.tibs.2015.07.006 chicago: Michael, Alicia K., Hande Asimgil, and Carrie L. Partch. “Cytosolic BMAL1 Moonlights as a Translation Factor.” Trends in Biochemical Sciences. Elsevier, 2015. https://doi.org/10.1016/j.tibs.2015.07.006. ieee: A. K. Michael, H. Asimgil, and C. L. Partch, “Cytosolic BMAL1 moonlights as a translation factor,” Trends in Biochemical Sciences, vol. 40, no. 9. Elsevier, pp. 489–490, 2015. ista: Michael AK, Asimgil H, Partch CL. 2015. Cytosolic BMAL1 moonlights as a translation factor. Trends in Biochemical Sciences. 40(9), 489–490. mla: Michael, Alicia K., et al. “Cytosolic BMAL1 Moonlights as a Translation Factor.” Trends in Biochemical Sciences, vol. 40, no. 9, Elsevier, 2015, pp. 489–90, doi:10.1016/j.tibs.2015.07.006. short: A.K. Michael, H. Asimgil, C.L. Partch, Trends in Biochemical Sciences 40 (2015) 489–490. date_created: 2024-03-21T07:57:44Z date_published: 2015-09-01T00:00:00Z date_updated: 2024-03-25T11:53:58Z day: '01' doi: 10.1016/j.tibs.2015.07.006 extern: '1' intvolume: ' 40' issue: '9' keyword: - Molecular Biology - Biochemistry language: - iso: eng month: '09' oa_version: None page: 489-490 publication: Trends in Biochemical Sciences publication_identifier: issn: - 0968-0004 publication_status: published publisher: Elsevier quality_controlled: '1' scopus_import: '1' status: public title: Cytosolic BMAL1 moonlights as a translation factor type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 40 year: '2015' ... --- _id: '1619' abstract: - lang: eng text: The emergence of drug resistant pathogens is a serious public health problem. It is a long-standing goal to predict rates of resistance evolution and design optimal treatment strategies accordingly. To this end, it is crucial to reveal the underlying causes of drug-specific differences in the evolutionary dynamics leading to resistance. However, it remains largely unknown why the rates of resistance evolution via spontaneous mutations and the diversity of mutational paths vary substantially between drugs. Here we comprehensively quantify the distribution of fitness effects (DFE) of mutations, a key determinant of evolutionary dynamics, in the presence of eight antibiotics representing the main modes of action. Using precise high-throughput fitness measurements for genome-wide Escherichia coli gene deletion strains, we find that the width of the DFE varies dramatically between antibiotics and, contrary to conventional wisdom, for some drugs the DFE width is lower than in the absence of stress. We show that this previously underappreciated divergence in DFE width among antibiotics is largely caused by their distinct drug-specific dose-response characteristics. Unlike the DFE, the magnitude of the changes in tolerated drug concentration resulting from genome-wide mutations is similar for most drugs but exceptionally small for the antibiotic nitrofurantoin, i.e., mutations generally have considerably smaller resistance effects for nitrofurantoin than for other drugs. A population genetics model predicts that resistance evolution for drugs with this property is severely limited and confined to reproducible mutational paths. We tested this prediction in laboratory evolution experiments using the “morbidostat”, a device for evolving bacteria in well-controlled drug environments. Nitrofurantoin resistance indeed evolved extremely slowly via reproducible mutations—an almost paradoxical behavior since this drug causes DNA damage and increases the mutation rate. Overall, we identified novel quantitative characteristics of the evolutionary landscape that provide the conceptual foundation for predicting the dynamics of drug resistance evolution. article_number: e1002299 author: - first_name: Guillaume full_name: Chevereau, Guillaume id: 424D78A0-F248-11E8-B48F-1D18A9856A87 last_name: Chevereau - first_name: Marta full_name: Dravecka, Marta id: 4342E402-F248-11E8-B48F-1D18A9856A87 last_name: Dravecka orcid: 0000-0002-2519-8004 - first_name: Tugce full_name: Batur, Tugce last_name: Batur - first_name: Aysegul full_name: Guvenek, Aysegul last_name: Guvenek - first_name: Dilay full_name: Ayhan, Dilay last_name: Ayhan - first_name: Erdal full_name: Toprak, Erdal last_name: Toprak - first_name: Mark Tobias full_name: Bollenbach, Mark Tobias id: 3E6DB97A-F248-11E8-B48F-1D18A9856A87 last_name: Bollenbach orcid: 0000-0003-4398-476X citation: ama: Chevereau G, Lukacisinova M, Batur T, et al. Quantifying the determinants of evolutionary dynamics leading to drug resistance. PLoS Biology. 2015;13(11). doi:10.1371/journal.pbio.1002299 apa: Chevereau, G., Lukacisinova, M., Batur, T., Guvenek, A., Ayhan, D., Toprak, E., & Bollenbach, M. T. (2015). Quantifying the determinants of evolutionary dynamics leading to drug resistance. PLoS Biology. Public Library of Science. https://doi.org/10.1371/journal.pbio.1002299 chicago: Chevereau, Guillaume, Marta Lukacisinova, Tugce Batur, Aysegul Guvenek, Dilay Ayhan, Erdal Toprak, and Mark Tobias Bollenbach. “Quantifying the Determinants of Evolutionary Dynamics Leading to Drug Resistance.” PLoS Biology. Public Library of Science, 2015. https://doi.org/10.1371/journal.pbio.1002299. ieee: G. Chevereau et al., “Quantifying the determinants of evolutionary dynamics leading to drug resistance,” PLoS Biology, vol. 13, no. 11. Public Library of Science, 2015. ista: Chevereau G, Lukacisinova M, Batur T, Guvenek A, Ayhan D, Toprak E, Bollenbach MT. 2015. Quantifying the determinants of evolutionary dynamics leading to drug resistance. PLoS Biology. 13(11), e1002299. mla: Chevereau, Guillaume, et al. “Quantifying the Determinants of Evolutionary Dynamics Leading to Drug Resistance.” PLoS Biology, vol. 13, no. 11, e1002299, Public Library of Science, 2015, doi:10.1371/journal.pbio.1002299. short: G. Chevereau, M. Lukacisinova, T. Batur, A. Guvenek, D. Ayhan, E. Toprak, M.T. Bollenbach, PLoS Biology 13 (2015). date_created: 2018-12-11T11:53:04Z date_published: 2015-11-18T00:00:00Z date_updated: 2024-03-27T23:30:28Z day: '18' ddc: - '570' department: - _id: ToBo doi: 10.1371/journal.pbio.1002299 ec_funded: 1 file: - access_level: open_access checksum: 0e82e3279f50b15c6c170c042627802b content_type: application/pdf creator: system date_created: 2018-12-12T10:09:00Z date_updated: 2020-07-14T12:45:07Z file_id: '4723' file_name: IST-2016-468-v1+1_journal.pbio.1002299.pdf file_size: 1387760 relation: main_file file_date_updated: 2020-07-14T12:45:07Z has_accepted_license: '1' intvolume: ' 13' issue: '11' language: - iso: eng month: '11' oa: 1 oa_version: Published Version project: - _id: 25EB3A80-B435-11E9-9278-68D0E5697425 grant_number: RGP0042/2013 name: Revealing the fundamental limits of cell growth - _id: 25E9AF9E-B435-11E9-9278-68D0E5697425 call_identifier: FWF grant_number: P27201-B22 name: Revealing the mechanisms underlying drug interactions - _id: 25E83C2C-B435-11E9-9278-68D0E5697425 call_identifier: FP7 grant_number: '303507' name: Optimality principles in responses to antibiotics publication: PLoS Biology publication_status: published publisher: Public Library of Science publist_id: '5547' pubrep_id: '468' quality_controlled: '1' related_material: record: - id: '9711' relation: research_data status: public - id: '9765' relation: research_data status: public - id: '6263' relation: dissertation_contains status: public scopus_import: 1 status: public title: Quantifying the determinants of evolutionary dynamics leading to drug resistance tmp: image: /images/cc_by.png legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0) short: CC BY (4.0) type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 13 year: '2015' ... --- _id: '10382' abstract: - lang: eng text: 'Protein oligomers have been implicated as toxic agents in a wide range of amyloid-related diseases. However, it has remained unsolved whether the oligomers are a necessary step in the formation of amyloid fibrils or just a dangerous byproduct. Analogously, it has not been resolved if the amyloid nucleation process is a classical one-step nucleation process or a two-step process involving prenucleation clusters. We use coarse-grained computer simulations to study the effect of nonspecific attractions between peptides on the primary nucleation process underlying amyloid fibrillization. We find that, for peptides that do not attract, the classical one-step nucleation mechanism is possible but only at nonphysiologically high peptide concentrations. At low peptide concentrations, which mimic the physiologically relevant regime, attractive interpeptide interactions are essential for fibril formation. Nucleation then inevitably takes place through a two-step mechanism involving prefibrillar oligomers. We show that oligomers not only help peptides meet each other but also, create an environment that facilitates the conversion of monomers into the β-sheet–rich form characteristic of fibrils. Nucleation typically does not proceed through the most prevalent oligomers but through an oligomer size that is only observed in rare fluctuations, which is why such aggregates might be hard to capture experimentally. Finally, we find that the nucleation of amyloid fibrils cannot be described by classical nucleation theory: in the two-step mechanism, the critical nucleus size increases with increases in both concentration and interpeptide interactions, which is in direct contrast with predictions from classical nucleation theory.' acknowledgement: We thank Michele Vendruscolo, Iskra Staneva, and William M. Jacobs, for helpful discussions. A.Š. acknowledges support from the Human Frontier Science Program and Emmanuel College. Y.C.C. and D.F. are supported by Engineering and Physical Sciences Research Council Programme Grant EP/I001352/1. T.P.J.K. acknowledges the Frances and Augustus Newman Foundation, the European Research Council, and the Biotechnology and Biological Sciences Research Council. D.F. acknowledges European Research Council Advanced Grant 227758. article_processing_charge: No article_type: original author: - first_name: Anđela full_name: Šarić, Anđela id: bf63d406-f056-11eb-b41d-f263a6566d8b last_name: Šarić orcid: 0000-0002-7854-2139 - first_name: Yassmine C. full_name: Chebaro, Yassmine C. last_name: Chebaro - first_name: Tuomas P. J. full_name: Knowles, Tuomas P. J. last_name: Knowles - first_name: Daan full_name: Frenkel, Daan last_name: Frenkel citation: ama: Šarić A, Chebaro YC, Knowles TPJ, Frenkel D. Crucial role of nonspecific interactions in amyloid nucleation. Proceedings of the National Academy of Sciences. 2014;111(50):17869-17874. doi:10.1073/pnas.1410159111 apa: Šarić, A., Chebaro, Y. C., Knowles, T. P. J., & Frenkel, D. (2014). Crucial role of nonspecific interactions in amyloid nucleation. Proceedings of the National Academy of Sciences. National Academy of Sciences. https://doi.org/10.1073/pnas.1410159111 chicago: Šarić, Anđela, Yassmine C. Chebaro, Tuomas P. J. Knowles, and Daan Frenkel. “Crucial Role of Nonspecific Interactions in Amyloid Nucleation.” Proceedings of the National Academy of Sciences. National Academy of Sciences, 2014. https://doi.org/10.1073/pnas.1410159111. ieee: A. Šarić, Y. C. Chebaro, T. P. J. Knowles, and D. Frenkel, “Crucial role of nonspecific interactions in amyloid nucleation,” Proceedings of the National Academy of Sciences, vol. 111, no. 50. National Academy of Sciences, pp. 17869–17874, 2014. ista: Šarić A, Chebaro YC, Knowles TPJ, Frenkel D. 2014. Crucial role of nonspecific interactions in amyloid nucleation. Proceedings of the National Academy of Sciences. 111(50), 17869–17874. mla: Šarić, Anđela, et al. “Crucial Role of Nonspecific Interactions in Amyloid Nucleation.” Proceedings of the National Academy of Sciences, vol. 111, no. 50, National Academy of Sciences, 2014, pp. 17869–74, doi:10.1073/pnas.1410159111. short: A. Šarić, Y.C. Chebaro, T.P.J. Knowles, D. Frenkel, Proceedings of the National Academy of Sciences 111 (2014) 17869–17874. date_created: 2021-11-29T13:09:53Z date_published: 2014-12-01T00:00:00Z date_updated: 2021-11-29T13:29:05Z day: '01' doi: 10.1073/pnas.1410159111 extern: '1' external_id: arxiv: - '1412.0897' pmid: - '25453085' intvolume: ' 111' issue: '50' keyword: - multidisciplinary language: - iso: eng main_file_link: - open_access: '1' url: https://www.pnas.org/content/111/50/17869 month: '12' oa: 1 oa_version: Published Version page: 17869-17874 pmid: 1 publication: Proceedings of the National Academy of Sciences publication_identifier: eissn: - 1091-6490 issn: - 0027-8424 publication_status: published publisher: National Academy of Sciences quality_controlled: '1' scopus_import: '1' status: public title: Crucial role of nonspecific interactions in amyloid nucleation type: journal_article user_id: 8b945eb4-e2f2-11eb-945a-df72226e66a9 volume: 111 year: '2014' ... --- _id: '10383' abstract: - lang: eng text: We use numerical simulations to compute the equation of state of a suspension of spherical self-propelled nanoparticles in two and three dimensions. We study in detail the effect of excluded volume interactions and confinement as a function of the system's temperature, concentration, and strength of the propulsion. We find a striking nonmonotonic dependence of the pressure on the temperature and provide simple scaling arguments to predict and explain the occurrence of such anomalous behavior. We explicitly show how our results have important implications for the effective forces on passive components suspended in a bath of active particles. article_number: '052303' article_processing_charge: No article_type: original author: - first_name: S. A. full_name: Mallory, S. A. last_name: Mallory - first_name: Anđela full_name: Šarić, Anđela id: bf63d406-f056-11eb-b41d-f263a6566d8b last_name: Šarić orcid: 0000-0002-7854-2139 - first_name: C. full_name: Valeriani, C. last_name: Valeriani - first_name: A. full_name: Cacciuto, A. last_name: Cacciuto citation: ama: Mallory SA, Šarić A, Valeriani C, Cacciuto A. Anomalous thermomechanical properties of a self-propelled colloidal fluid. Physical Review E. 2014;89(5). doi:10.1103/physreve.89.052303 apa: Mallory, S. A., Šarić, A., Valeriani, C., & Cacciuto, A. (2014). Anomalous thermomechanical properties of a self-propelled colloidal fluid. Physical Review E. American Physical Society. https://doi.org/10.1103/physreve.89.052303 chicago: Mallory, S. A., Anđela Šarić, C. Valeriani, and A. Cacciuto. “Anomalous Thermomechanical Properties of a Self-Propelled Colloidal Fluid.” Physical Review E. American Physical Society, 2014. https://doi.org/10.1103/physreve.89.052303. ieee: S. A. Mallory, A. Šarić, C. Valeriani, and A. Cacciuto, “Anomalous thermomechanical properties of a self-propelled colloidal fluid,” Physical Review E, vol. 89, no. 5. American Physical Society, 2014. ista: Mallory SA, Šarić A, Valeriani C, Cacciuto A. 2014. Anomalous thermomechanical properties of a self-propelled colloidal fluid. Physical Review E. 89(5), 052303. mla: Mallory, S. A., et al. “Anomalous Thermomechanical Properties of a Self-Propelled Colloidal Fluid.” Physical Review E, vol. 89, no. 5, 052303, American Physical Society, 2014, doi:10.1103/physreve.89.052303. short: S.A. Mallory, A. Šarić, C. Valeriani, A. Cacciuto, Physical Review E 89 (2014). date_created: 2021-11-29T13:10:33Z date_published: 2014-05-06T00:00:00Z date_updated: 2021-11-29T13:29:01Z day: '06' doi: 10.1103/physreve.89.052303 extern: '1' external_id: arxiv: - '1310.0826' pmid: - '25353796' intvolume: ' 89' issue: '5' language: - iso: eng main_file_link: - open_access: '1' url: https://arxiv.org/abs/1310.0826 month: '05' oa: 1 oa_version: Preprint pmid: 1 publication: Physical Review E publication_identifier: eissn: - 1550-2376 issn: - 1539-3755 publication_status: published publisher: American Physical Society quality_controlled: '1' scopus_import: '1' status: public title: Anomalous thermomechanical properties of a self-propelled colloidal fluid type: journal_article user_id: 8b945eb4-e2f2-11eb-945a-df72226e66a9 volume: 89 year: '2014' ... --- _id: '1058' abstract: - lang: eng text: Diffraction-unlimited far-field super-resolution fluorescence (nanoscopy) methods typically rely on transiently transferring fluorophores between two states, whereby this transfer is usually laid out as a switch. However, depending on whether this is induced in a spatially controlled manner using a pattern of light (coordinate-targeted) or stochastically on a single-molecule basis, specific requirements on the fluorophores are imposed. Therefore, the fluorophores are usually utilized just for one class of methods only. In this study we demonstrate that the reversibly switchable fluorescent protein Dreiklang enables live-cell recordings in both spatially controlled and stochastic modes. We show that the Dreiklang chromophore entails three different light-induced switching mechanisms, namely a reversible photochemical one, off-switching by stimulated emission, and a reversible transfer to a long-lived dark state from the S1 state, all of which can be utilized to overcome the diffraction barrier. We also find that for the single-molecule- based stochastic GSDIM approach (ground-state depletion followed by individual molecule return), Dreiklang provides a larger number of on-off localization events as compared to its progenitor Citrine. Altogether, Dreiklang is a versatile probe for essentially all popular forms of live-cell fluorescence nanoscopy. article_processing_charge: No author: - first_name: Nickels full_name: Jensen, Nickels last_name: Jensen - first_name: Johann G full_name: Danzl, Johann G id: 42EFD3B6-F248-11E8-B48F-1D18A9856A87 last_name: Danzl orcid: 0000-0001-8559-3973 - first_name: Katrin full_name: Willig, Katrin last_name: Willig - first_name: Flavie full_name: Lavoie Cardinal, Flavie last_name: Lavoie Cardinal - first_name: Tanja full_name: Brakemann, Tanja last_name: Brakemann - first_name: Stefan full_name: Hell, Stefan last_name: Hell - first_name: Stefan full_name: Jakobs, Stefan last_name: Jakobs citation: ama: Jensen N, Danzl JG, Willig K, et al. Coordinate-targeted and coordinate-stochastic super-resolution microscopy with the reversibly switchable fluorescent protein dreiklang. ChemPhysChem. 2014;15(4):756-762. doi:10.1002/cphc.201301034 apa: Jensen, N., Danzl, J. G., Willig, K., Lavoie Cardinal, F., Brakemann, T., Hell, S., & Jakobs, S. (2014). Coordinate-targeted and coordinate-stochastic super-resolution microscopy with the reversibly switchable fluorescent protein dreiklang. ChemPhysChem. Wiley-Blackwell. https://doi.org/10.1002/cphc.201301034 chicago: Jensen, Nickels, Johann G Danzl, Katrin Willig, Flavie Lavoie Cardinal, Tanja Brakemann, Stefan Hell, and Stefan Jakobs. “Coordinate-Targeted and Coordinate-Stochastic Super-Resolution Microscopy with the Reversibly Switchable Fluorescent Protein Dreiklang.” ChemPhysChem. Wiley-Blackwell, 2014. https://doi.org/10.1002/cphc.201301034. ieee: N. Jensen et al., “Coordinate-targeted and coordinate-stochastic super-resolution microscopy with the reversibly switchable fluorescent protein dreiklang,” ChemPhysChem, vol. 15, no. 4. Wiley-Blackwell, pp. 756–762, 2014. ista: Jensen N, Danzl JG, Willig K, Lavoie Cardinal F, Brakemann T, Hell S, Jakobs S. 2014. Coordinate-targeted and coordinate-stochastic super-resolution microscopy with the reversibly switchable fluorescent protein dreiklang. ChemPhysChem. 15(4), 756–762. mla: Jensen, Nickels, et al. “Coordinate-Targeted and Coordinate-Stochastic Super-Resolution Microscopy with the Reversibly Switchable Fluorescent Protein Dreiklang.” ChemPhysChem, vol. 15, no. 4, Wiley-Blackwell, 2014, pp. 756–62, doi:10.1002/cphc.201301034. short: N. Jensen, J.G. Danzl, K. Willig, F. Lavoie Cardinal, T. Brakemann, S. Hell, S. Jakobs, ChemPhysChem 15 (2014) 756–762. date_created: 2018-12-11T11:49:55Z date_published: 2014-03-17T00:00:00Z date_updated: 2021-01-12T06:47:58Z day: '17' doi: 10.1002/cphc.201301034 extern: '1' intvolume: ' 15' issue: '4' language: - iso: eng month: '03' oa_version: None page: 756 - 762 publication: ChemPhysChem publication_status: published publisher: Wiley-Blackwell publist_id: '6332' status: public title: Coordinate-targeted and coordinate-stochastic super-resolution microscopy with the reversibly switchable fluorescent protein dreiklang type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 15 year: '2014' ... --- _id: '10815' abstract: - lang: eng text: In the last several decades, developmental biology has clarified the molecular mechanisms of embryogenesis and organogenesis. In particular, it has demonstrated that the “tool-kit genes” essential for regulating developmental processes are not only highly conserved among species, but are also used as systems at various times and places in an organism to control distinct developmental events. Therefore, mutations in many of these tool-kit genes may cause congenital diseases involving morphological abnormalities. This link between genes and abnormal morphological phenotypes underscores the importance of understanding how cells behave and contribute to morphogenesis as a result of gene function. Recent improvements in live imaging and in quantitative analyses of cellular dynamics will advance our understanding of the cellular pathogenesis of congenital diseases associated with aberrant morphologies. In these studies, it is critical to select an appropriate model organism for the particular phenomenon of interest. acknowledgement: The authors thank all the members of the Division of Morphogenesis, National Institute for Basic Biology, for their contributions to the research, their encouragement, and helpful discussions, particularly Dr M. Suzuki for his critical reading of the manuscript. We also thank the Model Animal Research and Spectrography and Bioimaging Facilities, NIBB Core Research Facilities, for technical support. M.H. was supported by a research fellowship from the Japan Society for the Promotion of Science (JSPS). Our work introduced in this review was supported by a Grant-in-Aid for Scientific Research on Innovative Areas from the Ministry of Education, Culture, Sports, Science, and Technology (MEXT), Japan, to N.U. article_processing_charge: No article_type: original author: - first_name: Masakazu full_name: Hashimoto, Masakazu last_name: Hashimoto - first_name: Hitoshi full_name: Morita, Hitoshi id: 4C6E54C6-F248-11E8-B48F-1D18A9856A87 last_name: Morita - first_name: Naoto full_name: Ueno, Naoto last_name: Ueno citation: ama: Hashimoto M, Morita H, Ueno N. Molecular and cellular mechanisms of development underlying congenital diseases. Congenital Anomalies. 2014;54(1):1-7. doi:10.1111/cga.12039 apa: Hashimoto, M., Morita, H., & Ueno, N. (2014). Molecular and cellular mechanisms of development underlying congenital diseases. Congenital Anomalies. Wiley. https://doi.org/10.1111/cga.12039 chicago: Hashimoto, Masakazu, Hitoshi Morita, and Naoto Ueno. “Molecular and Cellular Mechanisms of Development Underlying Congenital Diseases.” Congenital Anomalies. Wiley, 2014. https://doi.org/10.1111/cga.12039. ieee: M. Hashimoto, H. Morita, and N. Ueno, “Molecular and cellular mechanisms of development underlying congenital diseases,” Congenital Anomalies, vol. 54, no. 1. Wiley, pp. 1–7, 2014. ista: Hashimoto M, Morita H, Ueno N. 2014. Molecular and cellular mechanisms of development underlying congenital diseases. Congenital Anomalies. 54(1), 1–7. mla: Hashimoto, Masakazu, et al. “Molecular and Cellular Mechanisms of Development Underlying Congenital Diseases.” Congenital Anomalies, vol. 54, no. 1, Wiley, 2014, pp. 1–7, doi:10.1111/cga.12039. short: M. Hashimoto, H. Morita, N. Ueno, Congenital Anomalies 54 (2014) 1–7. date_created: 2022-03-04T08:17:25Z date_published: 2014-02-01T00:00:00Z date_updated: 2022-03-04T08:26:05Z day: '01' department: - _id: CaHe doi: 10.1111/cga.12039 external_id: pmid: - '24666178' intvolume: ' 54' issue: '1' keyword: - Developmental Biology - Embryology - General Medicine - Pediatrics - Perinatology - and Child Health language: - iso: eng main_file_link: - open_access: '1' url: https://doi.org/10.1111/cga.12039 month: '02' oa: 1 oa_version: None page: 1-7 pmid: 1 publication: Congenital Anomalies publication_identifier: issn: - 0914-3505 publication_status: published publisher: Wiley quality_controlled: '1' scopus_import: '1' status: public title: Molecular and cellular mechanisms of development underlying congenital diseases type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 54 year: '2014' ... --- _id: '10811' abstract: - lang: eng text: Auxin is an important signaling compound in plants and vital for plant development and growth. The present book, Auxin and its Role in Plant Development, provides the reader with detailed and comprehensive insight into the functioning of the molecule on the whole and specifically in plant development. In the first part, the functioning, metabolism and signaling pathways of auxin in plants are explained, the second part depicts the specific role of auxin in plant development and the third part describes the interaction and functioning of the signaling compound upon stimuli of the environment. Each chapter is written by international experts in the respective field and designed for scientists and researchers in plant biology, plant development and cell biology to summarize the recent progress in understanding the role of auxin and suggest future perspectives for auxin research. article_processing_charge: No citation: ama: 'Zažímalová E, Petrášek J, Benková E, eds. Auxin and Its Role in Plant Development. 1st ed. Vienna: Springer Nature; 2014. doi:10.1007/978-3-7091-1526-8' apa: 'Zažímalová, E., Petrášek, J., & Benková, E. (Eds.). (2014). Auxin and Its Role in Plant Development (1st ed.). Vienna: Springer Nature. https://doi.org/10.1007/978-3-7091-1526-8' chicago: 'Zažímalová, Eva, Jan Petrášek, and Eva Benková, eds. Auxin and Its Role in Plant Development. 1st ed. Vienna: Springer Nature, 2014. https://doi.org/10.1007/978-3-7091-1526-8.' ieee: 'E. Zažímalová, J. Petrášek, and E. Benková, Eds., Auxin and Its Role in Plant Development, 1st ed. Vienna: Springer Nature, 2014.' ista: 'Zažímalová E, Petrášek J, Benková E eds. 2014. Auxin and Its Role in Plant Development 1st ed., Vienna: Springer Nature, 444p.' mla: Zažímalová, Eva, et al., editors. Auxin and Its Role in Plant Development. 1st ed., Springer Nature, 2014, doi:10.1007/978-3-7091-1526-8. short: E. Zažímalová, J. Petrášek, E. Benková, eds., Auxin and Its Role in Plant Development, 1st ed., Springer Nature, Vienna, 2014. date_created: 2022-03-03T11:52:44Z date_published: 2014-04-01T00:00:00Z date_updated: 2022-03-04T07:38:15Z day: '01' department: - _id: EvBe doi: 10.1007/978-3-7091-1526-8 edition: '1' editor: - first_name: Eva full_name: Zažímalová, Eva last_name: Zažímalová - first_name: Jan full_name: Petrášek, Jan last_name: Petrášek - first_name: Eva full_name: Benková, Eva id: 38F4F166-F248-11E8-B48F-1D18A9856A87 last_name: Benková orcid: 0000-0002-8510-9739 language: - iso: eng month: '04' oa_version: None page: '444' place: Vienna publication_identifier: eisbn: - '9783709115268' isbn: - '9783709115251' publication_status: published publisher: Springer Nature quality_controlled: '1' scopus_import: '1' status: public title: Auxin and Its Role in Plant Development type: book_editor user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 year: '2014' ... --- _id: '10884' abstract: - lang: eng text: "We revisit the parameterized model checking problem for token-passing systems and specifications in indexed CTL  ∗ \\X. Emerson and Namjoshi (1995, 2003) have shown that parameterized model checking of indexed CTL  ∗ \\X in uni-directional token rings can be reduced to checking rings up to some cutoff size. Clarke et al. (2004) have shown a similar result for general topologies and indexed LTL \\X, provided processes cannot choose the directions for sending or receiving the token.\r\nWe unify and substantially extend these results by systematically exploring fragments of indexed CTL  ∗ \\X with respect to general topologies. For each fragment we establish whether a cutoff exists, and for some concrete topologies, such as rings, cliques and stars, we infer small cutoffs. Finally, we show that the problem becomes undecidable, and thus no cutoffs exist, if processes are allowed to choose the directions in which they send or from which they receive the token." acknowledgement: "This work was supported by the Austrian Science Fund through grant P23499-N23\r\nand through the RiSE network (S11403, S11405, S11406, S11407-N23); ERC Starting Grant (279307: Graph Games); Vienna Science and Technology Fund (WWTF)\r\ngrants PROSEED, ICT12-059, and VRG11-005." alternative_title: - LNCS article_processing_charge: No author: - first_name: Benjamin full_name: Aminof, Benjamin id: 4A55BD00-F248-11E8-B48F-1D18A9856A87 last_name: Aminof - first_name: Swen full_name: Jacobs, Swen last_name: Jacobs - first_name: Ayrat full_name: Khalimov, Ayrat last_name: Khalimov - first_name: Sasha full_name: Rubin, Sasha id: 2EC51194-F248-11E8-B48F-1D18A9856A87 last_name: Rubin citation: ama: 'Aminof B, Jacobs S, Khalimov A, Rubin S. Parameterized model checking of token-passing systems. In: Verification, Model Checking, and Abstract Interpretation. Vol 8318. Springer Nature; 2014:262-281. doi:10.1007/978-3-642-54013-4_15' apa: 'Aminof, B., Jacobs, S., Khalimov, A., & Rubin, S. (2014). Parameterized model checking of token-passing systems. In Verification, Model Checking, and Abstract Interpretation (Vol. 8318, pp. 262–281). San Diego, CA, United States: Springer Nature. https://doi.org/10.1007/978-3-642-54013-4_15' chicago: Aminof, Benjamin, Swen Jacobs, Ayrat Khalimov, and Sasha Rubin. “Parameterized Model Checking of Token-Passing Systems.” In Verification, Model Checking, and Abstract Interpretation, 8318:262–81. Springer Nature, 2014. https://doi.org/10.1007/978-3-642-54013-4_15. ieee: B. Aminof, S. Jacobs, A. Khalimov, and S. Rubin, “Parameterized model checking of token-passing systems,” in Verification, Model Checking, and Abstract Interpretation, San Diego, CA, United States, 2014, vol. 8318, pp. 262–281. ista: 'Aminof B, Jacobs S, Khalimov A, Rubin S. 2014. Parameterized model checking of token-passing systems. Verification, Model Checking, and Abstract Interpretation. VMCAI: Verifcation, Model Checking, and Abstract Interpretation, LNCS, vol. 8318, 262–281.' mla: Aminof, Benjamin, et al. “Parameterized Model Checking of Token-Passing Systems.” Verification, Model Checking, and Abstract Interpretation, vol. 8318, Springer Nature, 2014, pp. 262–81, doi:10.1007/978-3-642-54013-4_15. short: B. Aminof, S. Jacobs, A. Khalimov, S. Rubin, in:, Verification, Model Checking, and Abstract Interpretation, Springer Nature, 2014, pp. 262–281. conference: end_date: 2014-01-21 location: San Diego, CA, United States name: 'VMCAI: Verifcation, Model Checking, and Abstract Interpretation' start_date: 2014-01-19 date_created: 2022-03-18T13:01:22Z date_published: 2014-01-30T00:00:00Z date_updated: 2022-05-17T08:36:01Z day: '30' department: - _id: KrCh doi: 10.1007/978-3-642-54013-4_15 ec_funded: 1 external_id: arxiv: - '1311.4425' intvolume: ' 8318' language: - iso: eng main_file_link: - open_access: '1' url: ' https://doi.org/10.48550/arXiv.1311.4425' month: '01' oa: 1 oa_version: Preprint page: 262-281 project: - _id: 2584A770-B435-11E9-9278-68D0E5697425 call_identifier: FWF grant_number: P 23499-N23 name: Modern Graph Algorithmic Techniques in Formal Verification - _id: 25863FF4-B435-11E9-9278-68D0E5697425 call_identifier: FWF grant_number: S11407 name: Game Theory - _id: 2581B60A-B435-11E9-9278-68D0E5697425 call_identifier: FP7 grant_number: '279307' name: 'Quantitative Graph Games: Theory and Applications' publication: Verification, Model Checking, and Abstract Interpretation publication_identifier: eisbn: - '9783642540134' eissn: - 1611-3349 isbn: - '9783642540127' issn: - 0302-9743 publication_status: published publisher: Springer Nature quality_controlled: '1' scopus_import: '1' status: public title: Parameterized model checking of token-passing systems type: conference user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 8318 year: '2014' ... --- _id: '10893' abstract: - lang: eng text: Saddle periodic orbits are an essential and stable part of the topological skeleton of a 3D vector field. Nevertheless, there is currently no efficient algorithm to robustly extract these features. In this chapter, we present a novel technique to extract saddle periodic orbits. Exploiting the analytic properties of such an orbit, we propose a scalar measure based on the finite-time Lyapunov exponent (FTLE) that indicates its presence. Using persistent homology, we can then extract the robust cycles of this field. These cycles thereby represent the saddle periodic orbits of the given vector field. We discuss the different existing FTLE approximation schemes regarding their applicability to this specific problem and propose an adapted version of FTLE called Normalized Velocity Separation. Finally, we evaluate our method using simple analytic vector field data. acknowledgement: First, we thank the reviewers of this paper for their ideas and critical comments. In addition, we thank Ronny Peikert and Filip Sadlo for a fruitful discussions. This research is supported by the European Commission under the TOPOSYS project FP7-ICT-318493-STREP, the European Social Fund (ESF App. No. 100098251), and the European Science Foundation under the ACAT Research Network Program. article_processing_charge: No author: - first_name: Jens full_name: Kasten, Jens last_name: Kasten - first_name: Jan full_name: Reininghaus, Jan id: 4505473A-F248-11E8-B48F-1D18A9856A87 last_name: Reininghaus - first_name: Wieland full_name: Reich, Wieland last_name: Reich - first_name: Gerik full_name: Scheuermann, Gerik last_name: Scheuermann citation: ama: 'Kasten J, Reininghaus J, Reich W, Scheuermann G. Toward the extraction of saddle periodic orbits. In: Bremer P-T, Hotz I, Pascucci V, Peikert R, eds. Topological Methods in Data Analysis and Visualization III . Vol 1. Mathematics and Visualization. Cham: Springer; 2014:55-69. doi:10.1007/978-3-319-04099-8_4' apa: 'Kasten, J., Reininghaus, J., Reich, W., & Scheuermann, G. (2014). Toward the extraction of saddle periodic orbits. In P.-T. Bremer, I. Hotz, V. Pascucci, & R. Peikert (Eds.), Topological Methods in Data Analysis and Visualization III (Vol. 1, pp. 55–69). Cham: Springer. https://doi.org/10.1007/978-3-319-04099-8_4' chicago: 'Kasten, Jens, Jan Reininghaus, Wieland Reich, and Gerik Scheuermann. “Toward the Extraction of Saddle Periodic Orbits.” In Topological Methods in Data Analysis and Visualization III , edited by Peer-Timo Bremer, Ingrid Hotz, Valerio Pascucci, and Ronald Peikert, 1:55–69. Mathematics and Visualization. Cham: Springer, 2014. https://doi.org/10.1007/978-3-319-04099-8_4.' ieee: 'J. Kasten, J. Reininghaus, W. Reich, and G. Scheuermann, “Toward the extraction of saddle periodic orbits,” in Topological Methods in Data Analysis and Visualization III , vol. 1, P.-T. Bremer, I. Hotz, V. Pascucci, and R. Peikert, Eds. Cham: Springer, 2014, pp. 55–69.' ista: 'Kasten J, Reininghaus J, Reich W, Scheuermann G. 2014.Toward the extraction of saddle periodic orbits. In: Topological Methods in Data Analysis and Visualization III . vol. 1, 55–69.' mla: Kasten, Jens, et al. “Toward the Extraction of Saddle Periodic Orbits.” Topological Methods in Data Analysis and Visualization III , edited by Peer-Timo Bremer et al., vol. 1, Springer, 2014, pp. 55–69, doi:10.1007/978-3-319-04099-8_4. short: J. Kasten, J. Reininghaus, W. Reich, G. Scheuermann, in:, P.-T. Bremer, I. Hotz, V. Pascucci, R. Peikert (Eds.), Topological Methods in Data Analysis and Visualization III , Springer, Cham, 2014, pp. 55–69. date_created: 2022-03-21T07:11:23Z date_published: 2014-03-19T00:00:00Z date_updated: 2022-06-21T12:01:47Z day: '19' department: - _id: HeEd doi: 10.1007/978-3-319-04099-8_4 ec_funded: 1 editor: - first_name: Peer-Timo full_name: Bremer, Peer-Timo last_name: Bremer - first_name: Ingrid full_name: Hotz, Ingrid last_name: Hotz - first_name: Valerio full_name: Pascucci, Valerio last_name: Pascucci - first_name: Ronald full_name: Peikert, Ronald last_name: Peikert intvolume: ' 1' language: - iso: eng month: '03' oa_version: None page: 55-69 place: Cham project: - _id: 255D761E-B435-11E9-9278-68D0E5697425 call_identifier: FP7 grant_number: '318493' name: Topological Complex Systems publication: 'Topological Methods in Data Analysis and Visualization III ' publication_identifier: eisbn: - '9783319040998' eissn: - 2197-666X isbn: - '9783319040981' issn: - 1612-3786 publication_status: published publisher: Springer quality_controlled: '1' scopus_import: '1' series_title: Mathematics and Visualization status: public title: Toward the extraction of saddle periodic orbits type: book_chapter user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 1 year: '2014' ...