--- _id: '6091' abstract: - lang: eng text: Cortical networks are characterized by sparse connectivity, with synapses found at only a subset of axo-dendritic contacts. Yet within these networks, neurons can exhibit high connection probabilities, suggesting that cell-intrinsic factors, not proximity, determine connectivity. Here, we identify ephrin-B3 (eB3) as a factor that determines synapse density by mediating a cell-cell competition that requires ephrin-B-EphB signaling. In a microisland culture system designed to isolate cell-cell competition, we find that eB3 determines winning and losing neurons in a contest for synapses. In a Mosaic Analysis with Double Markers (MADM) genetic mouse model system in vivo the relative levels of eB3 control spine density in layer 5 and 6 neurons. MADM cortical neurons in vitro reveal that eB3 controls synapse density independently of action potential-driven activity. Our findings illustrate a new class of competitive mechanism mediated by trans-synaptic organizing proteins which control the number of synapses neurons receive relative to neighboring neurons. article_number: e41563 article_processing_charge: No author: - first_name: Nathan T. full_name: Henderson, Nathan T. last_name: Henderson - first_name: Sylvain J. full_name: Le Marchand, Sylvain J. last_name: Le Marchand - first_name: Martin full_name: Hruska, Martin last_name: Hruska - first_name: Simon full_name: Hippenmeyer, Simon id: 37B36620-F248-11E8-B48F-1D18A9856A87 last_name: Hippenmeyer orcid: 0000-0003-2279-1061 - first_name: Liqun full_name: Luo, Liqun last_name: Luo - first_name: Matthew B. full_name: Dalva, Matthew B. last_name: Dalva citation: ama: Henderson NT, Le Marchand SJ, Hruska M, Hippenmeyer S, Luo L, Dalva MB. Ephrin-B3 controls excitatory synapse density through cell-cell competition for EphBs. eLife. 2019;8. doi:10.7554/eLife.41563 apa: Henderson, N. T., Le Marchand, S. J., Hruska, M., Hippenmeyer, S., Luo, L., & Dalva, M. B. (2019). Ephrin-B3 controls excitatory synapse density through cell-cell competition for EphBs. ELife. eLife Sciences Publications. https://doi.org/10.7554/eLife.41563 chicago: Henderson, Nathan T., Sylvain J. Le Marchand, Martin Hruska, Simon Hippenmeyer, Liqun Luo, and Matthew B. Dalva. “Ephrin-B3 Controls Excitatory Synapse Density through Cell-Cell Competition for EphBs.” ELife. eLife Sciences Publications, 2019. https://doi.org/10.7554/eLife.41563. ieee: N. T. Henderson, S. J. Le Marchand, M. Hruska, S. Hippenmeyer, L. Luo, and M. B. Dalva, “Ephrin-B3 controls excitatory synapse density through cell-cell competition for EphBs,” eLife, vol. 8. eLife Sciences Publications, 2019. ista: Henderson NT, Le Marchand SJ, Hruska M, Hippenmeyer S, Luo L, Dalva MB. 2019. Ephrin-B3 controls excitatory synapse density through cell-cell competition for EphBs. eLife. 8, e41563. mla: Henderson, Nathan T., et al. “Ephrin-B3 Controls Excitatory Synapse Density through Cell-Cell Competition for EphBs.” ELife, vol. 8, e41563, eLife Sciences Publications, 2019, doi:10.7554/eLife.41563. short: N.T. Henderson, S.J. Le Marchand, M. Hruska, S. Hippenmeyer, L. Luo, M.B. Dalva, ELife 8 (2019). date_created: 2019-03-10T22:59:20Z date_published: 2019-02-21T00:00:00Z date_updated: 2023-08-24T14:50:50Z day: '21' ddc: - '570' department: - _id: SiHi doi: 10.7554/eLife.41563 external_id: isi: - '000459380600001' pmid: - '30789343' file: - access_level: open_access checksum: 7b0800d003f14cd06b1802dea0c52941 content_type: application/pdf creator: dernst date_created: 2019-03-11T16:15:37Z date_updated: 2020-07-14T12:47:19Z file_id: '6098' file_name: 2019_eLife_Henderson.pdf file_size: 7260753 relation: main_file file_date_updated: 2020-07-14T12:47:19Z has_accepted_license: '1' intvolume: ' 8' isi: 1 language: - iso: eng month: '02' oa: 1 oa_version: Published Version pmid: 1 publication: eLife publication_status: published publisher: eLife Sciences Publications quality_controlled: '1' scopus_import: '1' status: public title: Ephrin-B3 controls excitatory synapse density through cell-cell competition for EphBs 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: 4359f0d1-fa6c-11eb-b949-802e58b17ae8 volume: 8 year: '2019' ... --- _id: '6046' abstract: - lang: eng text: Sudden stress often triggers diverse, temporally structured gene expression responses in microbes, but it is largely unknown how variable in time such responses are and if genes respond in the same temporal order in every single cell. Here, we quantified timing variability of individual promoters responding to sublethal antibiotic stress using fluorescent reporters, microfluidics, and time‐lapse microscopy. We identified lower and upper bounds that put definite constraints on timing variability, which varies strongly among promoters and conditions. Timing variability can be interpreted using results from statistical kinetics, which enable us to estimate the number of rate‐limiting molecular steps underlying different responses. We found that just a few critical steps control some responses while others rely on dozens of steps. To probe connections between different stress responses, we then tracked the temporal order and response time correlations of promoter pairs in individual cells. Our results support that, when bacteria are exposed to the antibiotic nitrofurantoin, the ensuing oxidative stress and SOS responses are part of the same causal chain of molecular events. In contrast, under trimethoprim, the acid stress response and the SOS response are part of different chains of events running in parallel. Our approach reveals fundamental constraints on gene expression timing and provides new insights into the molecular events that underlie the timing of stress responses. acknowledged_ssus: - _id: Bio article_number: e8470 article_processing_charge: No author: - first_name: Karin full_name: Mitosch, Karin id: 39B66846-F248-11E8-B48F-1D18A9856A87 last_name: Mitosch - first_name: Georg full_name: Rieckh, Georg id: 34DA8BD6-F248-11E8-B48F-1D18A9856A87 last_name: Rieckh - 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: Mitosch K, Rieckh G, Bollenbach MT. Temporal order and precision of complex stress responses in individual bacteria. Molecular systems biology. 2019;15(2). doi:10.15252/msb.20188470 apa: Mitosch, K., Rieckh, G., & Bollenbach, M. T. (2019). Temporal order and precision of complex stress responses in individual bacteria. Molecular Systems Biology. Embo Press. https://doi.org/10.15252/msb.20188470 chicago: Mitosch, Karin, Georg Rieckh, and Mark Tobias Bollenbach. “Temporal Order and Precision of Complex Stress Responses in Individual Bacteria.” Molecular Systems Biology. Embo Press, 2019. https://doi.org/10.15252/msb.20188470. ieee: K. Mitosch, G. Rieckh, and M. T. Bollenbach, “Temporal order and precision of complex stress responses in individual bacteria,” Molecular systems biology, vol. 15, no. 2. Embo Press, 2019. ista: Mitosch K, Rieckh G, Bollenbach MT. 2019. Temporal order and precision of complex stress responses in individual bacteria. Molecular systems biology. 15(2), e8470. mla: Mitosch, Karin, et al. “Temporal Order and Precision of Complex Stress Responses in Individual Bacteria.” Molecular Systems Biology, vol. 15, no. 2, e8470, Embo Press, 2019, doi:10.15252/msb.20188470. short: K. Mitosch, G. Rieckh, M.T. Bollenbach, Molecular Systems Biology 15 (2019). date_created: 2019-02-24T22:59:18Z date_published: 2019-02-14T00:00:00Z date_updated: 2023-08-24T14:49:53Z day: '14' department: - _id: GaTk doi: 10.15252/msb.20188470 external_id: isi: - '000459628300003' pmid: - '30765425' intvolume: ' 15' isi: 1 issue: '2' language: - iso: eng main_file_link: - open_access: '1' url: https://www.ncbi.nlm.nih.gov/pubmed/30765425 month: '02' oa: 1 oa_version: Submitted Version pmid: 1 project: - _id: 25E9AF9E-B435-11E9-9278-68D0E5697425 call_identifier: FWF grant_number: P27201-B22 name: Revealing the mechanisms underlying drug interactions - _id: 25EB3A80-B435-11E9-9278-68D0E5697425 grant_number: RGP0042/2013 name: Revealing the fundamental limits of cell growth publication: Molecular systems biology publication_status: published publisher: Embo Press quality_controlled: '1' scopus_import: '1' status: public title: Temporal order and precision of complex stress responses in individual bacteria type: journal_article user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8 volume: 15 year: '2019' ... --- _id: '6105' abstract: - lang: eng text: " Hosts can alter their strategy towards pathogens during their lifetime; that is, they can show phenotypic plasticity in immunity or life history. Immune priming is one such example, where a previous encounter with a pathogen confers enhanced protection upon secondary challenge, resulting in reduced pathogen load (i.e., resistance) and improved host survival. However, an initial encounter might also enhance tolerance, particularly to less virulent opportunistic pathogens that establish persistent infections. In this scenario, individuals are better able to reduce the negative fecundity consequences that result from a high pathogen burden. Finally, previous exposure may also lead to life‐history adjustments, such as terminal investment into reproduction.\r\n Using different Drosophila melanogaster host genotypes and two bacterial pathogens, Lactococcus lactis and Pseudomonas entomophila, we tested whether previous exposure results in resistance or tolerance and whether it modifies immune gene expression during an acute‐phase infection (one day post‐challenge). We then asked whether previous pathogen exposure affects chronic‐phase pathogen persistence and longer‐term survival (28 days post‐challenge).\r\n \ We predicted that previous exposure would increase host resistance to an early stage bacterial infection while it might come at a cost to host fecundity tolerance. We reasoned that resistance would be due in part to stronger immune gene expression after challenge. We expected that previous exposure would improve long‐term survival, that it would reduce infection persistence, and we expected to find genetic variation in these responses.\r\n We found that previous exposure to P. entomophila weakened host resistance to a second infection independent of genotype and had no effect on immune gene expression. Fecundity tolerance showed genotypic variation but was not influenced by previous exposure. However, L. lactis persisted as a chronic infection, whereas survivors cleared the more pathogenic P. entomophila infection.\r\n \ To our knowledge, this is the first study that addresses host tolerance to bacteria in relation to previous exposure, taking a multi‐faceted approach to address the topic. Our results suggest that previous exposure comes with transient costs to resistance during the early stage of infection in this host–pathogen system and that infection persistence may be bacterium‐specific.\r\n" article_processing_charge: No article_type: original author: - first_name: Megan full_name: Kutzer, Megan id: 29D0B332-F248-11E8-B48F-1D18A9856A87 last_name: Kutzer orcid: 0000-0002-8696-6978 - first_name: Joachim full_name: Kurtz, Joachim last_name: Kurtz - first_name: Sophie A.O. full_name: Armitage, Sophie A.O. last_name: Armitage citation: ama: Kutzer M, Kurtz J, Armitage SAO. A multi-faceted approach testing the effects of previous bacterial exposure on resistance and tolerance. Journal of Animal Ecology. 2019;88(4):566-578. doi:10.1111/1365-2656.12953 apa: Kutzer, M., Kurtz, J., & Armitage, S. A. O. (2019). A multi-faceted approach testing the effects of previous bacterial exposure on resistance and tolerance. Journal of Animal Ecology. Wiley. https://doi.org/10.1111/1365-2656.12953 chicago: Kutzer, Megan, Joachim Kurtz, and Sophie A.O. Armitage. “A Multi-Faceted Approach Testing the Effects of Previous Bacterial Exposure on Resistance and Tolerance.” Journal of Animal Ecology. Wiley, 2019. https://doi.org/10.1111/1365-2656.12953. ieee: M. Kutzer, J. Kurtz, and S. A. O. Armitage, “A multi-faceted approach testing the effects of previous bacterial exposure on resistance and tolerance,” Journal of Animal Ecology, vol. 88, no. 4. Wiley, pp. 566–578, 2019. ista: Kutzer M, Kurtz J, Armitage SAO. 2019. A multi-faceted approach testing the effects of previous bacterial exposure on resistance and tolerance. Journal of Animal Ecology. 88(4), 566–578. mla: Kutzer, Megan, et al. “A Multi-Faceted Approach Testing the Effects of Previous Bacterial Exposure on Resistance and Tolerance.” Journal of Animal Ecology, vol. 88, no. 4, Wiley, 2019, pp. 566–78, doi:10.1111/1365-2656.12953. short: M. Kutzer, J. Kurtz, S.A.O. Armitage, Journal of Animal Ecology 88 (2019) 566–578. date_created: 2019-03-17T22:59:15Z date_published: 2019-04-01T00:00:00Z date_updated: 2023-08-25T08:04:53Z day: '01' ddc: - '570' department: - _id: SyCr doi: 10.1111/1365-2656.12953 ec_funded: 1 external_id: isi: - '000467994800007' file: - access_level: open_access checksum: 405cde15120de26018b3bd0dfa29986c content_type: application/pdf creator: dernst date_created: 2019-03-18T07:43:06Z date_updated: 2020-07-14T12:47:19Z file_id: '6107' file_name: 2019_JournalAnimalEcology_Kutzer.pdf file_size: 1460662 relation: main_file file_date_updated: 2020-07-14T12:47:19Z has_accepted_license: '1' intvolume: ' 88' isi: 1 issue: '4' language: - iso: eng month: '04' oa: 1 oa_version: Published Version page: 566-578 project: - _id: 25681D80-B435-11E9-9278-68D0E5697425 call_identifier: FP7 grant_number: '291734' name: International IST Postdoc Fellowship Programme publication: Journal of Animal Ecology publication_identifier: eissn: - '13652656' issn: - '00218790' publication_status: published publisher: Wiley quality_controlled: '1' related_material: record: - id: '9806' relation: research_data status: public scopus_import: '1' status: public title: A multi-faceted approach testing the effects of previous bacterial exposure on resistance and tolerance 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: 4359f0d1-fa6c-11eb-b949-802e58b17ae8 volume: 88 year: '2019' ... --- _id: '6088' abstract: - lang: eng text: P-Glycoprotein (ABCB1) and breast cancer resistance protein (ABCG2) are two efflux transporters at the blood–brain barrier (BBB), which effectively restrict brain distribution of diverse drugs, such as tyrosine kinase inhibitors. There is a crucial need for pharmacological ABCB1 and ABCG2 inhibition protocols for a more effective treatment of brain diseases. In the present study, seven marketed drugs (osimertinib, erlotinib, nilotinib, imatinib, lapatinib, pazopanib, and cyclosporine A) and one nonmarketed drug (tariquidar), with known in vitro ABCB1/ABCG2 inhibitory properties, were screened for their inhibitory potency at the BBB in vivo. Positron emission tomography (PET) using the model ABCB1/ABCG2 substrate [11C]erlotinib was performed in mice. Tested inhibitors were administered as i.v. bolus injections at 30 min before the start of the PET scan, followed by a continuous i.v. infusion for the duration of the PET scan. Five of the tested drugs increased total distribution volume of [11C]erlotinib in the brain (VT,brain) compared to vehicle-treated animals (tariquidar, + 69%; erlotinib, + 19% and +23% for the 21.5 mg/kg and the 43 mg/kg dose, respectively; imatinib, + 22%; lapatinib, + 25%; and cyclosporine A, + 49%). For all drugs, increases in [11C]erlotinib brain distribution were lower than in Abcb1a/b(−/−)Abcg2(−/−) mice (+149%), which suggested that only partial ABCB1/ABCG2 inhibition was reached at the mouse BBB. The plasma concentrations of the tested drugs at the time of the PET scan were higher than clinically achievable plasma concentrations. Some of the tested drugs led to significant increases in blood radioactivity concentrations measured at the end of the PET scan (erlotinib, + 103% and +113% for the 21.5 mg/kg and the 43 mg/kg dose, respectively; imatinib, + 125%; and cyclosporine A, + 101%), which was most likely caused by decreased hepatobiliary excretion of radioactivity. Taken together, our data suggest that some marketed tyrosine kinase inhibitors may be repurposed to inhibit ABCB1 and ABCG2 at the BBB. From a clinical perspective, moderate increases in brain delivery despite the administration of high i.v. doses as well as peripheral drug–drug interactions due to transporter inhibition in clearance organs question the translatability of this concept. article_processing_charge: No author: - first_name: Alexander full_name: Traxl, Alexander last_name: Traxl - first_name: Severin full_name: Mairinger, Severin last_name: Mairinger - first_name: Thomas full_name: Filip, Thomas last_name: Filip - first_name: Michael full_name: Sauberer, Michael last_name: Sauberer - first_name: Johann full_name: Stanek, Johann last_name: Stanek - first_name: Stefan full_name: Poschner, Stefan last_name: Poschner - first_name: Walter full_name: Jäger, Walter last_name: Jäger - first_name: Viktoria full_name: Zoufal, Viktoria last_name: Zoufal - first_name: Gaia full_name: Novarino, Gaia id: 3E57A680-F248-11E8-B48F-1D18A9856A87 last_name: Novarino orcid: 0000-0002-7673-7178 - first_name: Nicolas full_name: Tournier, Nicolas last_name: Tournier - first_name: Martin full_name: Bauer, Martin last_name: Bauer - first_name: Thomas full_name: Wanek, Thomas last_name: Wanek - first_name: Oliver full_name: Langer, Oliver last_name: Langer citation: ama: Traxl A, Mairinger S, Filip T, et al. Inhibition of ABCB1 and ABCG2 at the mouse blood-brain barrier with marketed drugs to improve brain delivery of the model ABCB1/ABCG2 substrate [11C]erlotinib. Molecular Pharmaceutics. 2019;16(3):1282-1293. doi:10.1021/acs.molpharmaceut.8b01217 apa: Traxl, A., Mairinger, S., Filip, T., Sauberer, M., Stanek, J., Poschner, S., … Langer, O. (2019). Inhibition of ABCB1 and ABCG2 at the mouse blood-brain barrier with marketed drugs to improve brain delivery of the model ABCB1/ABCG2 substrate [11C]erlotinib. Molecular Pharmaceutics. American Chemical Society. https://doi.org/10.1021/acs.molpharmaceut.8b01217 chicago: Traxl, Alexander, Severin Mairinger, Thomas Filip, Michael Sauberer, Johann Stanek, Stefan Poschner, Walter Jäger, et al. “Inhibition of ABCB1 and ABCG2 at the Mouse Blood-Brain Barrier with Marketed Drugs to Improve Brain Delivery of the Model ABCB1/ABCG2 Substrate [11C]Erlotinib.” Molecular Pharmaceutics. American Chemical Society, 2019. https://doi.org/10.1021/acs.molpharmaceut.8b01217. ieee: A. Traxl et al., “Inhibition of ABCB1 and ABCG2 at the mouse blood-brain barrier with marketed drugs to improve brain delivery of the model ABCB1/ABCG2 substrate [11C]erlotinib,” Molecular Pharmaceutics, vol. 16, no. 3. American Chemical Society, pp. 1282–1293, 2019. ista: Traxl A, Mairinger S, Filip T, Sauberer M, Stanek J, Poschner S, Jäger W, Zoufal V, Novarino G, Tournier N, Bauer M, Wanek T, Langer O. 2019. Inhibition of ABCB1 and ABCG2 at the mouse blood-brain barrier with marketed drugs to improve brain delivery of the model ABCB1/ABCG2 substrate [11C]erlotinib. Molecular Pharmaceutics. 16(3), 1282–1293. mla: Traxl, Alexander, et al. “Inhibition of ABCB1 and ABCG2 at the Mouse Blood-Brain Barrier with Marketed Drugs to Improve Brain Delivery of the Model ABCB1/ABCG2 Substrate [11C]Erlotinib.” Molecular Pharmaceutics, vol. 16, no. 3, American Chemical Society, 2019, pp. 1282–93, doi:10.1021/acs.molpharmaceut.8b01217. short: A. Traxl, S. Mairinger, T. Filip, M. Sauberer, J. Stanek, S. Poschner, W. Jäger, V. Zoufal, G. Novarino, N. Tournier, M. Bauer, T. Wanek, O. Langer, Molecular Pharmaceutics 16 (2019) 1282–1293. date_created: 2019-03-10T22:59:19Z date_published: 2019-03-04T00:00:00Z date_updated: 2023-08-25T08:02:51Z day: '04' department: - _id: GaNo doi: 10.1021/acs.molpharmaceut.8b01217 external_id: isi: - '000460600400031' pmid: - '30694684' intvolume: ' 16' isi: 1 issue: '3' language: - iso: eng month: '03' oa_version: None page: 1282-1293 pmid: 1 publication: Molecular Pharmaceutics publication_status: published publisher: American Chemical Society quality_controlled: '1' scopus_import: '1' status: public title: Inhibition of ABCB1 and ABCG2 at the mouse blood-brain barrier with marketed drugs to improve brain delivery of the model ABCB1/ABCG2 substrate [11C]erlotinib type: journal_article user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8 volume: 16 year: '2019' ... --- _id: '6087' abstract: - lang: eng text: Cell fate specification by lateral inhibition typically involves contact signaling through the Delta-Notch signaling pathway. However, whether this is the only signaling mode mediating lateral inhibition remains unclear. Here we show that in zebrafish oogenesis, a group of cells within the granulosa cell layer at the oocyte animal pole acquire elevated levels of the transcriptional coactivator TAZ in their nuclei. One of these cells, the future micropyle precursor cell (MPC), accumulates increasingly high levels of nuclear TAZ and grows faster than its surrounding cells, mechanically compressing those cells, which ultimately lose TAZ from their nuclei. Strikingly, relieving neighbor-cell compression by MPC ablation or aspiration restores nuclear TAZ accumulation in neighboring cells, eventually leading to MPC re-specification from these cells. Conversely, MPC specification is defective in taz−/− follicles. These findings uncover a novel mode of lateral inhibition in cell fate specification based on mechanical signals controlling TAZ activity. acknowledged_ssus: - _id: Bio - _id: EM-Fac - _id: LifeSc acknowledgement: We thank Roland Dosch, Makoto Furutani-Seiki, Brian Link, Mary Mullins, and Masazumi Tada for providing transgenic and/or mutant zebrafish lines; Alexandra Schauer, Shayan Shami-Pour, and the rest of the Heisenberg lab for technical assistance and feedback on the manuscript; and the Bioimaging, Electron Microscopy, and Zebrafish facilities of IST Austria for continuous support. This work was supported by an ERC advanced grant ( MECSPEC to C.-P.H.). article_processing_charge: No article_type: original author: - first_name: Peng full_name: Xia, Peng id: 4AB6C7D0-F248-11E8-B48F-1D18A9856A87 last_name: Xia orcid: 0000-0002-5419-7756 - first_name: Daniel J full_name: Gütl, Daniel J id: 381929CE-F248-11E8-B48F-1D18A9856A87 last_name: Gütl - first_name: Vanessa full_name: Zheden, Vanessa id: 39C5A68A-F248-11E8-B48F-1D18A9856A87 last_name: Zheden orcid: 0000-0002-9438-4783 - first_name: Carl-Philipp J full_name: Heisenberg, Carl-Philipp J id: 39427864-F248-11E8-B48F-1D18A9856A87 last_name: Heisenberg orcid: 0000-0002-0912-4566 citation: ama: Xia P, Gütl DJ, Zheden V, Heisenberg C-PJ. Lateral inhibition in cell specification mediated by mechanical signals modulating TAZ activity. Cell. 2019;176(6):1379-1392.e14. doi:10.1016/j.cell.2019.01.019 apa: Xia, P., Gütl, D. J., Zheden, V., & Heisenberg, C.-P. J. (2019). Lateral inhibition in cell specification mediated by mechanical signals modulating TAZ activity. Cell. Elsevier. https://doi.org/10.1016/j.cell.2019.01.019 chicago: Xia, Peng, Daniel J Gütl, Vanessa Zheden, and Carl-Philipp J Heisenberg. “Lateral Inhibition in Cell Specification Mediated by Mechanical Signals Modulating TAZ Activity.” Cell. Elsevier, 2019. https://doi.org/10.1016/j.cell.2019.01.019. ieee: P. Xia, D. J. Gütl, V. Zheden, and C.-P. J. Heisenberg, “Lateral inhibition in cell specification mediated by mechanical signals modulating TAZ activity,” Cell, vol. 176, no. 6. Elsevier, p. 1379–1392.e14, 2019. ista: Xia P, Gütl DJ, Zheden V, Heisenberg C-PJ. 2019. Lateral inhibition in cell specification mediated by mechanical signals modulating TAZ activity. Cell. 176(6), 1379–1392.e14. mla: Xia, Peng, et al. “Lateral Inhibition in Cell Specification Mediated by Mechanical Signals Modulating TAZ Activity.” Cell, vol. 176, no. 6, Elsevier, 2019, p. 1379–1392.e14, doi:10.1016/j.cell.2019.01.019. short: P. Xia, D.J. Gütl, V. Zheden, C.-P.J. Heisenberg, Cell 176 (2019) 1379–1392.e14. date_created: 2019-03-10T22:59:19Z date_published: 2019-03-07T00:00:00Z date_updated: 2023-08-25T08:02:23Z day: '07' department: - _id: CaHe - _id: EM-Fac doi: 10.1016/j.cell.2019.01.019 ec_funded: 1 external_id: isi: - '000460509600013' pmid: - '30773315' intvolume: ' 176' isi: 1 issue: '6' language: - iso: eng main_file_link: - open_access: '1' url: https://doi.org/10.1016/j.cell.2019.01.019 month: '03' oa: 1 oa_version: Published Version page: 1379-1392.e14 pmid: 1 project: - _id: 260F1432-B435-11E9-9278-68D0E5697425 call_identifier: H2020 grant_number: '742573' name: Interaction and feedback between cell mechanics and fate specification in vertebrate gastrulation publication: Cell publication_status: published publisher: Elsevier quality_controlled: '1' related_material: link: - description: News on IST Homepage relation: press_release url: https://ist.ac.at/en/news/in-zebrafish-eggs-most-rapidly-growing-cell-inhibits-its-neighbours-through-mechanical-signals/ scopus_import: '1' status: public title: Lateral inhibition in cell specification mediated by mechanical signals modulating TAZ activity type: journal_article user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8 volume: 176 year: '2019' ... --- _id: '9806' abstract: - lang: eng text: 1. Hosts can alter their strategy towards pathogens during their lifetime, i.e., they can show phenotypic plasticity in immunity or life history. Immune priming is one such example, where a previous encounter with a pathogen confers enhanced protection upon secondary challenge, resulting in reduced pathogen load (i.e. resistance) and improved host survival. However, an initial encounter might also enhance tolerance, particularly to less virulent opportunistic pathogens that establish persistent infections. In this scenario, individuals are better able to reduce the negative fitness consequences that result from a high pathogen load. Finally, previous exposure may also lead to life history adjustments, such as terminal investment into reproduction. 2. Using different Drosophila melanogaster host genotypes and two bacterial pathogens, Lactococcus lactis and Pseudomonas entomophila, we tested if previous exposure results in resistance or tolerance and whether it modifies immune gene expression during an acute-phase infection (one day post-challenge). We then asked if previous pathogen exposure affects chronic-phase pathogen persistence and longer-term survival (28 days post-challenge). 3. We predicted that previous exposure would increase host resistance to an early stage bacterial infection while it might come at a cost to host fecundity tolerance. We reasoned that resistance would be due in part to stronger immune gene expression after challenge. We expected that previous exposure would improve long-term survival, that it would reduce infection persistence, and we expected to find genetic variation in these responses. 4. We found that previous exposure to P. entomophila weakened host resistance to a second infection independent of genotype and had no effect on immune gene expression. Fecundity tolerance showed genotypic variation but was not influenced by previous exposure. However, L. lactis persisted as a chronic infection, whereas survivors cleared the more pathogenic P. entomophila infection. 5. To our knowledge, this is the first study that addresses host tolerance to bacteria in relation to previous exposure, taking a multi-faceted approach to address the topic. Our results suggest that previous exposure comes with transient costs to resistance during the early stage of infection in this host-pathogen system and that infection persistence may be bacterium-specific. article_processing_charge: No author: - first_name: Megan full_name: Kutzer, Megan id: 29D0B332-F248-11E8-B48F-1D18A9856A87 last_name: Kutzer orcid: 0000-0002-8696-6978 - first_name: Joachim full_name: Kurtz, Joachim last_name: Kurtz - first_name: Sophie A.O. full_name: Armitage, Sophie A.O. last_name: Armitage citation: ama: 'Kutzer M, Kurtz J, Armitage SAO. Data from: A multi-faceted approach testing the effects of previous bacterial exposure on resistance and tolerance. 2019. doi:10.5061/dryad.9kj41f0' apa: 'Kutzer, M., Kurtz, J., & Armitage, S. A. O. (2019). Data from: A multi-faceted approach testing the effects of previous bacterial exposure on resistance and tolerance. Dryad. https://doi.org/10.5061/dryad.9kj41f0' chicago: 'Kutzer, Megan, Joachim Kurtz, and Sophie A.O. Armitage. “Data from: A Multi-Faceted Approach Testing the Effects of Previous Bacterial Exposure on Resistance and Tolerance.” Dryad, 2019. https://doi.org/10.5061/dryad.9kj41f0.' ieee: 'M. Kutzer, J. Kurtz, and S. A. O. Armitage, “Data from: A multi-faceted approach testing the effects of previous bacterial exposure on resistance and tolerance.” Dryad, 2019.' ista: 'Kutzer M, Kurtz J, Armitage SAO. 2019. Data from: A multi-faceted approach testing the effects of previous bacterial exposure on resistance and tolerance, Dryad, 10.5061/dryad.9kj41f0.' mla: 'Kutzer, Megan, et al. Data from: A Multi-Faceted Approach Testing the Effects of Previous Bacterial Exposure on Resistance and Tolerance. Dryad, 2019, doi:10.5061/dryad.9kj41f0.' short: M. Kutzer, J. Kurtz, S.A.O. Armitage, (2019). date_created: 2021-08-06T12:06:40Z date_published: 2019-02-05T00:00:00Z date_updated: 2023-08-25T08:04:52Z day: '05' department: - _id: SyCr doi: 10.5061/dryad.9kj41f0 main_file_link: - open_access: '1' url: https://doi.org/10.5061/dryad.9kj41f0 month: '02' oa: 1 oa_version: Published Version publisher: Dryad related_material: record: - id: '6105' relation: used_in_publication status: public status: public title: 'Data from: A multi-faceted approach testing the effects of previous bacterial exposure on resistance and tolerance' type: research_data_reference user_id: 6785fbc1-c503-11eb-8a32-93094b40e1cf year: '2019' ... --- _id: '6086' abstract: - lang: eng text: We show that linear analytic cocycles where all Lyapunov exponents are negative infinite are nilpotent. For such one-frequency cocycles we show that they can be analytically conjugated to an upper triangular cocycle or a Jordan normal form. As a consequence, an arbitrarily small analytic perturbation leads to distinct Lyapunov exponents. Moreover, in the one-frequency case where the th Lyapunov exponent is finite and the st negative infinite, we obtain a simple criterion for domination in which case there is a splitting into a nilpotent part and an invertible part. article_processing_charge: No author: - first_name: Christian full_name: Sadel, Christian id: 4760E9F8-F248-11E8-B48F-1D18A9856A87 last_name: Sadel orcid: 0000-0001-8255-3968 - first_name: Disheng full_name: Xu, Disheng last_name: Xu citation: ama: Sadel C, Xu D. Singular analytic linear cocycles with negative infinite Lyapunov exponents. Ergodic Theory and Dynamical Systems. 2019;39(4):1082-1098. doi:10.1017/etds.2017.52 apa: Sadel, C., & Xu, D. (2019). Singular analytic linear cocycles with negative infinite Lyapunov exponents. Ergodic Theory and Dynamical Systems. Cambridge University Press. https://doi.org/10.1017/etds.2017.52 chicago: Sadel, Christian, and Disheng Xu. “Singular Analytic Linear Cocycles with Negative Infinite Lyapunov Exponents.” Ergodic Theory and Dynamical Systems. Cambridge University Press, 2019. https://doi.org/10.1017/etds.2017.52. ieee: C. Sadel and D. Xu, “Singular analytic linear cocycles with negative infinite Lyapunov exponents,” Ergodic Theory and Dynamical Systems, vol. 39, no. 4. Cambridge University Press, pp. 1082–1098, 2019. ista: Sadel C, Xu D. 2019. Singular analytic linear cocycles with negative infinite Lyapunov exponents. Ergodic Theory and Dynamical Systems. 39(4), 1082–1098. mla: Sadel, Christian, and Disheng Xu. “Singular Analytic Linear Cocycles with Negative Infinite Lyapunov Exponents.” Ergodic Theory and Dynamical Systems, vol. 39, no. 4, Cambridge University Press, 2019, pp. 1082–98, doi:10.1017/etds.2017.52. short: C. Sadel, D. Xu, Ergodic Theory and Dynamical Systems 39 (2019) 1082–1098. date_created: 2019-03-10T22:59:18Z date_published: 2019-04-01T00:00:00Z date_updated: 2023-08-25T08:03:30Z day: '01' department: - _id: LaEr doi: 10.1017/etds.2017.52 ec_funded: 1 external_id: arxiv: - '1601.06118' isi: - '000459725600012' intvolume: ' 39' isi: 1 issue: '4' language: - iso: eng main_file_link: - open_access: '1' url: https://arxiv.org/abs/1601.06118 month: '04' oa: 1 oa_version: Preprint page: 1082-1098 project: - _id: 25681D80-B435-11E9-9278-68D0E5697425 call_identifier: FP7 grant_number: '291734' name: International IST Postdoc Fellowship Programme publication: Ergodic Theory and Dynamical Systems publication_status: published publisher: Cambridge University Press quality_controlled: '1' scopus_import: '1' status: public title: Singular analytic linear cocycles with negative infinite Lyapunov exponents type: journal_article user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8 volume: 39 year: '2019' ... --- _id: '6102' abstract: - lang: eng text: 'Light is a union of electric and magnetic fields, and nowhere is the complex relationship between these fields more evident than in the near fields of nanophotonic structures. There, complicated electric and magnetic fields varying over subwavelength scales are generally present, which results in photonic phenomena such as extraordinary optical momentum, superchiral fields, and a complex spatial evolution of optical singularities. An understanding of such phenomena requires nanoscale measurements of the complete optical field vector. Although the sensitivity of near- field scanning optical microscopy to the complete electromagnetic field was recently demonstrated, a separation of different components required a priori knowledge of the sample. Here, we introduce a robust algorithm that can disentangle all six electric and magnetic field components from a single near-field measurement without any numerical modeling of the structure. As examples, we unravel the fields of two prototypical nanophotonic structures: a photonic crystal waveguide and a plasmonic nanowire. These results pave the way for new studies of complex photonic phenomena at the nanoscale and for the design of structures that optimize their optical behavior.' article_number: '28' article_processing_charge: No author: - first_name: B. full_name: Le Feber, B. last_name: Le Feber - first_name: J. E. full_name: Sipe, J. E. last_name: Sipe - first_name: Matthias full_name: Wulf, Matthias id: 45598606-F248-11E8-B48F-1D18A9856A87 last_name: Wulf orcid: 0000-0001-6613-1378 - first_name: L. full_name: Kuipers, L. last_name: Kuipers - first_name: N. full_name: Rotenberg, N. last_name: Rotenberg citation: ama: 'Le Feber B, Sipe JE, Wulf M, Kuipers L, Rotenberg N. A full vectorial mapping of nanophotonic light fields. Light: Science and Applications. 2019;8(1). doi:10.1038/s41377-019-0124-3' apa: 'Le Feber, B., Sipe, J. E., Wulf, M., Kuipers, L., & Rotenberg, N. (2019). A full vectorial mapping of nanophotonic light fields. Light: Science and Applications. Springer Nature. https://doi.org/10.1038/s41377-019-0124-3' chicago: 'Le Feber, B., J. E. Sipe, Matthias Wulf, L. Kuipers, and N. Rotenberg. “A Full Vectorial Mapping of Nanophotonic Light Fields.” Light: Science and Applications. Springer Nature, 2019. https://doi.org/10.1038/s41377-019-0124-3.' ieee: 'B. Le Feber, J. E. Sipe, M. Wulf, L. Kuipers, and N. Rotenberg, “A full vectorial mapping of nanophotonic light fields,” Light: Science and Applications, vol. 8, no. 1. Springer Nature, 2019.' ista: 'Le Feber B, Sipe JE, Wulf M, Kuipers L, Rotenberg N. 2019. A full vectorial mapping of nanophotonic light fields. Light: Science and Applications. 8(1), 28.' mla: 'Le Feber, B., et al. “A Full Vectorial Mapping of Nanophotonic Light Fields.” Light: Science and Applications, vol. 8, no. 1, 28, Springer Nature, 2019, doi:10.1038/s41377-019-0124-3.' short: 'B. Le Feber, J.E. Sipe, M. Wulf, L. Kuipers, N. Rotenberg, Light: Science and Applications 8 (2019).' date_created: 2019-03-17T22:59:13Z date_published: 2019-03-06T00:00:00Z date_updated: 2023-08-25T08:06:10Z day: '06' ddc: - '530' department: - _id: JoFi doi: 10.1038/s41377-019-0124-3 external_id: arxiv: - '1803.10145' isi: - '000460470700004' file: - access_level: open_access checksum: d71e528cff9c56f70ccc29dd7005257f content_type: application/pdf creator: dernst date_created: 2019-03-18T08:08:22Z date_updated: 2020-07-14T12:47:19Z file_id: '6108' file_name: 2019_Light_LeFeber.pdf file_size: 1119947 relation: main_file file_date_updated: 2020-07-14T12:47:19Z has_accepted_license: '1' intvolume: ' 8' isi: 1 issue: '1' language: - iso: eng month: '03' oa: 1 oa_version: Published Version publication: 'Light: Science and Applications' publication_identifier: eissn: - '20477538' issn: - '20955545' publication_status: published publisher: Springer Nature quality_controlled: '1' scopus_import: '1' status: public title: A full vectorial mapping of nanophotonic light fields 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: 4359f0d1-fa6c-11eb-b949-802e58b17ae8 volume: 8 year: '2019' ... --- _id: '6104' abstract: - lang: eng text: Abiotic stress poses constant challenges for plant survival and is a serious problem for global agricultural productivity. On a molecular level, stress conditions result in elevation of reactive oxygen species (ROS) production causing oxidative stress associated with oxidation of proteins and nucleic acids as well as impairment of membrane functions. Adaptation of root growth to ROS accumulation is facilitated through modification of auxin and cytokinin hormone homeostasis. Here, we report that in Arabidopsis root meristem, ROS-induced changes of auxin levels correspond to decreased abundance of PIN auxin efflux carriers at the plasma membrane (PM). Specifically, increase in H2O2 levels affects PIN2 endocytic recycling. We show that the PIN2 intracellular trafficking during adaptation to oxidative stress requires the function of the ADP-ribosylation factor (ARF)-guanine-nucleotide exchange factor (GEF) BEN1, an actin-associated regulator of the trafficking from the PM to early endosomes and, presumably, indirectly, trafficking to the vacuoles. We propose that H2O2 levels affect the actin dynamics thus modulating ARF-GEF-dependent trafficking of PIN2. This mechanism provides a way how root growth acclimates to stress and adapts to a changing environment. article_processing_charge: No author: - first_name: Marta full_name: Zwiewka, Marta last_name: Zwiewka - first_name: Agnieszka full_name: Bielach, Agnieszka last_name: Bielach - first_name: Prashanth full_name: Tamizhselvan, Prashanth last_name: Tamizhselvan - first_name: Sharmila full_name: Madhavan, Sharmila last_name: Madhavan - first_name: Eman Elrefaay full_name: Ryad, Eman Elrefaay last_name: Ryad - first_name: Shutang full_name: Tan, Shutang id: 2DE75584-F248-11E8-B48F-1D18A9856A87 last_name: Tan orcid: 0000-0002-0471-8285 - first_name: Mónika full_name: Hrtyan, Mónika id: 45A71A74-F248-11E8-B48F-1D18A9856A87 last_name: Hrtyan - first_name: Petre full_name: Dobrev, Petre last_name: Dobrev - first_name: Radomira full_name: Vanková, Radomira last_name: Vanková - first_name: Jiří full_name: Friml, Jiří id: 4159519E-F248-11E8-B48F-1D18A9856A87 last_name: Friml orcid: 0000-0002-8302-7596 - first_name: Vanesa B. full_name: Tognetti, Vanesa B. last_name: Tognetti citation: ama: Zwiewka M, Bielach A, Tamizhselvan P, et al. Root adaptation to H2O2-induced oxidative stress by ARF-GEF BEN1- and cytoskeleton-mediated PIN2 trafficking. Plant and Cell Physiology. 2019;60(2):255-273. doi:10.1093/pcp/pcz001 apa: Zwiewka, M., Bielach, A., Tamizhselvan, P., Madhavan, S., Ryad, E. E., Tan, S., … Tognetti, V. B. (2019). Root adaptation to H2O2-induced oxidative stress by ARF-GEF BEN1- and cytoskeleton-mediated PIN2 trafficking. Plant and Cell Physiology. Oxford University Press. https://doi.org/10.1093/pcp/pcz001 chicago: Zwiewka, Marta, Agnieszka Bielach, Prashanth Tamizhselvan, Sharmila Madhavan, Eman Elrefaay Ryad, Shutang Tan, Mónika Hrtyan, et al. “Root Adaptation to H2O2-Induced Oxidative Stress by ARF-GEF BEN1- and Cytoskeleton-Mediated PIN2 Trafficking.” Plant and Cell Physiology. Oxford University Press, 2019. https://doi.org/10.1093/pcp/pcz001. ieee: M. Zwiewka et al., “Root adaptation to H2O2-induced oxidative stress by ARF-GEF BEN1- and cytoskeleton-mediated PIN2 trafficking,” Plant and Cell Physiology, vol. 60, no. 2. Oxford University Press, pp. 255–273, 2019. ista: Zwiewka M, Bielach A, Tamizhselvan P, Madhavan S, Ryad EE, Tan S, Hrtyan M, Dobrev P, Vanková R, Friml J, Tognetti VB. 2019. Root adaptation to H2O2-induced oxidative stress by ARF-GEF BEN1- and cytoskeleton-mediated PIN2 trafficking. Plant and Cell Physiology. 60(2), 255–273. mla: Zwiewka, Marta, et al. “Root Adaptation to H2O2-Induced Oxidative Stress by ARF-GEF BEN1- and Cytoskeleton-Mediated PIN2 Trafficking.” Plant and Cell Physiology, vol. 60, no. 2, Oxford University Press, 2019, pp. 255–73, doi:10.1093/pcp/pcz001. short: M. Zwiewka, A. Bielach, P. Tamizhselvan, S. Madhavan, E.E. Ryad, S. Tan, M. Hrtyan, P. Dobrev, R. Vanková, J. Friml, V.B. Tognetti, Plant and Cell Physiology 60 (2019) 255–273. date_created: 2019-03-17T22:59:14Z date_published: 2019-02-01T00:00:00Z date_updated: 2023-08-25T08:05:28Z day: '01' department: - _id: JiFr doi: 10.1093/pcp/pcz001 external_id: isi: - '000459634300002' pmid: - '30668780' intvolume: ' 60' isi: 1 issue: '2' language: - iso: eng month: '02' oa_version: None page: 255-273 pmid: 1 publication: Plant and Cell Physiology publication_identifier: eissn: - 1471-9053 issn: - 0032-0781 publication_status: published publisher: Oxford University Press quality_controlled: '1' scopus_import: '1' status: public title: Root adaptation to H2O2-induced oxidative stress by ARF-GEF BEN1- and cytoskeleton-mediated PIN2 trafficking type: journal_article user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8 volume: 60 year: '2019' ... --- _id: '6191' abstract: - lang: eng text: The formation of self-organized patterns is key to the morphogenesis of multicellular organisms, although a comprehensive theory of biological pattern formation is still lacking. Here, we propose a minimal model combining tissue mechanics with morphogen turnover and transport to explore routes to patterning. Our active description couples morphogen reaction and diffusion, which impact cell differentiation and tissue mechanics, to a two-phase poroelastic rheology, where one tissue phase consists of a poroelastic cell network and the other one of a permeating extracellular fluid, which provides a feedback by actively transporting morphogens. While this model encompasses previous theories approximating tissues to inert monophasic media, such as Turing’s reaction–diffusion model, it overcomes some of their key limitations permitting pattern formation via any two-species biochemical kinetics due to mechanically induced cross-diffusion flows. Moreover, we describe a qualitatively different advection-driven Keller–Segel instability which allows for the formation of patterns with a single morphogen and whose fundamental mode pattern robustly scales with tissue size. We discuss the potential relevance of these findings for tissue morphogenesis. article_processing_charge: No author: - first_name: Pierre full_name: Recho, Pierre last_name: Recho - first_name: Adrien full_name: Hallou, Adrien last_name: Hallou - first_name: Edouard B full_name: Hannezo, Edouard B id: 3A9DB764-F248-11E8-B48F-1D18A9856A87 last_name: Hannezo orcid: 0000-0001-6005-1561 citation: ama: Recho P, Hallou A, Hannezo EB. Theory of mechanochemical patterning in biphasic biological tissues. Proceedings of the National Academy of Sciences of the United States of America. 2019;116(12):5344-5349. doi:10.1073/pnas.1813255116 apa: Recho, P., Hallou, A., & Hannezo, E. B. (2019). Theory of mechanochemical patterning in biphasic biological tissues. Proceedings of the National Academy of Sciences of the United States of America. National Academy of Sciences. https://doi.org/10.1073/pnas.1813255116 chicago: Recho, Pierre, Adrien Hallou, and Edouard B Hannezo. “Theory of Mechanochemical Patterning in Biphasic Biological Tissues.” Proceedings of the National Academy of Sciences of the United States of America. National Academy of Sciences, 2019. https://doi.org/10.1073/pnas.1813255116. ieee: P. Recho, A. Hallou, and E. B. Hannezo, “Theory of mechanochemical patterning in biphasic biological tissues,” Proceedings of the National Academy of Sciences of the United States of America, vol. 116, no. 12. National Academy of Sciences, pp. 5344–5349, 2019. ista: Recho P, Hallou A, Hannezo EB. 2019. Theory of mechanochemical patterning in biphasic biological tissues. Proceedings of the National Academy of Sciences of the United States of America. 116(12), 5344–5349. mla: Recho, Pierre, et al. “Theory of Mechanochemical Patterning in Biphasic Biological Tissues.” Proceedings of the National Academy of Sciences of the United States of America, vol. 116, no. 12, National Academy of Sciences, 2019, pp. 5344–49, doi:10.1073/pnas.1813255116. short: P. Recho, A. Hallou, E.B. Hannezo, Proceedings of the National Academy of Sciences of the United States of America 116 (2019) 5344–5349. date_created: 2019-03-31T21:59:13Z date_published: 2019-03-19T00:00:00Z date_updated: 2023-08-25T08:57:30Z day: '19' ddc: - '570' department: - _id: EdHa doi: 10.1073/pnas.1813255116 external_id: isi: - '000461679000027' pmid: - '30819884' file: - access_level: open_access checksum: 8b67eee0ea8e5db61583e4d485215258 content_type: application/pdf creator: dernst date_created: 2019-04-03T14:10:30Z date_updated: 2020-07-14T12:47:23Z file_id: '6193' file_name: 2019_PNAS_Recho.pdf file_size: 3456045 relation: main_file file_date_updated: 2020-07-14T12:47:23Z has_accepted_license: '1' intvolume: ' 116' isi: 1 issue: '12' language: - iso: eng month: '03' oa: 1 oa_version: Published Version page: 5344-5349 pmid: 1 project: - _id: 268294B6-B435-11E9-9278-68D0E5697425 call_identifier: FWF grant_number: P31639 name: Active mechano-chemical description of the cell cytoskeleton publication: Proceedings of the National Academy of Sciences of the United States of America publication_identifier: eissn: - '10916490' issn: - '00278424' publication_status: published publisher: National Academy of Sciences quality_controlled: '1' related_material: link: - relation: supplementary_material url: www.pnas.org/lookup/suppl/doi:10.1073/pnas.1813255116/-/DCSupplemental scopus_import: '1' status: public title: Theory of mechanochemical patterning in biphasic biological tissues 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: 4359f0d1-fa6c-11eb-b949-802e58b17ae8 volume: 116 year: '2019' ...