[{"month":"06","day":"01","scopus_import":1,"doi":"10.1016/j.tibtech.2015.03.009","date_published":"2015-06-01T00:00:00Z","language":[{"iso":"eng"}],"publication":"Trends in Biotechnology","citation":{"chicago":"Angermayr, Andreas, Aleix Gorchs, and Klaas Hellingwerf. “Metabolic Engineering of Cyanobacteria for the Synthesis of Commodity Products.” Trends in Biotechnology. Elsevier, 2015. https://doi.org/10.1016/j.tibtech.2015.03.009.","mla":"Angermayr, Andreas, et al. “Metabolic Engineering of Cyanobacteria for the Synthesis of Commodity Products.” Trends in Biotechnology, vol. 33, no. 6, Elsevier, 2015, pp. 352–61, doi:10.1016/j.tibtech.2015.03.009.","short":"A. Angermayr, A. Gorchs, K. Hellingwerf, Trends in Biotechnology 33 (2015) 352–361.","ista":"Angermayr A, Gorchs A, Hellingwerf K. 2015. Metabolic engineering of cyanobacteria for the synthesis of commodity products. Trends in Biotechnology. 33(6), 352–361.","apa":"Angermayr, A., Gorchs, A., & Hellingwerf, K. (2015). Metabolic engineering of cyanobacteria for the synthesis of commodity products. Trends in Biotechnology. Elsevier. https://doi.org/10.1016/j.tibtech.2015.03.009","ieee":"A. Angermayr, A. Gorchs, and K. Hellingwerf, “Metabolic engineering of cyanobacteria for the synthesis of commodity products,” Trends in Biotechnology, vol. 33, no. 6. Elsevier, pp. 352–361, 2015.","ama":"Angermayr A, Gorchs A, Hellingwerf K. Metabolic engineering of cyanobacteria for the synthesis of commodity products. Trends in Biotechnology. 2015;33(6):352-361. doi:10.1016/j.tibtech.2015.03.009"},"quality_controlled":"1","page":"352 - 361","abstract":[{"text":"Through metabolic engineering cyanobacteria can be employed in biotechnology. Combining the capacity for oxygenic photosynthesis and carbon fixation with an engineered metabolic pathway allows carbon-based product formation from CO2, light, and water directly. Such cyanobacterial 'cell factories' are constructed to produce biofuels, bioplastics, and commodity chemicals. Efforts of metabolic engineers and synthetic biologists allow the modification of the intermediary metabolism at various branching points, expanding the product range. The new biosynthesis routes 'tap' the metabolism ever more efficiently, particularly through the engineering of driving forces and utilization of cofactors generated during the light reactions of photosynthesis, resulting in higher product titers. High rates of carbon rechanneling ultimately allow an almost-complete allocation of fixed carbon to product above biomass.","lang":"eng"}],"publist_id":"5585","issue":"6","type":"journal_article","author":[{"full_name":"Angermayr, Andreas","id":"4677C796-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0001-8619-2223","first_name":"Andreas","last_name":"Angermayr"},{"full_name":"Gorchs, Aleix","last_name":"Gorchs","first_name":"Aleix"},{"last_name":"Hellingwerf","first_name":"Klaas","full_name":"Hellingwerf, Klaas"}],"date_updated":"2021-01-12T06:51:46Z","date_created":"2018-12-11T11:52:52Z","oa_version":"None","volume":33,"year":"2015","_id":"1586","user_id":"3E5EF7F0-F248-11E8-B48F-1D18A9856A87","status":"public","title":"Metabolic engineering of cyanobacteria for the synthesis of commodity products","publication_status":"published","intvolume":" 33","department":[{"_id":"ToBo"}],"publisher":"Elsevier"},{"author":[{"last_name":"Hammar","first_name":"Petter","full_name":"Hammar, Petter"},{"orcid":"0000-0001-8619-2223","id":"4677C796-F248-11E8-B48F-1D18A9856A87","last_name":"Angermayr","first_name":"Andreas","full_name":"Angermayr, Andreas"},{"first_name":"Staffan","last_name":"Sjostrom","full_name":"Sjostrom, Staffan"},{"full_name":"Van Der Meer, Josefin","last_name":"Van Der Meer","first_name":"Josefin"},{"full_name":"Hellingwerf, Klaas","last_name":"Hellingwerf","first_name":"Klaas"},{"full_name":"Hudson, Elton","last_name":"Hudson","first_name":"Elton"},{"full_name":"Joensson, Hakaan","first_name":"Hakaan","last_name":"Joensson"}],"date_created":"2018-12-11T11:53:05Z","date_updated":"2021-01-12T06:52:04Z","volume":8,"year":"2015","publication_status":"published","publisher":"BioMed Central","department":[{"_id":"ToBo"}],"file_date_updated":"2020-07-14T12:45:07Z","publist_id":"5537","article_number":"193","doi":"10.1186/s13068-015-0380-2","language":[{"iso":"eng"}],"tmp":{"name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","short":"CC BY (4.0)","image":"/images/cc_by.png"},"oa":1,"quality_controlled":"1","month":"11","pubrep_id":"467","oa_version":"Published Version","file":[{"access_level":"open_access","file_name":"IST-2016-467-v1+1_s13068-015-0380-2.pdf","creator":"system","content_type":"application/pdf","file_size":2914089,"file_id":"4796","relation":"main_file","checksum":"172b0b6f4eb2e5c22b7cec1d57dc0107","date_created":"2018-12-12T10:10:11Z","date_updated":"2020-07-14T12:45:07Z"}],"user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","_id":"1623","title":"Single-cell screening of photosynthetic growth and lactate production by cyanobacteria","status":"public","ddc":["570"],"intvolume":" 8","abstract":[{"lang":"eng","text":"Background\r\nPhotosynthetic cyanobacteria are attractive for a range of biotechnological applications including biofuel production. However, due to slow growth, screening of mutant libraries using microtiter plates is not feasible.\r\nResults\r\nWe present a method for high-throughput, single-cell analysis and sorting of genetically engineered l-lactate-producing strains of Synechocystis sp. PCC6803. A microfluidic device is used to encapsulate single cells in picoliter droplets, assay the droplets for l-lactate production, and sort strains with high productivity. We demonstrate the separation of low- and high-producing reference strains, as well as enrichment of a more productive l-lactate-synthesizing population after UV-induced mutagenesis. The droplet platform also revealed population heterogeneity in photosynthetic growth and lactate production, as well as the presence of metabolically stalled cells.\r\nConclusions\r\nThe workflow will facilitate metabolic engineering and directed evolution studies and will be useful in studies of cyanobacteria biochemistry and physiology.\r\n"}],"issue":"1","type":"journal_article","date_published":"2015-11-25T00:00:00Z","publication":"Biotechnology for Biofuels","citation":{"ama":"Hammar P, Angermayr A, Sjostrom S, et al. Single-cell screening of photosynthetic growth and lactate production by cyanobacteria. Biotechnology for Biofuels. 2015;8(1). doi:10.1186/s13068-015-0380-2","ieee":"P. Hammar et al., “Single-cell screening of photosynthetic growth and lactate production by cyanobacteria,” Biotechnology for Biofuels, vol. 8, no. 1. BioMed Central, 2015.","apa":"Hammar, P., Angermayr, A., Sjostrom, S., Van Der Meer, J., Hellingwerf, K., Hudson, E., & Joensson, H. (2015). Single-cell screening of photosynthetic growth and lactate production by cyanobacteria. Biotechnology for Biofuels. BioMed Central. https://doi.org/10.1186/s13068-015-0380-2","ista":"Hammar P, Angermayr A, Sjostrom S, Van Der Meer J, Hellingwerf K, Hudson E, Joensson H. 2015. Single-cell screening of photosynthetic growth and lactate production by cyanobacteria. Biotechnology for Biofuels. 8(1), 193.","short":"P. Hammar, A. Angermayr, S. Sjostrom, J. Van Der Meer, K. Hellingwerf, E. Hudson, H. Joensson, Biotechnology for Biofuels 8 (2015).","mla":"Hammar, Petter, et al. “Single-Cell Screening of Photosynthetic Growth and Lactate Production by Cyanobacteria.” Biotechnology for Biofuels, vol. 8, no. 1, 193, BioMed Central, 2015, doi:10.1186/s13068-015-0380-2.","chicago":"Hammar, Petter, Andreas Angermayr, Staffan Sjostrom, Josefin Van Der Meer, Klaas Hellingwerf, Elton Hudson, and Hakaan Joensson. “Single-Cell Screening of Photosynthetic Growth and Lactate Production by Cyanobacteria.” Biotechnology for Biofuels. BioMed Central, 2015. https://doi.org/10.1186/s13068-015-0380-2."},"day":"25","has_accepted_license":"1","scopus_import":1},{"volume":27,"date_updated":"2021-01-12T06:53:21Z","date_created":"2018-12-11T11:54:08Z","author":[{"id":"3E6DB97A-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0003-4398-476X","first_name":"Mark Tobias","last_name":"Bollenbach","full_name":"Bollenbach, Mark Tobias"}],"department":[{"_id":"ToBo"}],"publisher":"Elsevier","publication_status":"published","year":"2015","ec_funded":1,"publist_id":"5298","file_date_updated":"2020-07-14T12:45:17Z","language":[{"iso":"eng"}],"doi":"10.1016/j.mib.2015.05.008","project":[{"name":"Revealing the mechanisms underlying drug interactions","call_identifier":"FWF","grant_number":"P27201-B22","_id":"25E9AF9E-B435-11E9-9278-68D0E5697425"},{"grant_number":"303507","_id":"25E83C2C-B435-11E9-9278-68D0E5697425","name":"Optimality principles in responses to antibiotics","call_identifier":"FP7"},{"_id":"25EB3A80-B435-11E9-9278-68D0E5697425","grant_number":"RGP0042/2013","name":"Revealing the fundamental limits of cell growth"}],"quality_controlled":"1","tmp":{"name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","short":"CC BY (4.0)","image":"/images/cc_by.png"},"oa":1,"month":"06","oa_version":"Published Version","file":[{"file_name":"IST-2016-493-v1+1_1-s2.0-S1369527415000594-main.pdf","access_level":"open_access","file_size":1047255,"content_type":"application/pdf","creator":"system","relation":"main_file","file_id":"5277","date_updated":"2020-07-14T12:45:17Z","date_created":"2018-12-12T10:17:23Z","checksum":"1683bb0f42ef892a5b3b71a050d65d25"}],"pubrep_id":"493","intvolume":" 27","status":"public","ddc":["570"],"title":"Antimicrobial interactions: Mechanisms and implications for drug discovery and resistance evolution","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","_id":"1810","abstract":[{"text":"Combining antibiotics is a promising strategy for increasing treatment efficacy and for controlling resistance evolution. When drugs are combined, their effects on cells may be amplified or weakened, that is the drugs may show synergistic or antagonistic interactions. Recent work revealed the underlying mechanisms of such drug interactions by elucidating the drugs'; joint effects on cell physiology. Moreover, new treatment strategies that use drug combinations to exploit evolutionary tradeoffs were shown to affect the rate of resistance evolution in predictable ways. High throughput studies have further identified drug candidates based on their interactions with established antibiotics and general principles that enable the prediction of drug interactions were suggested. Overall, the conceptual and technical foundation for the rational design of potent drug combinations is rapidly developing.","lang":"eng"}],"type":"journal_article","date_published":"2015-06-01T00:00:00Z","page":"1 - 9","citation":{"chicago":"Bollenbach, Mark Tobias. “Antimicrobial Interactions: Mechanisms and Implications for Drug Discovery and Resistance Evolution.” Current Opinion in Microbiology. Elsevier, 2015. https://doi.org/10.1016/j.mib.2015.05.008.","mla":"Bollenbach, Mark Tobias. “Antimicrobial Interactions: Mechanisms and Implications for Drug Discovery and Resistance Evolution.” Current Opinion in Microbiology, vol. 27, Elsevier, 2015, pp. 1–9, doi:10.1016/j.mib.2015.05.008.","short":"M.T. Bollenbach, Current Opinion in Microbiology 27 (2015) 1–9.","ista":"Bollenbach MT. 2015. Antimicrobial interactions: Mechanisms and implications for drug discovery and resistance evolution. Current Opinion in Microbiology. 27, 1–9.","ieee":"M. T. Bollenbach, “Antimicrobial interactions: Mechanisms and implications for drug discovery and resistance evolution,” Current Opinion in Microbiology, vol. 27. Elsevier, pp. 1–9, 2015.","apa":"Bollenbach, M. T. (2015). Antimicrobial interactions: Mechanisms and implications for drug discovery and resistance evolution. Current Opinion in Microbiology. Elsevier. https://doi.org/10.1016/j.mib.2015.05.008","ama":"Bollenbach MT. Antimicrobial interactions: Mechanisms and implications for drug discovery and resistance evolution. Current Opinion in Microbiology. 2015;27:1-9. doi:10.1016/j.mib.2015.05.008"},"publication":"Current Opinion in Microbiology","has_accepted_license":"1","day":"01","scopus_import":1},{"month":"04","doi":"10.15252/msb.20156098","language":[{"iso":"eng"}],"oa":1,"tmp":{"name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","short":"CC BY (4.0)","image":"/images/cc_by.png"},"project":[{"name":"Revealing the mechanisms underlying drug interactions","call_identifier":"FWF","grant_number":"P27201-B22","_id":"25E9AF9E-B435-11E9-9278-68D0E5697425"},{"name":"Revealing the fundamental limits of cell growth","_id":"25EB3A80-B435-11E9-9278-68D0E5697425","grant_number":"RGP0042/2013"},{"grant_number":"303507","_id":"25E83C2C-B435-11E9-9278-68D0E5697425","call_identifier":"FP7","name":"Optimality principles in responses to antibiotics"}],"quality_controlled":"1","publist_id":"5283","ec_funded":1,"file_date_updated":"2020-07-14T12:45:17Z","article_number":"807","author":[{"full_name":"Chevereau, Guillaume","id":"424D78A0-F248-11E8-B48F-1D18A9856A87","last_name":"Chevereau","first_name":"Guillaume"},{"orcid":"0000-0003-4398-476X","id":"3E6DB97A-F248-11E8-B48F-1D18A9856A87","last_name":"Bollenbach","first_name":"Mark Tobias","full_name":"Bollenbach, Mark Tobias"}],"volume":11,"date_updated":"2021-01-12T06:53:26Z","date_created":"2018-12-11T11:54:12Z","year":"2015","department":[{"_id":"ToBo"}],"publisher":"Nature Publishing Group","publication_status":"published","has_accepted_license":"1","day":"01","scopus_import":1,"date_published":"2015-04-01T00:00:00Z","citation":{"ama":"Chevereau G, Bollenbach MT. Systematic discovery of drug interaction mechanisms. Molecular Systems Biology. 2015;11(4). doi:10.15252/msb.20156098","ista":"Chevereau G, Bollenbach MT. 2015. Systematic discovery of drug interaction mechanisms. Molecular Systems Biology. 11(4), 807.","apa":"Chevereau, G., & Bollenbach, M. T. (2015). Systematic discovery of drug interaction mechanisms. Molecular Systems Biology. Nature Publishing Group. https://doi.org/10.15252/msb.20156098","ieee":"G. Chevereau and M. T. Bollenbach, “Systematic discovery of drug interaction mechanisms,” Molecular Systems Biology, vol. 11, no. 4. Nature Publishing Group, 2015.","mla":"Chevereau, Guillaume, and Mark Tobias Bollenbach. “Systematic Discovery of Drug Interaction Mechanisms.” Molecular Systems Biology, vol. 11, no. 4, 807, Nature Publishing Group, 2015, doi:10.15252/msb.20156098.","short":"G. Chevereau, M.T. Bollenbach, Molecular Systems Biology 11 (2015).","chicago":"Chevereau, Guillaume, and Mark Tobias Bollenbach. “Systematic Discovery of Drug Interaction Mechanisms.” Molecular Systems Biology. Nature Publishing Group, 2015. https://doi.org/10.15252/msb.20156098."},"publication":"Molecular Systems Biology","issue":"4","abstract":[{"lang":"eng","text":"Abstract Drug combinations are increasingly important in disease treatments, for combating drug resistance, and for elucidating fundamental relationships in cell physiology. When drugs are combined, their individual effects on cells may be amplified or weakened. Such drug interactions are crucial for treatment efficacy, but their underlying mechanisms remain largely unknown. To uncover the causes of drug interactions, we developed a systematic approach based on precise quantification of the individual and joint effects of antibiotics on growth of genome-wide Escherichia coli gene deletion strains. We found that drug interactions between antibiotics representing the main modes of action are highly robust to genetic perturbation. This robustness is encapsulated in a general principle of bacterial growth, which enables the quantitative prediction of mutant growth rates under drug combinations. Rare violations of this principle exposed recurring cellular functions controlling drug interactions. In particular, we found that polysaccharide and ATP synthesis control multiple drug interactions with previously unexplained mechanisms, and small molecule adjuvants targeting these functions synthetically reshape drug interactions in predictable ways. These results provide a new conceptual framework for the design of multidrug combinations and suggest that there are universal mechanisms at the heart of most drug interactions. Synopsis A general principle of bacterial growth enables the prediction of mutant growth rates under drug combinations. Rare violations of this principle expose cellular functions that control drug interactions and can be targeted by small molecules to alter drug interactions in predictable ways. Drug interactions between antibiotics are highly robust to genetic perturbations. A general principle of bacterial growth enables the prediction of mutant growth rates under drug combinations. Rare violations of this principle expose cellular functions that control drug interactions. Diverse drug interactions are controlled by recurring cellular functions, including LPS synthesis and ATP synthesis. A general principle of bacterial growth enables the prediction of mutant growth rates under drug combinations. Rare violations of this principle expose cellular functions that control drug interactions and can be targeted by small molecules to alter drug interactions in predictable ways."}],"type":"journal_article","pubrep_id":"395","file":[{"relation":"main_file","file_id":"5087","checksum":"4289b518fbe2166682fb1a1ef9b405f3","date_created":"2018-12-12T10:14:34Z","date_updated":"2020-07-14T12:45:17Z","access_level":"open_access","file_name":"IST-2015-395-v1+1_807.full.pdf","content_type":"application/pdf","file_size":1273573,"creator":"system"}],"oa_version":"Published Version","_id":"1823","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","intvolume":" 11","status":"public","title":"Systematic discovery of drug interaction mechanisms","ddc":["570"]},{"type":"research_data_reference","_id":"9711","year":"2015","user_id":"6785fbc1-c503-11eb-8a32-93094b40e1cf","publisher":"Public Library of Science","department":[{"_id":"ToBo"}],"title":"Excel file containing the raw data for all figures","status":"public","related_material":{"record":[{"id":"1619","relation":"used_in_publication","status":"public"}]},"author":[{"id":"424D78A0-F248-11E8-B48F-1D18A9856A87","last_name":"Chevereau","first_name":"Guillaume","full_name":"Chevereau, Guillaume"},{"last_name":"Lukacisinova","first_name":"Marta","orcid":"0000-0002-2519-8004","id":"4342E402-F248-11E8-B48F-1D18A9856A87","full_name":"Lukacisinova, Marta"},{"last_name":"Batur","first_name":"Tugce","full_name":"Batur, Tugce"},{"full_name":"Guvenek, Aysegul","first_name":"Aysegul","last_name":"Guvenek"},{"full_name":"Ayhan, Dilay Hazal","first_name":"Dilay Hazal","last_name":"Ayhan"},{"full_name":"Toprak, Erdal","last_name":"Toprak","first_name":"Erdal"},{"full_name":"Bollenbach, Mark Tobias","id":"3E6DB97A-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0003-4398-476X","first_name":"Mark Tobias","last_name":"Bollenbach"}],"oa_version":"Published Version","date_created":"2021-07-23T11:53:50Z","date_updated":"2023-02-23T10:07:02Z","article_processing_charge":"No","day":"18","month":"11","citation":{"short":"G. Chevereau, M. Lukacisinova, T. Batur, A. Guvenek, D.H. Ayhan, E. Toprak, M.T. Bollenbach, (2015).","mla":"Chevereau, Guillaume, et al. Excel File Containing the Raw Data for All Figures. Public Library of Science, 2015, doi:10.1371/journal.pbio.1002299.s001.","chicago":"Chevereau, Guillaume, Marta Lukacisinova, Tugce Batur, Aysegul Guvenek, Dilay Hazal Ayhan, Erdal Toprak, and Mark Tobias Bollenbach. “Excel File Containing the Raw Data for All Figures.” Public Library of Science, 2015. https://doi.org/10.1371/journal.pbio.1002299.s001.","ama":"Chevereau G, Lukacisinova M, Batur T, et al. Excel file containing the raw data for all figures. 2015. doi:10.1371/journal.pbio.1002299.s001","ieee":"G. Chevereau et al., “Excel file containing the raw data for all figures.” Public Library of Science, 2015.","apa":"Chevereau, G., Lukacisinova, M., Batur, T., Guvenek, A., Ayhan, D. H., Toprak, E., & Bollenbach, M. T. (2015). Excel file containing the raw data for all figures. Public Library of Science. https://doi.org/10.1371/journal.pbio.1002299.s001","ista":"Chevereau G, Lukacisinova M, Batur T, Guvenek A, Ayhan DH, Toprak E, Bollenbach MT. 2015. Excel file containing the raw data for all figures, Public Library of Science, 10.1371/journal.pbio.1002299.s001."},"doi":"10.1371/journal.pbio.1002299.s001","date_published":"2015-11-18T00:00:00Z"},{"month":"11","day":"18","article_processing_charge":"No","citation":{"chicago":"Chevereau, Guillaume, Marta Lukacisinova, Tugce Batur, Aysegul Guvenek, Dilay Hazal Ayhan, Erdal Toprak, and Mark Tobias Bollenbach. “Gene Ontology Enrichment Analysis for the Most Sensitive Gene Deletion Strains for All Drugs.” Public Library of Science, 2015. https://doi.org/10.1371/journal.pbio.1002299.s008.","mla":"Chevereau, Guillaume, et al. Gene Ontology Enrichment Analysis for the Most Sensitive Gene Deletion Strains for All Drugs. Public Library of Science, 2015, doi:10.1371/journal.pbio.1002299.s008.","short":"G. Chevereau, M. Lukacisinova, T. Batur, A. Guvenek, D.H. Ayhan, E. Toprak, M.T. Bollenbach, (2015).","ista":"Chevereau G, Lukacisinova M, Batur T, Guvenek A, Ayhan DH, Toprak E, Bollenbach MT. 2015. Gene ontology enrichment analysis for the most sensitive gene deletion strains for all drugs, Public Library of Science, 10.1371/journal.pbio.1002299.s008.","apa":"Chevereau, G., Lukacisinova, M., Batur, T., Guvenek, A., Ayhan, D. H., Toprak, E., & Bollenbach, M. T. (2015). Gene ontology enrichment analysis for the most sensitive gene deletion strains for all drugs. Public Library of Science. https://doi.org/10.1371/journal.pbio.1002299.s008","ieee":"G. Chevereau et al., “Gene ontology enrichment analysis for the most sensitive gene deletion strains for all drugs.” Public Library of Science, 2015.","ama":"Chevereau G, Lukacisinova M, Batur T, et al. Gene ontology enrichment analysis for the most sensitive gene deletion strains for all drugs. 2015. doi:10.1371/journal.pbio.1002299.s008"},"doi":"10.1371/journal.pbio.1002299.s008","date_published":"2015-11-18T00:00:00Z","type":"research_data_reference","user_id":"6785fbc1-c503-11eb-8a32-93094b40e1cf","_id":"9765","year":"2015","status":"public","title":"Gene ontology enrichment analysis for the most sensitive gene deletion strains for all drugs","department":[{"_id":"ToBo"}],"publisher":"Public Library of Science","author":[{"id":"424D78A0-F248-11E8-B48F-1D18A9856A87","last_name":"Chevereau","first_name":"Guillaume","full_name":"Chevereau, Guillaume"},{"orcid":"0000-0002-2519-8004","id":"4342E402-F248-11E8-B48F-1D18A9856A87","last_name":"Lukacisinova","first_name":"Marta","full_name":"Lukacisinova, Marta"},{"full_name":"Batur, Tugce","last_name":"Batur","first_name":"Tugce"},{"full_name":"Guvenek, Aysegul","last_name":"Guvenek","first_name":"Aysegul"},{"last_name":"Ayhan","first_name":"Dilay Hazal","full_name":"Ayhan, Dilay Hazal"},{"full_name":"Toprak, Erdal","last_name":"Toprak","first_name":"Erdal"},{"orcid":"0000-0003-4398-476X","id":"3E6DB97A-F248-11E8-B48F-1D18A9856A87","last_name":"Bollenbach","first_name":"Mark Tobias","full_name":"Bollenbach, Mark Tobias"}],"related_material":{"record":[{"status":"public","relation":"used_in_publication","id":"1619"}]},"date_created":"2021-08-03T07:05:16Z","date_updated":"2023-02-23T10:07:02Z","oa_version":"Published Version"},{"month":"10","quality_controlled":"1","project":[{"_id":"25716A02-B435-11E9-9278-68D0E5697425","grant_number":"282300","call_identifier":"FP7","name":"Polarity and subcellular dynamics in plants"}],"tmp":{"name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","short":"CC BY (4.0)","image":"/images/cc_by.png"},"oa":1,"language":[{"iso":"eng"}],"doi":"10.12688/f1000research.7143.1","file_date_updated":"2020-07-14T12:44:59Z","publist_id":"5668","ec_funded":1,"publication_status":"published","department":[{"_id":"JiFr"},{"_id":"ToBo"}],"publisher":"F1000 Research","acknowledgement":"This work was supported by ERC Independent Research grant (ERC-2011-StG-20101109-PSDP to JF). JM internship was supported by the grant “Action Austria – Slovakia”.\r\nData associated with the article are available under the terms of the Creative Commons Zero \"No rights reserved\" data waiver (CC0 1.0 Public domain dedication). \r\n\r\nData availability: \r\nF1000Research: Dataset 1. Dataset 1, 10.5256/f1000research.7143.d104552\r\n\r\nF1000Research: Dataset 2. Dataset 2, 10.5256/f1000research.7143.d104553\r\n\r\nF1000Research: Dataset 3. Dataset 3, 10.5256/f1000research.7143.d104554","year":"2015","date_updated":"2023-10-10T14:10:24Z","date_created":"2018-12-11T11:52:26Z","volume":4,"author":[{"last_name":"Michalko","first_name":"Jaroslav","id":"483727CA-F248-11E8-B48F-1D18A9856A87","full_name":"Michalko, Jaroslav"},{"first_name":"Marta","last_name":"Dravecka","id":"4342E402-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-2519-8004","full_name":"Dravecka, Marta"},{"full_name":"Bollenbach, Tobias","last_name":"Bollenbach","first_name":"Tobias","orcid":"0000-0003-4398-476X","id":"3E6DB97A-F248-11E8-B48F-1D18A9856A87"},{"full_name":"Friml, Jirí","id":"4159519E-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-8302-7596","first_name":"Jirí","last_name":"Friml"}],"scopus_import":"1","day":"01","article_processing_charge":"No","has_accepted_license":"1","publication":"F1000 Research ","citation":{"mla":"Michalko, Jaroslav, et al. “Embryo-Lethal Phenotypes in Early Abp1 Mutants Are Due to Disruption of the Neighboring BSM Gene.” F1000 Research , vol. 4, F1000 Research, 2015, doi:10.12688/f1000research.7143.1.","short":"J. Michalko, M. Lukacisinova, M.T. Bollenbach, J. Friml, F1000 Research 4 (2015).","chicago":"Michalko, Jaroslav, Marta Lukacisinova, Mark Tobias Bollenbach, and Jiří Friml. “Embryo-Lethal Phenotypes in Early Abp1 Mutants Are Due to Disruption of the Neighboring BSM Gene.” F1000 Research . F1000 Research, 2015. https://doi.org/10.12688/f1000research.7143.1.","ama":"Michalko J, Lukacisinova M, Bollenbach MT, Friml J. Embryo-lethal phenotypes in early abp1 mutants are due to disruption of the neighboring BSM gene. F1000 Research . 2015;4. doi:10.12688/f1000research.7143.1","ista":"Michalko J, Lukacisinova M, Bollenbach MT, Friml J. 2015. Embryo-lethal phenotypes in early abp1 mutants are due to disruption of the neighboring BSM gene. F1000 Research . 4.","ieee":"J. Michalko, M. Lukacisinova, M. T. Bollenbach, and J. Friml, “Embryo-lethal phenotypes in early abp1 mutants are due to disruption of the neighboring BSM gene,” F1000 Research , vol. 4. F1000 Research, 2015.","apa":"Michalko, J., Lukacisinova, M., Bollenbach, M. T., & Friml, J. (2015). Embryo-lethal phenotypes in early abp1 mutants are due to disruption of the neighboring BSM gene. F1000 Research . F1000 Research. https://doi.org/10.12688/f1000research.7143.1"},"date_published":"2015-10-01T00:00:00Z","type":"journal_article","abstract":[{"lang":"eng","text":"The Auxin Binding Protein1 (ABP1) has been identified based on its ability to bind auxin with high affinity and studied for a long time as a prime candidate for the extracellular auxin receptor responsible for mediating in particular the fast non-transcriptional auxin responses. However, the contradiction between the embryo-lethal phenotypes of the originally described Arabidopsis T-DNA insertional knock-out alleles (abp1-1 and abp1-1s) and the wild type-like phenotypes of other recently described loss-of-function alleles (abp1-c1 and abp1-TD1) questions the biological importance of ABP1 and relevance of the previous genetic studies. Here we show that there is no hidden copy of the ABP1 gene in the Arabidopsis genome but the embryo-lethal phenotypes of abp1-1 and abp1-1s alleles are very similar to the knock-out phenotypes of the neighboring gene, BELAYA SMERT (BSM). Furthermore, the allelic complementation test between bsm and abp1 alleles shows that the embryo-lethality in the abp1-1 and abp1-1s alleles is caused by the off-target disruption of the BSM locus by the T-DNA insertions. This clarifies the controversy of different phenotypes among published abp1 knock-out alleles and asks for reflections on the developmental role of ABP1."}],"status":"public","title":"Embryo-lethal phenotypes in early abp1 mutants are due to disruption of the neighboring BSM gene","ddc":["570"],"intvolume":" 4","_id":"1509","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","file":[{"checksum":"8beae5cbe988e1060265ae7de2ee8306","date_updated":"2020-07-14T12:44:59Z","date_created":"2018-12-12T10:16:12Z","relation":"main_file","file_id":"5198","file_size":4414248,"content_type":"application/pdf","creator":"system","access_level":"open_access","file_name":"IST-2016-497-v1+1_10.12688_f1000research.7143.1_20151102.pdf"}],"oa_version":"Published Version","pubrep_id":"497"},{"ec_funded":1,"publist_id":"5547","file_date_updated":"2020-07-14T12:45:07Z","article_number":"e1002299","related_material":{"record":[{"relation":"research_data","status":"public","id":"9711"},{"status":"public","relation":"research_data","id":"9765"},{"id":"6263","status":"public","relation":"dissertation_contains"}]},"author":[{"full_name":"Chevereau, Guillaume","id":"424D78A0-F248-11E8-B48F-1D18A9856A87","last_name":"Chevereau","first_name":"Guillaume"},{"last_name":"Dravecka","first_name":"Marta","orcid":"0000-0002-2519-8004","id":"4342E402-F248-11E8-B48F-1D18A9856A87","full_name":"Dravecka, Marta"},{"first_name":"Tugce","last_name":"Batur","full_name":"Batur, Tugce"},{"full_name":"Guvenek, Aysegul","last_name":"Guvenek","first_name":"Aysegul"},{"last_name":"Ayhan","first_name":"Dilay","full_name":"Ayhan, Dilay"},{"first_name":"Erdal","last_name":"Toprak","full_name":"Toprak, Erdal"},{"full_name":"Bollenbach, Mark Tobias","last_name":"Bollenbach","first_name":"Mark Tobias","orcid":"0000-0003-4398-476X","id":"3E6DB97A-F248-11E8-B48F-1D18A9856A87"}],"volume":13,"date_updated":"2024-03-28T23:30:28Z","date_created":"2018-12-11T11:53:04Z","year":"2015","publisher":"Public Library of Science","department":[{"_id":"ToBo"}],"publication_status":"published","month":"11","doi":"10.1371/journal.pbio.1002299","language":[{"iso":"eng"}],"tmp":{"name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","short":"CC BY (4.0)","image":"/images/cc_by.png"},"oa":1,"project":[{"name":"Revealing the fundamental limits of cell growth","grant_number":"RGP0042/2013","_id":"25EB3A80-B435-11E9-9278-68D0E5697425"},{"grant_number":"P27201-B22","_id":"25E9AF9E-B435-11E9-9278-68D0E5697425","call_identifier":"FWF","name":"Revealing the mechanisms underlying drug interactions"},{"grant_number":"303507","_id":"25E83C2C-B435-11E9-9278-68D0E5697425","name":"Optimality principles in responses to antibiotics","call_identifier":"FP7"}],"quality_controlled":"1","issue":"11","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."}],"type":"journal_article","pubrep_id":"468","file":[{"content_type":"application/pdf","file_size":1387760,"creator":"system","file_name":"IST-2016-468-v1+1_journal.pbio.1002299.pdf","access_level":"open_access","date_created":"2018-12-12T10:09:00Z","date_updated":"2020-07-14T12:45:07Z","checksum":"0e82e3279f50b15c6c170c042627802b","relation":"main_file","file_id":"4723"}],"oa_version":"Published Version","_id":"1619","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","intvolume":" 13","ddc":["570"],"title":"Quantifying the determinants of evolutionary dynamics leading to drug resistance","status":"public","has_accepted_license":"1","day":"18","scopus_import":1,"date_published":"2015-11-18T00:00:00Z","citation":{"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).","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.","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","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.","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","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."},"publication":"PLoS Biology"},{"date_updated":"2021-01-12T06:54:55Z","date_created":"2018-12-11T11:55:22Z","volume":345,"oa_version":"Submitted Version","author":[{"first_name":"Anna","last_name":"Kicheva","full_name":"Kicheva, Anna"},{"full_name":"Bollenbach, Mark Tobias","last_name":"Bollenbach","first_name":"Mark Tobias","orcid":"0000-0003-4398-476X","id":"3E6DB97A-F248-11E8-B48F-1D18A9856A87"},{"first_name":"Ana","last_name":"Ribeiro","full_name":"Ribeiro, Ana"},{"first_name":"Helena","last_name":"Pérez Valle","full_name":"Pérez Valle, Helena"},{"last_name":"Lovell Badge","first_name":"Robin","full_name":"Lovell Badge, Robin"},{"full_name":"Episkopou, Vasso","first_name":"Vasso","last_name":"Episkopou"},{"full_name":"Briscoe, James","first_name":"James","last_name":"Briscoe"}],"title":"Coordination of progenitor specification and growth in mouse and chick spinal cord","status":"public","publication_status":"published","intvolume":" 345","department":[{"_id":"ToBo"}],"publisher":"American Association for the Advancement of Science","user_id":"4435EBFC-F248-11E8-B48F-1D18A9856A87","_id":"2040","year":"2014","abstract":[{"lang":"eng","text":"Development requires tissue growth as well as cell diversification. To address how these processes are coordinated, we analyzed the development of molecularly distinct domains of neural progenitors in the mouse and chick neural tube. We show that during development, these domains undergo changes in size that do not scale with changes in overall tissue size. Our data show that domain proportions are first established by opposing morphogen gradients and subsequently controlled by domain-specific regulation of differentiation rate but not differences in proliferation rate. Regulation of differentiation rate is key to maintaining domain proportions while accommodating both intra- and interspecies variations in size. Thus, the sequential control of progenitor specification and differentiation elaborates pattern without requiring that signaling gradients grow as tissues expand. "}],"publist_id":"5011","issue":"6204","article_number":"1254927","type":"journal_article","language":[{"iso":"eng"}],"doi":"10.1126/science.1254927","date_published":"2014-09-26T00:00:00Z","quality_controlled":"1","publication":"Science","main_file_link":[{"open_access":"1","url":"http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4228193/"}],"oa":1,"citation":{"chicago":"Kicheva, Anna, Mark Tobias Bollenbach, Ana Ribeiro, Helena Pérez Valle, Robin Lovell Badge, Vasso Episkopou, and James Briscoe. “Coordination of Progenitor Specification and Growth in Mouse and Chick Spinal Cord.” Science. American Association for the Advancement of Science, 2014. https://doi.org/10.1126/science.1254927.","short":"A. Kicheva, M.T. Bollenbach, A. Ribeiro, H. Pérez Valle, R. Lovell Badge, V. Episkopou, J. Briscoe, Science 345 (2014).","mla":"Kicheva, Anna, et al. “Coordination of Progenitor Specification and Growth in Mouse and Chick Spinal Cord.” Science, vol. 345, no. 6204, 1254927, American Association for the Advancement of Science, 2014, doi:10.1126/science.1254927.","apa":"Kicheva, A., Bollenbach, M. T., Ribeiro, A., Pérez Valle, H., Lovell Badge, R., Episkopou, V., & Briscoe, J. (2014). Coordination of progenitor specification and growth in mouse and chick spinal cord. Science. American Association for the Advancement of Science. https://doi.org/10.1126/science.1254927","ieee":"A. Kicheva et al., “Coordination of progenitor specification and growth in mouse and chick spinal cord,” Science, vol. 345, no. 6204. American Association for the Advancement of Science, 2014.","ista":"Kicheva A, Bollenbach MT, Ribeiro A, Pérez Valle H, Lovell Badge R, Episkopou V, Briscoe J. 2014. Coordination of progenitor specification and growth in mouse and chick spinal cord. Science. 345(6204), 1254927.","ama":"Kicheva A, Bollenbach MT, Ribeiro A, et al. Coordination of progenitor specification and growth in mouse and chick spinal cord. Science. 2014;345(6204). doi:10.1126/science.1254927"},"month":"09","day":"26","scopus_import":1},{"scopus_import":1,"day":"24","citation":{"short":"M. de Vos, M.T. Bollenbach, Chemistry and Biology 21 (2014) 439–440.","mla":"de Vos, Marjon, and Mark Tobias Bollenbach. “Suppressive Drug Interactions between Antifungals.” Chemistry and Biology, vol. 21, no. 4, Cell Press, 2014, pp. 439–40, doi:10.1016/j.chembiol.2014.04.004.","chicago":"Vos, Marjon de, and Mark Tobias Bollenbach. “Suppressive Drug Interactions between Antifungals.” Chemistry and Biology. Cell Press, 2014. https://doi.org/10.1016/j.chembiol.2014.04.004.","ama":"de Vos M, Bollenbach MT. Suppressive drug interactions between antifungals. Chemistry and Biology. 2014;21(4):439-440. doi:10.1016/j.chembiol.2014.04.004","ieee":"M. de Vos and M. T. Bollenbach, “Suppressive drug interactions between antifungals,” Chemistry and Biology, vol. 21, no. 4. Cell Press, pp. 439–440, 2014.","apa":"de Vos, M., & Bollenbach, M. T. (2014). Suppressive drug interactions between antifungals. Chemistry and Biology. Cell Press. https://doi.org/10.1016/j.chembiol.2014.04.004","ista":"de Vos M, Bollenbach MT. 2014. Suppressive drug interactions between antifungals. Chemistry and Biology. 21(4), 439–440."},"publication":"Chemistry and Biology","page":"439 - 440","date_published":"2014-04-24T00:00:00Z","type":"journal_article","issue":"4","abstract":[{"lang":"eng","text":"In this issue of Chemistry & Biology, Cokol and colleagues report a systematic study of drug interactions between antifungal compounds. Suppressive drug interactions occur more frequently than previously realized and come in different flavors with interesting implications."}],"_id":"2220","user_id":"3E5EF7F0-F248-11E8-B48F-1D18A9856A87","intvolume":" 21","status":"public","title":"Suppressive drug interactions between antifungals","oa_version":"Published Version","publication_identifier":{"issn":["10745521"]},"month":"04","oa":1,"main_file_link":[{"url":"https://www.ncbi.nlm.nih.gov/pubmed/24766845","open_access":"1"}],"external_id":{"pmid":["24766845"]},"quality_controlled":"1","doi":"10.1016/j.chembiol.2014.04.004","language":[{"iso":"eng"}],"publist_id":"4747","pmid":1,"year":"2014","publisher":"Cell Press","department":[{"_id":"ToBo"}],"publication_status":"published","author":[{"first_name":"Marjon","last_name":"De Vos","id":"3111FFAC-F248-11E8-B48F-1D18A9856A87","full_name":"De Vos, Marjon"},{"orcid":"0000-0003-4398-476X","id":"3E6DB97A-F248-11E8-B48F-1D18A9856A87","last_name":"Bollenbach","first_name":"Mark Tobias","full_name":"Bollenbach, Mark Tobias"}],"volume":21,"date_created":"2018-12-11T11:56:24Z","date_updated":"2021-01-12T06:56:06Z"}]