--- _id: '503' abstract: - lang: eng text: Buffers are essential for diluting bacterial cultures for flow cytometry analysis in order to study bacterial physiology and gene expression parameters based on fluorescence signals. Using a variety of constitutively expressed fluorescent proteins in Escherichia coli K-12 strain MG1655, we found strong artifactual changes in fluorescence levels after dilution into the commonly used flow cytometry buffer phosphate-buffered saline (PBS) and two other buffer solutions, Tris-HCl and M9 salts. These changes appeared very rapidly after dilution, and were linked to increased membrane permeability and loss in cell viability. We observed buffer-related effects in several different E. coli strains, K-12, C and W, but not E. coli B, which can be partially explained by differences in lipopolysaccharide (LPS) and outer membrane composition. Supplementing the buffers with divalent cations responsible for outer membrane stability, Mg2+ and Ca2+, preserved fluorescence signals, membrane integrity and viability of E. coli. Thus, stabilizing the bacterial outer membrane is essential for precise and unbiased measurements of fluorescence parameters using flow cytometry. acknowledged_ssus: - _id: Bio acknowledgement: "We thank R Chait and M Lagator for sharing Bacillus subtilis CR_Y1 and pZS*_2R-cIPtet-Venus-Prm, respectively. We are grateful to T Pilizota and all members of the Guet lab for critically reading the manuscript. We also thank the Bioimaging facility at IST Austria for assistance using the FACSAria III system.\r\n\r\n" article_processing_charge: No author: - first_name: Kathrin full_name: Tomasek, Kathrin id: 3AEC8556-F248-11E8-B48F-1D18A9856A87 last_name: Tomasek orcid: 0000-0003-3768-877X - first_name: Tobias full_name: Bergmiller, Tobias id: 2C471CFA-F248-11E8-B48F-1D18A9856A87 last_name: Bergmiller orcid: 0000-0001-5396-4346 - first_name: Calin C full_name: Guet, Calin C id: 47F8433E-F248-11E8-B48F-1D18A9856A87 last_name: Guet orcid: 0000-0001-6220-2052 citation: ama: Tomasek K, Bergmiller T, Guet CC. Lack of cations in flow cytometry buffers affect fluorescence signals by reducing membrane stability and viability of Escherichia coli strains. Journal of Biotechnology. 2018;268:40-52. doi:10.1016/j.jbiotec.2018.01.008 apa: Tomasek, K., Bergmiller, T., & Guet, C. C. (2018). Lack of cations in flow cytometry buffers affect fluorescence signals by reducing membrane stability and viability of Escherichia coli strains. Journal of Biotechnology. Elsevier. https://doi.org/10.1016/j.jbiotec.2018.01.008 chicago: Tomasek, Kathrin, Tobias Bergmiller, and Calin C Guet. “Lack of Cations in Flow Cytometry Buffers Affect Fluorescence Signals by Reducing Membrane Stability and Viability of Escherichia Coli Strains.” Journal of Biotechnology. Elsevier, 2018. https://doi.org/10.1016/j.jbiotec.2018.01.008. ieee: K. Tomasek, T. Bergmiller, and C. C. Guet, “Lack of cations in flow cytometry buffers affect fluorescence signals by reducing membrane stability and viability of Escherichia coli strains,” Journal of Biotechnology, vol. 268. Elsevier, pp. 40–52, 2018. ista: Tomasek K, Bergmiller T, Guet CC. 2018. Lack of cations in flow cytometry buffers affect fluorescence signals by reducing membrane stability and viability of Escherichia coli strains. Journal of Biotechnology. 268, 40–52. mla: Tomasek, Kathrin, et al. “Lack of Cations in Flow Cytometry Buffers Affect Fluorescence Signals by Reducing Membrane Stability and Viability of Escherichia Coli Strains.” Journal of Biotechnology, vol. 268, Elsevier, 2018, pp. 40–52, doi:10.1016/j.jbiotec.2018.01.008. short: K. Tomasek, T. Bergmiller, C.C. Guet, Journal of Biotechnology 268 (2018) 40–52. date_created: 2018-12-11T11:46:50Z date_published: 2018-02-20T00:00:00Z date_updated: 2023-09-13T08:24:51Z day: '20' department: - _id: CaGu doi: 10.1016/j.jbiotec.2018.01.008 external_id: isi: - '000425715100006' intvolume: ' 268' isi: 1 language: - iso: eng month: '02' oa_version: None page: 40 - 52 publication: Journal of Biotechnology publication_status: published publisher: Elsevier publist_id: '7317' quality_controlled: '1' scopus_import: '1' status: public title: Lack of cations in flow cytometry buffers affect fluorescence signals by reducing membrane stability and viability of Escherichia coli strains type: journal_article user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1 volume: 268 year: '2018' ... --- _id: '438' abstract: - lang: eng text: The MazF toxin sequence-specifically cleaves single-stranded RNA upon various stressful conditions, and it is activated as a part of the mazEF toxin–antitoxin module in Escherichia coli. Although autoregulation of mazEF expression through the MazE antitoxin-dependent transcriptional repression has been biochemically characterized, less is known about post-transcriptional autoregulation, as well as how both of these autoregulatory features affect growth of single cells during conditions that promote MazF production. Here, we demonstrate post-transcriptional autoregulation of mazF expression dynamics by MazF cleaving its own transcript. Single-cell analyses of bacterial populations during ectopic MazF production indicated that two-level autoregulation of mazEF expression influences cell-to-cell growth rate heterogeneity. The increase in growth rate heterogeneity is governed by the MazE antitoxin, and tuned by the MazF-dependent mazF mRNA cleavage. Also, both autoregulatory features grant rapid exit from the stress caused by mazF overexpression. Time-lapse microscopy revealed that MazF-mediated cleavage of mazF mRNA leads to increased temporal variability in length of individual cells during ectopic mazF overexpression, as explained by a stochastic model indicating that mazEF mRNA cleavage underlies temporal fluctuations in MazF levels during stress. article_processing_charge: Yes (in subscription journal) author: - first_name: Nela full_name: Nikolic, Nela id: 42D9CABC-F248-11E8-B48F-1D18A9856A87 last_name: Nikolic orcid: 0000-0001-9068-6090 - first_name: Tobias full_name: Bergmiller, Tobias id: 2C471CFA-F248-11E8-B48F-1D18A9856A87 last_name: Bergmiller orcid: 0000-0001-5396-4346 - first_name: Alexandra full_name: Vandervelde, Alexandra last_name: Vandervelde - first_name: Tanino full_name: Albanese, Tanino last_name: Albanese - first_name: Lendert full_name: Gelens, Lendert last_name: Gelens - first_name: Isabella full_name: Moll, Isabella last_name: Moll citation: ama: Nikolic N, Bergmiller T, Vandervelde A, Albanese T, Gelens L, Moll I. Autoregulation of mazEF expression underlies growth heterogeneity in bacterial populations. Nucleic Acids Research. 2018;46(6):2918-2931. doi:10.1093/nar/gky079 apa: Nikolic, N., Bergmiller, T., Vandervelde, A., Albanese, T., Gelens, L., & Moll, I. (2018). Autoregulation of mazEF expression underlies growth heterogeneity in bacterial populations. Nucleic Acids Research. Oxford University Press. https://doi.org/10.1093/nar/gky079 chicago: Nikolic, Nela, Tobias Bergmiller, Alexandra Vandervelde, Tanino Albanese, Lendert Gelens, and Isabella Moll. “Autoregulation of MazEF Expression Underlies Growth Heterogeneity in Bacterial Populations.” Nucleic Acids Research. Oxford University Press, 2018. https://doi.org/10.1093/nar/gky079. ieee: N. Nikolic, T. Bergmiller, A. Vandervelde, T. Albanese, L. Gelens, and I. Moll, “Autoregulation of mazEF expression underlies growth heterogeneity in bacterial populations,” Nucleic Acids Research, vol. 46, no. 6. Oxford University Press, pp. 2918–2931, 2018. ista: Nikolic N, Bergmiller T, Vandervelde A, Albanese T, Gelens L, Moll I. 2018. Autoregulation of mazEF expression underlies growth heterogeneity in bacterial populations. Nucleic Acids Research. 46(6), 2918–2931. mla: Nikolic, Nela, et al. “Autoregulation of MazEF Expression Underlies Growth Heterogeneity in Bacterial Populations.” Nucleic Acids Research, vol. 46, no. 6, Oxford University Press, 2018, pp. 2918–31, doi:10.1093/nar/gky079. short: N. Nikolic, T. Bergmiller, A. Vandervelde, T. Albanese, L. Gelens, I. Moll, Nucleic Acids Research 46 (2018) 2918–2931. date_created: 2018-12-11T11:46:29Z date_published: 2018-04-06T00:00:00Z date_updated: 2024-02-21T13:44:45Z day: '06' ddc: - '576' department: - _id: CaGu doi: 10.1093/nar/gky079 external_id: isi: - '000429009500021' file: - access_level: open_access checksum: 3ff4f545c27e11a4cd20ccb30778793e content_type: application/pdf creator: system date_created: 2018-12-12T10:15:30Z date_updated: 2020-07-14T12:46:27Z file_id: '5151' file_name: IST-2018-971-v1+1_2018_Nikoloc_Autoregulation_of.pdf file_size: 5027978 relation: main_file file_date_updated: 2020-07-14T12:46:27Z has_accepted_license: '1' intvolume: ' 46' isi: 1 issue: '6' language: - iso: eng month: '04' oa: 1 oa_version: Published Version page: 2918-2931 project: - _id: 3AC91DDA-15DF-11EA-824D-93A3E7B544D1 call_identifier: FWF name: FWF Open Access Fund publication: Nucleic Acids Research publication_status: published publisher: Oxford University Press pubrep_id: '971' quality_controlled: '1' related_material: record: - id: '5569' relation: popular_science status: public scopus_import: '1' status: public title: Autoregulation of mazEF expression underlies growth heterogeneity in bacterial populations 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: c635000d-4b10-11ee-a964-aac5a93f6ac1 volume: 46 year: '2018' ... --- _id: '5569' abstract: - lang: eng text: "Nela Nikolic, Tobias Bergmiller, Alexandra Vandervelde, Tanino G. Albanese, Lendert Gelens, and Isabella Moll (2018)\r\n“Autoregulation of mazEF expression underlies growth heterogeneity in bacterial populations” Nucleic Acids Research, doi: 10.15479/AT:ISTA:74;\r\nmicroscopy experiments by Tobias Bergmiller; image and data analysis by Nela Nikolic." article_processing_charge: No author: - first_name: Tobias full_name: Bergmiller, Tobias id: 2C471CFA-F248-11E8-B48F-1D18A9856A87 last_name: Bergmiller orcid: 0000-0001-5396-4346 - first_name: Nela full_name: Nikolic, Nela id: 42D9CABC-F248-11E8-B48F-1D18A9856A87 last_name: Nikolic orcid: 0000-0001-9068-6090 citation: ama: Bergmiller T, Nikolic N. Time-lapse microscopy data. 2018. doi:10.15479/AT:ISTA:74 apa: Bergmiller, T., & Nikolic, N. (2018). Time-lapse microscopy data. Institute of Science and Technology Austria. https://doi.org/10.15479/AT:ISTA:74 chicago: Bergmiller, Tobias, and Nela Nikolic. “Time-Lapse Microscopy Data.” Institute of Science and Technology Austria, 2018. https://doi.org/10.15479/AT:ISTA:74. ieee: T. Bergmiller and N. Nikolic, “Time-lapse microscopy data.” Institute of Science and Technology Austria, 2018. ista: Bergmiller T, Nikolic N. 2018. Time-lapse microscopy data, Institute of Science and Technology Austria, 10.15479/AT:ISTA:74. mla: Bergmiller, Tobias, and Nela Nikolic. Time-Lapse Microscopy Data. Institute of Science and Technology Austria, 2018, doi:10.15479/AT:ISTA:74. short: T. Bergmiller, N. Nikolic, (2018). datarep_id: '74' date_created: 2018-12-12T12:31:35Z date_published: 2018-02-07T00:00:00Z date_updated: 2024-02-21T13:44:45Z day: '07' ddc: - '579' department: - _id: CaGu doi: 10.15479/AT:ISTA:74 file: - access_level: open_access checksum: 61ebb92213cfffeba3ddbaff984b81af content_type: application/zip creator: system date_created: 2018-12-12T13:04:39Z date_updated: 2020-07-14T12:47:04Z file_id: '5637' file_name: IST-2018-74-v1+2_15-11-05.zip file_size: 3558703796 relation: main_file - access_level: open_access checksum: bf26649af310ef6892d68576515cde6d content_type: application/zip creator: system date_created: 2018-12-12T13:04:55Z date_updated: 2020-07-14T12:47:04Z file_id: '5638' file_name: IST-2018-74-v1+3_15-07-31.zip file_size: 1830422606 relation: main_file - access_level: open_access checksum: 8e46eedce06f22acb2be1a9b9d3f56bd content_type: application/zip creator: system date_created: 2018-12-12T13:05:11Z date_updated: 2020-07-14T12:47:04Z file_id: '5639' file_name: IST-2018-74-v1+4_Images_for_analysis.zip file_size: 2140849248 relation: main_file file_date_updated: 2020-07-14T12:47:04Z has_accepted_license: '1' keyword: - microscopy - microfluidics license: https://creativecommons.org/publicdomain/zero/1.0/ month: '02' oa: 1 oa_version: Published Version publisher: Institute of Science and Technology Austria publist_id: '7385' related_material: record: - id: '438' relation: research_paper status: public status: public title: Time-lapse microscopy data tmp: image: /images/cc_0.png legal_code_url: https://creativecommons.org/publicdomain/zero/1.0/legalcode name: Creative Commons Public Domain Dedication (CC0 1.0) short: CC0 (1.0) type: research_data user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 year: '2018' ... --- _id: '161' abstract: - lang: eng text: 'Which properties of metabolic networks can be derived solely from stoichiometry? Predictive results have been obtained by flux balance analysis (FBA), by postulating that cells set metabolic fluxes to maximize growth rate. Here we consider a generalization of FBA to single-cell level using maximum entropy modeling, which we extend and test experimentally. Specifically, we define for Escherichia coli metabolism a flux distribution that yields the experimental growth rate: the model, containing FBA as a limit, provides a better match to measured fluxes and it makes a wide range of predictions: on flux variability, regulation, and correlations; on the relative importance of stoichiometry vs. optimization; on scaling relations for growth rate distributions. We validate the latter here with single-cell data at different sub-inhibitory antibiotic concentrations. The model quantifies growth optimization as emerging from the interplay of competitive dynamics in the population and regulation of metabolism at the level of single cells.' article_number: '2988' article_processing_charge: No author: - first_name: Daniele full_name: De Martino, Daniele id: 3FF5848A-F248-11E8-B48F-1D18A9856A87 last_name: De Martino orcid: 0000-0002-5214-4706 - first_name: Andersson Anna full_name: Mc, Andersson Anna last_name: Mc - first_name: Tobias full_name: Bergmiller, Tobias id: 2C471CFA-F248-11E8-B48F-1D18A9856A87 last_name: Bergmiller orcid: 0000-0001-5396-4346 - first_name: Calin C full_name: Guet, Calin C id: 47F8433E-F248-11E8-B48F-1D18A9856A87 last_name: Guet orcid: 0000-0001-6220-2052 - first_name: Gasper full_name: Tkacik, Gasper id: 3D494DCA-F248-11E8-B48F-1D18A9856A87 last_name: Tkacik orcid: 0000-0002-6699-1455 citation: ama: De Martino D, Mc AA, Bergmiller T, Guet CC, Tkačik G. Statistical mechanics for metabolic networks during steady state growth. Nature Communications. 2018;9(1). doi:10.1038/s41467-018-05417-9 apa: De Martino, D., Mc, A. A., Bergmiller, T., Guet, C. C., & Tkačik, G. (2018). Statistical mechanics for metabolic networks during steady state growth. Nature Communications. Springer Nature. https://doi.org/10.1038/s41467-018-05417-9 chicago: De Martino, Daniele, Andersson Anna Mc, Tobias Bergmiller, Calin C Guet, and Gašper Tkačik. “Statistical Mechanics for Metabolic Networks during Steady State Growth.” Nature Communications. Springer Nature, 2018. https://doi.org/10.1038/s41467-018-05417-9. ieee: D. De Martino, A. A. Mc, T. Bergmiller, C. C. Guet, and G. Tkačik, “Statistical mechanics for metabolic networks during steady state growth,” Nature Communications, vol. 9, no. 1. Springer Nature, 2018. ista: De Martino D, Mc AA, Bergmiller T, Guet CC, Tkačik G. 2018. Statistical mechanics for metabolic networks during steady state growth. Nature Communications. 9(1), 2988. mla: De Martino, Daniele, et al. “Statistical Mechanics for Metabolic Networks during Steady State Growth.” Nature Communications, vol. 9, no. 1, 2988, Springer Nature, 2018, doi:10.1038/s41467-018-05417-9. short: D. De Martino, A.A. Mc, T. Bergmiller, C.C. Guet, G. Tkačik, Nature Communications 9 (2018). date_created: 2018-12-11T11:44:57Z date_published: 2018-07-30T00:00:00Z date_updated: 2024-02-21T13:45:39Z day: '30' ddc: - '570' department: - _id: GaTk - _id: CaGu doi: 10.1038/s41467-018-05417-9 ec_funded: 1 external_id: isi: - '000440149300021' file: - access_level: open_access checksum: 3ba7ab27b27723c7dcf633e8fc1f8f18 content_type: application/pdf creator: dernst date_created: 2018-12-17T16:44:28Z date_updated: 2020-07-14T12:45:06Z file_id: '5728' file_name: 2018_NatureComm_DeMartino.pdf file_size: 1043205 relation: main_file file_date_updated: 2020-07-14T12:45:06Z has_accepted_license: '1' intvolume: ' 9' isi: 1 issue: '1' language: - iso: eng month: '07' oa: 1 oa_version: Published Version project: - _id: 254E9036-B435-11E9-9278-68D0E5697425 call_identifier: FWF grant_number: P28844-B27 name: Biophysics of information processing in gene regulation - _id: 25681D80-B435-11E9-9278-68D0E5697425 call_identifier: FP7 grant_number: '291734' name: International IST Postdoc Fellowship Programme publication: Nature Communications publication_status: published publisher: Springer Nature publist_id: '7760' quality_controlled: '1' related_material: record: - id: '5587' relation: popular_science status: public scopus_import: '1' status: public title: Statistical mechanics for metabolic networks during steady state growth 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: c635000d-4b10-11ee-a964-aac5a93f6ac1 volume: 9 year: '2018' ... --- _id: '613' abstract: - lang: eng text: 'Bacteria in groups vary individually, and interact with other bacteria and the environment to produce population-level patterns of gene expression. Investigating such behavior in detail requires measuring and controlling populations at the single-cell level alongside precisely specified interactions and environmental characteristics. Here we present an automated, programmable platform that combines image-based gene expression and growth measurements with on-line optogenetic expression control for hundreds of individual Escherichia coli cells over days, in a dynamically adjustable environment. This integrated platform broadly enables experiments that bridge individual and population behaviors. We demonstrate: (i) population structuring by independent closed-loop control of gene expression in many individual cells, (ii) cell-cell variation control during antibiotic perturbation, (iii) hybrid bio-digital circuits in single cells, and freely specifiable digital communication between individual bacteria. These examples showcase the potential for real-time integration of theoretical models with measurement and control of many individual cells to investigate and engineer microbial population behavior.' acknowledgement: We are grateful to M. Lang, H. Janovjak, M. Khammash, A. Milias-Argeitis, M. Rullan, G. Batt, A. Bosma-Moody, Aryan, S. Leibler, and members of the Guet and Tkačik groups for helpful discussion, comments, and suggestions. We thank A. Moglich, T. Mathes, J. Tabor, and S. Schmidl for kind gifts of strains, and R. Hauschild, B. Knep, M. Lang, T. Asenov, E. Papusheva, T. Menner, T. Adletzberger, and J. Merrin for technical assistance. The research leading to these results has received funding from the People Programme (Marie Curie Actions) of the European Union’s Seventh Framework Programme (FP7/2007–2013) under REA grant agreement no. [291734]. (to R.C. and J.R.), Austrian Science Fund grant FWF P28844 (to G.T.), and internal IST Austria Interdisciplinary Project Support. J.R. acknowledges support from the Agence Nationale de la Recherche (ANR) under Grant Nos. ANR-16-CE33-0018 (MEMIP), ANR-16-CE12-0025 (COGEX) and ANR-10-BINF-06-01 (ICEBERG). article_number: '1535' article_processing_charge: Yes (in subscription journal) author: - first_name: Remy P full_name: Chait, Remy P id: 3464AE84-F248-11E8-B48F-1D18A9856A87 last_name: Chait orcid: 0000-0003-0876-3187 - first_name: Jakob full_name: Ruess, Jakob id: 4A245D00-F248-11E8-B48F-1D18A9856A87 last_name: Ruess orcid: 0000-0003-1615-3282 - first_name: Tobias full_name: Bergmiller, Tobias id: 2C471CFA-F248-11E8-B48F-1D18A9856A87 last_name: Bergmiller orcid: 0000-0001-5396-4346 - first_name: Gasper full_name: Tkacik, Gasper id: 3D494DCA-F248-11E8-B48F-1D18A9856A87 last_name: Tkacik orcid: 0000-0002-6699-1455 - first_name: Calin C full_name: Guet, Calin C id: 47F8433E-F248-11E8-B48F-1D18A9856A87 last_name: Guet orcid: 0000-0001-6220-2052 citation: ama: Chait RP, Ruess J, Bergmiller T, Tkačik G, Guet CC. Shaping bacterial population behavior through computer interfaced control of individual cells. Nature Communications. 2017;8(1). doi:10.1038/s41467-017-01683-1 apa: Chait, R. P., Ruess, J., Bergmiller, T., Tkačik, G., & Guet, C. C. (2017). Shaping bacterial population behavior through computer interfaced control of individual cells. Nature Communications. Nature Publishing Group. https://doi.org/10.1038/s41467-017-01683-1 chicago: Chait, Remy P, Jakob Ruess, Tobias Bergmiller, Gašper Tkačik, and Calin C Guet. “Shaping Bacterial Population Behavior through Computer Interfaced Control of Individual Cells.” Nature Communications. Nature Publishing Group, 2017. https://doi.org/10.1038/s41467-017-01683-1. ieee: R. P. Chait, J. Ruess, T. Bergmiller, G. Tkačik, and C. C. Guet, “Shaping bacterial population behavior through computer interfaced control of individual cells,” Nature Communications, vol. 8, no. 1. Nature Publishing Group, 2017. ista: Chait RP, Ruess J, Bergmiller T, Tkačik G, Guet CC. 2017. Shaping bacterial population behavior through computer interfaced control of individual cells. Nature Communications. 8(1), 1535. mla: Chait, Remy P., et al. “Shaping Bacterial Population Behavior through Computer Interfaced Control of Individual Cells.” Nature Communications, vol. 8, no. 1, 1535, Nature Publishing Group, 2017, doi:10.1038/s41467-017-01683-1. short: R.P. Chait, J. Ruess, T. Bergmiller, G. Tkačik, C.C. Guet, Nature Communications 8 (2017). date_created: 2018-12-11T11:47:30Z date_published: 2017-12-01T00:00:00Z date_updated: 2021-01-12T08:06:15Z day: '01' ddc: - '576' - '579' department: - _id: CaGu - _id: GaTk doi: 10.1038/s41467-017-01683-1 ec_funded: 1 file: - access_level: open_access checksum: 44bb5d0229926c23a9955d9fe0f9723f content_type: application/pdf creator: system date_created: 2018-12-12T10:16:05Z date_updated: 2020-07-14T12:47:20Z file_id: '5190' file_name: IST-2017-911-v1+1_s41467-017-01683-1.pdf file_size: 1951699 relation: main_file file_date_updated: 2020-07-14T12:47:20Z has_accepted_license: '1' intvolume: ' 8' issue: '1' language: - iso: eng month: '12' oa: 1 oa_version: Published Version project: - _id: 25681D80-B435-11E9-9278-68D0E5697425 call_identifier: FP7 grant_number: '291734' name: International IST Postdoc Fellowship Programme - _id: 254E9036-B435-11E9-9278-68D0E5697425 call_identifier: FWF grant_number: P28844-B27 name: Biophysics of information processing in gene regulation publication: Nature Communications publication_identifier: issn: - '20411723' publication_status: published publisher: Nature Publishing Group publist_id: '7191' pubrep_id: '911' quality_controlled: '1' scopus_import: 1 status: public title: Shaping bacterial population behavior through computer interfaced control of individual cells 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: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87 volume: 8 year: '2017' ... --- _id: '655' abstract: - lang: eng text: 'The bacterial flagellum is a self-assembling nanomachine. The external flagellar filament, several times longer than a bacterial cell body, is made of a few tens of thousands subunits of a single protein: flagellin. A fundamental problem concerns the molecular mechanism of how the flagellum grows outside the cell, where no discernible energy source is available. Here, we monitored the dynamic assembly of individual flagella using in situ labelling and real-time immunostaining of elongating flagellar filaments. We report that the rate of flagellum growth, initially ~1,700 amino acids per second, decreases with length and that the previously proposed chain mechanism does not contribute to the filament elongation dynamics. Inhibition of the proton motive force-dependent export apparatus revealed a major contribution of substrate injection in driving filament elongation. The combination of experimental and mathematical evidence demonstrates that a simple, injection-diffusion mechanism controls bacterial flagella growth outside the cell.' article_number: e23136 author: - first_name: Thibaud full_name: Renault, Thibaud last_name: Renault - first_name: Anthony full_name: Abraham, Anthony last_name: Abraham - first_name: Tobias full_name: Bergmiller, Tobias id: 2C471CFA-F248-11E8-B48F-1D18A9856A87 last_name: Bergmiller orcid: 0000-0001-5396-4346 - first_name: Guillaume full_name: Paradis, Guillaume last_name: Paradis - first_name: Simon full_name: Rainville, Simon last_name: Rainville - first_name: Emmanuelle full_name: Charpentier, Emmanuelle last_name: Charpentier - first_name: Calin C full_name: Guet, Calin C id: 47F8433E-F248-11E8-B48F-1D18A9856A87 last_name: Guet orcid: 0000-0001-6220-2052 - first_name: Yuhai full_name: Tu, Yuhai last_name: Tu - first_name: Keiichi full_name: Namba, Keiichi last_name: Namba - first_name: James full_name: Keener, James last_name: Keener - first_name: Tohru full_name: Minamino, Tohru last_name: Minamino - first_name: Marc full_name: Erhardt, Marc last_name: Erhardt citation: ama: Renault T, Abraham A, Bergmiller T, et al. Bacterial flagella grow through an injection diffusion mechanism. eLife. 2017;6. doi:10.7554/eLife.23136 apa: Renault, T., Abraham, A., Bergmiller, T., Paradis, G., Rainville, S., Charpentier, E., … Erhardt, M. (2017). Bacterial flagella grow through an injection diffusion mechanism. ELife. eLife Sciences Publications. https://doi.org/10.7554/eLife.23136 chicago: Renault, Thibaud, Anthony Abraham, Tobias Bergmiller, Guillaume Paradis, Simon Rainville, Emmanuelle Charpentier, Calin C Guet, et al. “Bacterial Flagella Grow through an Injection Diffusion Mechanism.” ELife. eLife Sciences Publications, 2017. https://doi.org/10.7554/eLife.23136. ieee: T. Renault et al., “Bacterial flagella grow through an injection diffusion mechanism,” eLife, vol. 6. eLife Sciences Publications, 2017. ista: Renault T, Abraham A, Bergmiller T, Paradis G, Rainville S, Charpentier E, Guet CC, Tu Y, Namba K, Keener J, Minamino T, Erhardt M. 2017. Bacterial flagella grow through an injection diffusion mechanism. eLife. 6, e23136. mla: Renault, Thibaud, et al. “Bacterial Flagella Grow through an Injection Diffusion Mechanism.” ELife, vol. 6, e23136, eLife Sciences Publications, 2017, doi:10.7554/eLife.23136. short: T. Renault, A. Abraham, T. Bergmiller, G. Paradis, S. Rainville, E. Charpentier, C.C. Guet, Y. Tu, K. Namba, J. Keener, T. Minamino, M. Erhardt, ELife 6 (2017). date_created: 2018-12-11T11:47:44Z date_published: 2017-03-06T00:00:00Z date_updated: 2021-01-12T08:07:55Z day: '06' ddc: - '579' department: - _id: CaGu doi: 10.7554/eLife.23136 file: - access_level: open_access checksum: 39e1c3e82ddac83a30422fa72fa1a383 content_type: application/pdf creator: system date_created: 2018-12-12T10:08:53Z date_updated: 2020-07-14T12:47:33Z file_id: '4716' file_name: IST-2017-904-v1+1_elife-23136-v2.pdf file_size: 5520359 relation: main_file - access_level: open_access checksum: a6d542253028f52e00aa29739ddffe8f content_type: application/pdf creator: system date_created: 2018-12-12T10:08:54Z date_updated: 2020-07-14T12:47:33Z file_id: '4717' file_name: IST-2017-904-v1+2_elife-23136-figures-v2.pdf file_size: 11242920 relation: main_file file_date_updated: 2020-07-14T12:47:33Z has_accepted_license: '1' intvolume: ' 6' language: - iso: eng month: '03' oa: 1 oa_version: Published Version publication: eLife publication_identifier: issn: - 2050084X publication_status: published publisher: eLife Sciences Publications publist_id: '7082' pubrep_id: '904' quality_controlled: '1' scopus_import: 1 status: public title: Bacterial flagella grow through an injection diffusion mechanism 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: 6 year: '2017' ... --- _id: '541' abstract: - lang: eng text: 'While we have good understanding of bacterial metabolism at the population level, we know little about the metabolic behavior of individual cells: do single cells in clonal populations sometimes specialize on different metabolic pathways? Such metabolic specialization could be driven by stochastic gene expression and could provide individual cells with growth benefits of specialization. We measured the degree of phenotypic specialization in two parallel metabolic pathways, the assimilation of glucose and arabinose. We grew Escherichia coli in chemostats, and used isotope-labeled sugars in combination with nanometer-scale secondary ion mass spectrometry and mathematical modeling to quantify sugar assimilation at the single-cell level. We found large variation in metabolic activities between single cells, both in absolute assimilation and in the degree to which individual cells specialize in the assimilation of different sugars. Analysis of transcriptional reporters indicated that this variation was at least partially based on cell-to-cell variation in gene expression. Metabolic differences between cells in clonal populations could potentially reduce metabolic incompatibilities between different pathways, and increase the rate at which parallel reactions can be performed.' article_number: e1007122 author: - first_name: Nela full_name: Nikolic, Nela id: 42D9CABC-F248-11E8-B48F-1D18A9856A87 last_name: Nikolic orcid: 0000-0001-9068-6090 - first_name: Frank full_name: Schreiber, Frank last_name: Schreiber - first_name: Alma full_name: Dal Co, Alma last_name: Dal Co - first_name: Daniel full_name: Kiviet, Daniel last_name: Kiviet - first_name: Tobias full_name: Bergmiller, Tobias id: 2C471CFA-F248-11E8-B48F-1D18A9856A87 last_name: Bergmiller orcid: 0000-0001-5396-4346 - first_name: Sten full_name: Littmann, Sten last_name: Littmann - first_name: Marcel full_name: Kuypers, Marcel last_name: Kuypers - first_name: Martin full_name: Ackermann, Martin last_name: Ackermann citation: ama: Nikolic N, Schreiber F, Dal Co A, et al. Cell-to-cell variation and specialization in sugar metabolism in clonal bacterial populations. PLoS Genetics. 2017;13(12). doi:10.1371/journal.pgen.1007122 apa: Nikolic, N., Schreiber, F., Dal Co, A., Kiviet, D., Bergmiller, T., Littmann, S., … Ackermann, M. (2017). Cell-to-cell variation and specialization in sugar metabolism in clonal bacterial populations. PLoS Genetics. Public Library of Science. https://doi.org/10.1371/journal.pgen.1007122 chicago: Nikolic, Nela, Frank Schreiber, Alma Dal Co, Daniel Kiviet, Tobias Bergmiller, Sten Littmann, Marcel Kuypers, and Martin Ackermann. “Cell-to-Cell Variation and Specialization in Sugar Metabolism in Clonal Bacterial Populations.” PLoS Genetics. Public Library of Science, 2017. https://doi.org/10.1371/journal.pgen.1007122. ieee: N. Nikolic et al., “Cell-to-cell variation and specialization in sugar metabolism in clonal bacterial populations,” PLoS Genetics, vol. 13, no. 12. Public Library of Science, 2017. ista: Nikolic N, Schreiber F, Dal Co A, Kiviet D, Bergmiller T, Littmann S, Kuypers M, Ackermann M. 2017. Cell-to-cell variation and specialization in sugar metabolism in clonal bacterial populations. PLoS Genetics. 13(12), e1007122. mla: Nikolic, Nela, et al. “Cell-to-Cell Variation and Specialization in Sugar Metabolism in Clonal Bacterial Populations.” PLoS Genetics, vol. 13, no. 12, e1007122, Public Library of Science, 2017, doi:10.1371/journal.pgen.1007122. short: N. Nikolic, F. Schreiber, A. Dal Co, D. Kiviet, T. Bergmiller, S. Littmann, M. Kuypers, M. Ackermann, PLoS Genetics 13 (2017). date_created: 2018-12-11T11:47:04Z date_published: 2017-12-18T00:00:00Z date_updated: 2023-02-23T14:10:34Z day: '18' ddc: - '576' - '579' department: - _id: CaGu doi: 10.1371/journal.pgen.1007122 ec_funded: 1 file: - access_level: open_access checksum: 22426d9382f21554bad5fa5967afcfd0 content_type: application/pdf creator: system date_created: 2018-12-12T10:14:35Z date_updated: 2020-07-14T12:46:46Z file_id: '5088' file_name: IST-2018-959-v1+1_2017_Nikolic_Cell-to-cell.pdf file_size: 1308475 relation: main_file file_date_updated: 2020-07-14T12:46:46Z has_accepted_license: '1' intvolume: ' 13' issue: '12' language: - iso: eng month: '12' oa: 1 oa_version: Published Version project: - _id: 25681D80-B435-11E9-9278-68D0E5697425 call_identifier: FP7 grant_number: '291734' name: International IST Postdoc Fellowship Programme publication: PLoS Genetics publication_identifier: issn: - '15537390' publication_status: published publisher: Public Library of Science publist_id: '7275' pubrep_id: '959' quality_controlled: '1' related_material: record: - id: '9844' relation: research_data status: public - id: '9845' relation: research_data status: public - id: '9846' relation: research_data status: public scopus_import: 1 status: public title: Cell-to-cell variation and specialization in sugar metabolism in clonal bacterial populations 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: '2017' ... --- _id: '9845' abstract: - lang: eng text: "Estimates of 13 C-arabinose and 2 H-glucose uptake from the fractions of heavy isotopes measured\tin single cells" article_processing_charge: No author: - first_name: Nela full_name: Nikolic, Nela id: 42D9CABC-F248-11E8-B48F-1D18A9856A87 last_name: Nikolic orcid: 0000-0001-9068-6090 - first_name: Frank full_name: Schreiber, Frank last_name: Schreiber - first_name: Alma full_name: Dal Co, Alma last_name: Dal Co - first_name: Daniel full_name: Kiviet, Daniel last_name: Kiviet - first_name: Tobias full_name: Bergmiller, Tobias id: 2C471CFA-F248-11E8-B48F-1D18A9856A87 last_name: Bergmiller orcid: 0000-0001-5396-4346 - first_name: Sten full_name: Littmann, Sten last_name: Littmann - first_name: Marcel full_name: Kuypers, Marcel last_name: Kuypers - first_name: Martin full_name: Ackermann, Martin last_name: Ackermann citation: ama: Nikolic N, Schreiber F, Dal Co A, et al. Mathematical model. 2017. doi:10.1371/journal.pgen.1007122.s017 apa: Nikolic, N., Schreiber, F., Dal Co, A., Kiviet, D., Bergmiller, T., Littmann, S., … Ackermann, M. (2017). Mathematical model. Public Library of Science. https://doi.org/10.1371/journal.pgen.1007122.s017 chicago: Nikolic, Nela, Frank Schreiber, Alma Dal Co, Daniel Kiviet, Tobias Bergmiller, Sten Littmann, Marcel Kuypers, and Martin Ackermann. “Mathematical Model.” Public Library of Science, 2017. https://doi.org/10.1371/journal.pgen.1007122.s017. ieee: N. Nikolic et al., “Mathematical model.” Public Library of Science, 2017. ista: Nikolic N, Schreiber F, Dal Co A, Kiviet D, Bergmiller T, Littmann S, Kuypers M, Ackermann M. 2017. Mathematical model, Public Library of Science, 10.1371/journal.pgen.1007122.s017. mla: Nikolic, Nela, et al. Mathematical Model. Public Library of Science, 2017, doi:10.1371/journal.pgen.1007122.s017. short: N. Nikolic, F. Schreiber, A. Dal Co, D. Kiviet, T. Bergmiller, S. Littmann, M. Kuypers, M. Ackermann, (2017). date_created: 2021-08-09T13:31:51Z date_published: 2017-12-18T00:00:00Z date_updated: 2023-02-23T12:25:04Z day: '18' department: - _id: CaGu doi: 10.1371/journal.pgen.1007122.s017 month: '12' oa_version: None publisher: Public Library of Science related_material: record: - id: '541' relation: used_in_publication status: public status: public title: Mathematical model type: research_data_reference user_id: 6785fbc1-c503-11eb-8a32-93094b40e1cf year: '2017' ... --- _id: '9846' article_processing_charge: No author: - first_name: Nela full_name: Nikolic, Nela id: 42D9CABC-F248-11E8-B48F-1D18A9856A87 last_name: Nikolic orcid: 0000-0001-9068-6090 - first_name: Frank full_name: Schreiber, Frank last_name: Schreiber - first_name: Alma full_name: Dal Co, Alma last_name: Dal Co - first_name: Daniel full_name: Kiviet, Daniel last_name: Kiviet - first_name: Tobias full_name: Bergmiller, Tobias id: 2C471CFA-F248-11E8-B48F-1D18A9856A87 last_name: Bergmiller orcid: 0000-0001-5396-4346 - first_name: Sten full_name: Littmann, Sten last_name: Littmann - first_name: Marcel full_name: Kuypers, Marcel last_name: Kuypers - first_name: Martin full_name: Ackermann, Martin last_name: Ackermann citation: ama: Nikolic N, Schreiber F, Dal Co A, et al. Supplementary methods. 2017. doi:10.1371/journal.pgen.1007122.s016 apa: Nikolic, N., Schreiber, F., Dal Co, A., Kiviet, D., Bergmiller, T., Littmann, S., … Ackermann, M. (2017). Supplementary methods. Public Library of Science. https://doi.org/10.1371/journal.pgen.1007122.s016 chicago: Nikolic, Nela, Frank Schreiber, Alma Dal Co, Daniel Kiviet, Tobias Bergmiller, Sten Littmann, Marcel Kuypers, and Martin Ackermann. “Supplementary Methods.” Public Library of Science, 2017. https://doi.org/10.1371/journal.pgen.1007122.s016. ieee: N. Nikolic et al., “Supplementary methods.” Public Library of Science, 2017. ista: Nikolic N, Schreiber F, Dal Co A, Kiviet D, Bergmiller T, Littmann S, Kuypers M, Ackermann M. 2017. Supplementary methods, Public Library of Science, 10.1371/journal.pgen.1007122.s016. mla: Nikolic, Nela, et al. Supplementary Methods. Public Library of Science, 2017, doi:10.1371/journal.pgen.1007122.s016. short: N. Nikolic, F. Schreiber, A. Dal Co, D. Kiviet, T. Bergmiller, S. Littmann, M. Kuypers, M. Ackermann, (2017). date_created: 2021-08-09T13:35:17Z date_published: 2017-12-18T00:00:00Z date_updated: 2023-02-23T12:25:04Z day: '18' department: - _id: CaGu doi: 10.1371/journal.pgen.1007122.s016 month: '12' oa_version: Published Version publisher: Public Library of Science related_material: record: - id: '541' relation: used_in_publication status: public status: public title: Supplementary methods type: research_data_reference user_id: 6785fbc1-c503-11eb-8a32-93094b40e1cf year: '2017' ... --- _id: '9844' article_processing_charge: No author: - first_name: Nela full_name: Nikolic, Nela id: 42D9CABC-F248-11E8-B48F-1D18A9856A87 last_name: Nikolic orcid: 0000-0001-9068-6090 - first_name: Frank full_name: Schreiber, Frank last_name: Schreiber - first_name: Alma full_name: Dal Co, Alma last_name: Dal Co - first_name: Daniel full_name: Kiviet, Daniel last_name: Kiviet - first_name: Tobias full_name: Bergmiller, Tobias id: 2C471CFA-F248-11E8-B48F-1D18A9856A87 last_name: Bergmiller orcid: 0000-0001-5396-4346 - first_name: Sten full_name: Littmann, Sten last_name: Littmann - first_name: Marcel full_name: Kuypers, Marcel last_name: Kuypers - first_name: Martin full_name: Ackermann, Martin last_name: Ackermann citation: ama: Nikolic N, Schreiber F, Dal Co A, et al. Source data for figures and tables. 2017. doi:10.1371/journal.pgen.1007122.s018 apa: Nikolic, N., Schreiber, F., Dal Co, A., Kiviet, D., Bergmiller, T., Littmann, S., … Ackermann, M. (2017). Source data for figures and tables. Public Library of Science. https://doi.org/10.1371/journal.pgen.1007122.s018 chicago: Nikolic, Nela, Frank Schreiber, Alma Dal Co, Daniel Kiviet, Tobias Bergmiller, Sten Littmann, Marcel Kuypers, and Martin Ackermann. “Source Data for Figures and Tables.” Public Library of Science, 2017. https://doi.org/10.1371/journal.pgen.1007122.s018. ieee: N. Nikolic et al., “Source data for figures and tables.” Public Library of Science, 2017. ista: Nikolic N, Schreiber F, Dal Co A, Kiviet D, Bergmiller T, Littmann S, Kuypers M, Ackermann M. 2017. Source data for figures and tables, Public Library of Science, 10.1371/journal.pgen.1007122.s018. mla: Nikolic, Nela, et al. Source Data for Figures and Tables. Public Library of Science, 2017, doi:10.1371/journal.pgen.1007122.s018. short: N. Nikolic, F. Schreiber, A. Dal Co, D. Kiviet, T. Bergmiller, S. Littmann, M. Kuypers, M. Ackermann, (2017). date_created: 2021-08-09T13:27:16Z date_published: 2017-12-18T00:00:00Z date_updated: 2023-02-23T12:25:04Z day: '18' department: - _id: CaGu doi: 10.1371/journal.pgen.1007122.s018 month: '12' oa_version: Published Version publisher: Public Library of Science related_material: record: - id: '541' relation: used_in_publication status: public status: public title: Source data for figures and tables type: research_data_reference user_id: 6785fbc1-c503-11eb-8a32-93094b40e1cf year: '2017' ... --- _id: '5560' abstract: - lang: eng text: "This repository contains the data collected for the manuscript \"Biased partitioning of the multi-drug efflux pump AcrAB-TolC underlies long-lived phenotypic heterogeneity\".\r\nThe data is compressed into a single archive. Within the archive, different folders correspond to figures of the main text and the SI of the related publication.\r\nData is saved as plain text, with each folder containing a separate readme file describing the format. Typically, the data is from fluorescence microscopy measurements of single cells growing in a microfluidic \"mother machine\" device, and consists of relevant values (primarily arbitrary unit or normalized fluorescence measurements, and division times / growth rates) after raw microscopy images have been processed, segmented, and their features extracted, as described in the methods section of the related publication." article_processing_charge: No author: - first_name: Tobias full_name: Bergmiller, Tobias id: 2C471CFA-F248-11E8-B48F-1D18A9856A87 last_name: Bergmiller orcid: 0000-0001-5396-4346 - first_name: Anna M full_name: Andersson, Anna M id: 2B8A40DA-F248-11E8-B48F-1D18A9856A87 last_name: Andersson orcid: 0000-0003-2912-6769 - first_name: Kathrin full_name: Tomasek, Kathrin id: 3AEC8556-F248-11E8-B48F-1D18A9856A87 last_name: Tomasek orcid: 0000-0003-3768-877X - first_name: Enrique full_name: Balleza, Enrique last_name: Balleza - first_name: Daniel full_name: Kiviet, Daniel last_name: Kiviet - first_name: Robert full_name: Hauschild, Robert id: 4E01D6B4-F248-11E8-B48F-1D18A9856A87 last_name: Hauschild orcid: 0000-0001-9843-3522 - first_name: Gasper full_name: Tkacik, Gasper id: 3D494DCA-F248-11E8-B48F-1D18A9856A87 last_name: Tkacik orcid: 0000-0002-6699-1455 - first_name: Calin C full_name: Guet, Calin C id: 47F8433E-F248-11E8-B48F-1D18A9856A87 last_name: Guet orcid: 0000-0001-6220-2052 citation: ama: Bergmiller T, Andersson AM, Tomasek K, et al. Biased partitioning of the multi-drug efflux pump AcrAB-TolC underlies long-lived phenotypic heterogeneity. 2017. doi:10.15479/AT:ISTA:53 apa: Bergmiller, T., Andersson, A. M., Tomasek, K., Balleza, E., Kiviet, D., Hauschild, R., … Guet, C. C. (2017). Biased partitioning of the multi-drug efflux pump AcrAB-TolC underlies long-lived phenotypic heterogeneity. Institute of Science and Technology Austria. https://doi.org/10.15479/AT:ISTA:53 chicago: Bergmiller, Tobias, Anna M Andersson, Kathrin Tomasek, Enrique Balleza, Daniel Kiviet, Robert Hauschild, Gašper Tkačik, and Calin C Guet. “Biased Partitioning of the Multi-Drug Efflux Pump AcrAB-TolC Underlies Long-Lived Phenotypic Heterogeneity.” Institute of Science and Technology Austria, 2017. https://doi.org/10.15479/AT:ISTA:53. ieee: T. Bergmiller et al., “Biased partitioning of the multi-drug efflux pump AcrAB-TolC underlies long-lived phenotypic heterogeneity.” Institute of Science and Technology Austria, 2017. ista: Bergmiller T, Andersson AM, Tomasek K, Balleza E, Kiviet D, Hauschild R, Tkačik G, Guet CC. 2017. Biased partitioning of the multi-drug efflux pump AcrAB-TolC underlies long-lived phenotypic heterogeneity, Institute of Science and Technology Austria, 10.15479/AT:ISTA:53. mla: Bergmiller, Tobias, et al. Biased Partitioning of the Multi-Drug Efflux Pump AcrAB-TolC Underlies Long-Lived Phenotypic Heterogeneity. Institute of Science and Technology Austria, 2017, doi:10.15479/AT:ISTA:53. short: T. Bergmiller, A.M. Andersson, K. Tomasek, E. Balleza, D. Kiviet, R. Hauschild, G. Tkačik, C.C. Guet, (2017). datarep_id: '53' date_created: 2018-12-12T12:31:32Z date_published: 2017-03-10T00:00:00Z date_updated: 2024-02-21T13:49:00Z day: '10' ddc: - '571' department: - _id: CaGu - _id: GaTk - _id: Bio doi: 10.15479/AT:ISTA:53 file: - access_level: open_access checksum: d77859af757ac8025c50c7b12b52eaf3 content_type: application/zip creator: system date_created: 2018-12-12T13:02:38Z date_updated: 2020-07-14T12:47:03Z file_id: '5603' file_name: IST-2017-53-v1+1_Data_MDE.zip file_size: 6773204 relation: main_file file_date_updated: 2020-07-14T12:47:03Z has_accepted_license: '1' keyword: - single cell microscopy - mother machine microfluidic device - AcrAB-TolC pump - multi-drug efflux - Escherichia coli month: '03' oa: 1 oa_version: Published Version publisher: Institute of Science and Technology Austria related_material: record: - id: '665' relation: research_paper status: public status: public title: Biased partitioning of the multi-drug efflux pump AcrAB-TolC underlies long-lived phenotypic heterogeneity tmp: image: /images/cc_0.png legal_code_url: https://creativecommons.org/publicdomain/zero/1.0/legalcode name: Creative Commons Public Domain Dedication (CC0 1.0) short: CC0 (1.0) type: research_data user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 year: '2017' ... --- _id: '665' abstract: - lang: eng text: The molecular mechanisms underlying phenotypic variation in isogenic bacterial populations remain poorly understood.We report that AcrAB-TolC, the main multidrug efflux pump of Escherichia coli, exhibits a strong partitioning bias for old cell poles by a segregation mechanism that is mediated by ternary AcrAB-TolC complex formation. Mother cells inheriting old poles are phenotypically distinct and display increased drug efflux activity relative to daughters. Consequently, we find systematic and long-lived growth differences between mother and daughter cells in the presence of subinhibitory drug concentrations. A simple model for biased partitioning predicts a population structure of long-lived and highly heterogeneous phenotypes. This straightforward mechanism of generating sustained growth rate differences at subinhibitory antibiotic concentrations has implications for understanding the emergence of multidrug resistance in bacteria. article_processing_charge: No article_type: original author: - first_name: Tobias full_name: Bergmiller, Tobias id: 2C471CFA-F248-11E8-B48F-1D18A9856A87 last_name: Bergmiller orcid: 0000-0001-5396-4346 - first_name: Anna M full_name: Andersson, Anna M id: 2B8A40DA-F248-11E8-B48F-1D18A9856A87 last_name: Andersson orcid: 0000-0003-2912-6769 - first_name: Kathrin full_name: Tomasek, Kathrin id: 3AEC8556-F248-11E8-B48F-1D18A9856A87 last_name: Tomasek orcid: 0000-0003-3768-877X - first_name: Enrique full_name: Balleza, Enrique last_name: Balleza - first_name: Daniel full_name: Kiviet, Daniel last_name: Kiviet - first_name: Robert full_name: Hauschild, Robert id: 4E01D6B4-F248-11E8-B48F-1D18A9856A87 last_name: Hauschild orcid: 0000-0001-9843-3522 - first_name: Gasper full_name: Tkacik, Gasper id: 3D494DCA-F248-11E8-B48F-1D18A9856A87 last_name: Tkacik orcid: 0000-0002-6699-1455 - first_name: Calin C full_name: Guet, Calin C id: 47F8433E-F248-11E8-B48F-1D18A9856A87 last_name: Guet orcid: 0000-0001-6220-2052 citation: ama: Bergmiller T, Andersson AM, Tomasek K, et al. Biased partitioning of the multidrug efflux pump AcrAB TolC underlies long lived phenotypic heterogeneity. Science. 2017;356(6335):311-315. doi:10.1126/science.aaf4762 apa: Bergmiller, T., Andersson, A. M., Tomasek, K., Balleza, E., Kiviet, D., Hauschild, R., … Guet, C. C. (2017). Biased partitioning of the multidrug efflux pump AcrAB TolC underlies long lived phenotypic heterogeneity. Science. American Association for the Advancement of Science. https://doi.org/10.1126/science.aaf4762 chicago: Bergmiller, Tobias, Anna M Andersson, Kathrin Tomasek, Enrique Balleza, Daniel Kiviet, Robert Hauschild, Gašper Tkačik, and Calin C Guet. “Biased Partitioning of the Multidrug Efflux Pump AcrAB TolC Underlies Long Lived Phenotypic Heterogeneity.” Science. American Association for the Advancement of Science, 2017. https://doi.org/10.1126/science.aaf4762. ieee: T. Bergmiller et al., “Biased partitioning of the multidrug efflux pump AcrAB TolC underlies long lived phenotypic heterogeneity,” Science, vol. 356, no. 6335. American Association for the Advancement of Science, pp. 311–315, 2017. ista: Bergmiller T, Andersson AM, Tomasek K, Balleza E, Kiviet D, Hauschild R, Tkačik G, Guet CC. 2017. Biased partitioning of the multidrug efflux pump AcrAB TolC underlies long lived phenotypic heterogeneity. Science. 356(6335), 311–315. mla: Bergmiller, Tobias, et al. “Biased Partitioning of the Multidrug Efflux Pump AcrAB TolC Underlies Long Lived Phenotypic Heterogeneity.” Science, vol. 356, no. 6335, American Association for the Advancement of Science, 2017, pp. 311–15, doi:10.1126/science.aaf4762. short: T. Bergmiller, A.M. Andersson, K. Tomasek, E. Balleza, D. Kiviet, R. Hauschild, G. Tkačik, C.C. Guet, Science 356 (2017) 311–315. date_created: 2018-12-11T11:47:48Z date_published: 2017-04-21T00:00:00Z date_updated: 2024-02-21T13:49:00Z day: '21' department: - _id: CaGu - _id: GaTk - _id: Bio doi: 10.1126/science.aaf4762 intvolume: ' 356' issue: '6335' language: - iso: eng month: '04' oa_version: None page: 311 - 315 project: - _id: 254E9036-B435-11E9-9278-68D0E5697425 call_identifier: FWF grant_number: P28844-B27 name: Biophysics of information processing in gene regulation publication: Science publication_identifier: issn: - '00368075' publication_status: published publisher: American Association for the Advancement of Science publist_id: '7064' quality_controlled: '1' related_material: record: - id: '5560' relation: popular_science status: public scopus_import: 1 status: public title: Biased partitioning of the multidrug efflux pump AcrAB TolC underlies long lived phenotypic heterogeneity type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 356 year: '2017' ... --- _id: '1250' abstract: - lang: eng text: In bacteria, replicative aging manifests as a difference in growth or survival between the two cells emerging from division. One cell can be regarded as an aging mother with a decreased potential for future survival and division, the other as a rejuvenated daughter. Here, we aimed at investigating some of the processes involved in aging in the bacterium Escherichia coli, where the two types of cells can be distinguished by the age of their cell poles. We found that certain changes in the regulation of the carbohydrate metabolism can affect aging. A mutation in the carbon storage regulator gene, csrA, leads to a dramatically shorter replicative lifespan; csrA mutants stop dividing once their pole exceeds an age of about five divisions. These old-pole cells accumulate glycogen at their old cell poles; after their last division, they do not contain a chromosome, presumably because of spatial exclusion by the glycogen aggregates. The new-pole daughters produced by these aging mothers are born young; they only express the deleterious phenotype once their pole is old. These results demonstrate how manipulations of nutrient allocation can lead to the exclusion of the chromosome and limit replicative lifespan in E. coli, and illustrate how mutations can have phenotypic effects that are specific for cells with old poles. This raises the question how bacteria can avoid the accumulation of such mutations in their genomes over evolutionary times, and how they can achieve the long replicative lifespans that have recently been reported. acknowledgement: This manuscript is dedicated to the memory of Alex Böhm, who was a great friend and a passionate biologist. Alex passed away after the initial submission of this manuscript. We thank Vesna Olivera and Ursula Sauder from the Zentrum für Mikroskopie Uni Basel for excellent service, and Olin Silander, Nikki Freed, and Nela Nikolic for helpful discussions. This work was supported by the Swiss National Science Foundation grants to M. Ackermann and Urs Jenal (supporting AB). article_number: e1005974 author: - first_name: Alex full_name: Boehm, Alex last_name: Boehm - first_name: Markus full_name: Arnoldini, Markus last_name: Arnoldini - first_name: Tobias full_name: Bergmiller, Tobias id: 2C471CFA-F248-11E8-B48F-1D18A9856A87 last_name: Bergmiller orcid: 0000-0001-5396-4346 - first_name: Thomas full_name: Röösli, Thomas last_name: Röösli - first_name: Colette full_name: Bigosch, Colette last_name: Bigosch - first_name: Martin full_name: Ackermann, Martin last_name: Ackermann citation: ama: Boehm A, Arnoldini M, Bergmiller T, Röösli T, Bigosch C, Ackermann M. Genetic manipulation of glycogen allocation affects replicative lifespan in E coli. PLoS Genetics. 2016;12(4). doi:10.1371/journal.pgen.1005974 apa: Boehm, A., Arnoldini, M., Bergmiller, T., Röösli, T., Bigosch, C., & Ackermann, M. (2016). Genetic manipulation of glycogen allocation affects replicative lifespan in E coli. PLoS Genetics. Public Library of Science. https://doi.org/10.1371/journal.pgen.1005974 chicago: Boehm, Alex, Markus Arnoldini, Tobias Bergmiller, Thomas Röösli, Colette Bigosch, and Martin Ackermann. “Genetic Manipulation of Glycogen Allocation Affects Replicative Lifespan in E Coli.” PLoS Genetics. Public Library of Science, 2016. https://doi.org/10.1371/journal.pgen.1005974. ieee: A. Boehm, M. Arnoldini, T. Bergmiller, T. Röösli, C. Bigosch, and M. Ackermann, “Genetic manipulation of glycogen allocation affects replicative lifespan in E coli,” PLoS Genetics, vol. 12, no. 4. Public Library of Science, 2016. ista: Boehm A, Arnoldini M, Bergmiller T, Röösli T, Bigosch C, Ackermann M. 2016. Genetic manipulation of glycogen allocation affects replicative lifespan in E coli. PLoS Genetics. 12(4), e1005974. mla: Boehm, Alex, et al. “Genetic Manipulation of Glycogen Allocation Affects Replicative Lifespan in E Coli.” PLoS Genetics, vol. 12, no. 4, e1005974, Public Library of Science, 2016, doi:10.1371/journal.pgen.1005974. short: A. Boehm, M. Arnoldini, T. Bergmiller, T. Röösli, C. Bigosch, M. Ackermann, PLoS Genetics 12 (2016). date_created: 2018-12-11T11:50:56Z date_published: 2016-04-19T00:00:00Z date_updated: 2023-02-23T14:11:39Z day: '19' ddc: - '576' - '579' department: - _id: CaGu doi: 10.1371/journal.pgen.1005974 file: - access_level: open_access checksum: 53d22b2b39e5adc243d34f18b2615a85 content_type: application/pdf creator: system date_created: 2018-12-12T10:14:17Z date_updated: 2020-07-14T12:44:41Z file_id: '5067' file_name: IST-2016-705-v1+1_journal.pgen.1005974.PDF file_size: 6273249 relation: main_file file_date_updated: 2020-07-14T12:44:41Z has_accepted_license: '1' intvolume: ' 12' issue: '4' language: - iso: eng month: '04' oa: 1 oa_version: Published Version publication: PLoS Genetics publication_status: published publisher: Public Library of Science publist_id: '6077' pubrep_id: '705' quality_controlled: '1' related_material: record: - id: '9873' relation: research_data status: public scopus_import: 1 status: public title: Genetic manipulation of glycogen allocation affects replicative lifespan in E coli 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: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87 volume: 12 year: '2016' ... --- _id: '9873' article_processing_charge: No author: - first_name: Alex full_name: Boehm, Alex last_name: Boehm - first_name: Markus full_name: Arnoldini, Markus last_name: Arnoldini - first_name: Tobias full_name: Bergmiller, Tobias id: 2C471CFA-F248-11E8-B48F-1D18A9856A87 last_name: Bergmiller orcid: 0000-0001-5396-4346 - first_name: Thomas full_name: Röösli, Thomas last_name: Röösli - first_name: Colette full_name: Bigosch, Colette last_name: Bigosch - first_name: Martin full_name: Ackermann, Martin last_name: Ackermann citation: ama: Boehm A, Arnoldini M, Bergmiller T, Röösli T, Bigosch C, Ackermann M. Quantification of the growth rate reduction as a consequence of age-specific mortality. 2016. doi:10.1371/journal.pgen.1005974.s015 apa: Boehm, A., Arnoldini, M., Bergmiller, T., Röösli, T., Bigosch, C., & Ackermann, M. (2016). Quantification of the growth rate reduction as a consequence of age-specific mortality. Public Library of Science. https://doi.org/10.1371/journal.pgen.1005974.s015 chicago: Boehm, Alex, Markus Arnoldini, Tobias Bergmiller, Thomas Röösli, Colette Bigosch, and Martin Ackermann. “Quantification of the Growth Rate Reduction as a Consequence of Age-Specific Mortality.” Public Library of Science, 2016. https://doi.org/10.1371/journal.pgen.1005974.s015. ieee: A. Boehm, M. Arnoldini, T. Bergmiller, T. Röösli, C. Bigosch, and M. Ackermann, “Quantification of the growth rate reduction as a consequence of age-specific mortality.” Public Library of Science, 2016. ista: Boehm A, Arnoldini M, Bergmiller T, Röösli T, Bigosch C, Ackermann M. 2016. Quantification of the growth rate reduction as a consequence of age-specific mortality, Public Library of Science, 10.1371/journal.pgen.1005974.s015. mla: Boehm, Alex, et al. Quantification of the Growth Rate Reduction as a Consequence of Age-Specific Mortality. Public Library of Science, 2016, doi:10.1371/journal.pgen.1005974.s015. short: A. Boehm, M. Arnoldini, T. Bergmiller, T. Röösli, C. Bigosch, M. Ackermann, (2016). date_created: 2021-08-10T09:42:34Z date_updated: 2023-02-21T16:50:13Z day: '19' department: - _id: CaGu doi: 10.1371/journal.pgen.1005974.s015 month: '04' oa_version: Published Version publisher: Public Library of Science related_material: record: - id: '1250' relation: used_in_publication status: public status: public title: Quantification of the growth rate reduction as a consequence of age-specific mortality type: research_data_reference user_id: 6785fbc1-c503-11eb-8a32-93094b40e1cf year: '2016' ... --- _id: '5749' abstract: - lang: eng text: Parasitism creates selection for resistance mechanisms in host populations and is hypothesized to promote increased host evolvability. However, the influence of these traits on host evolution when parasites are no longer present is unclear. We used experimental evolution and whole-genome sequencing of Escherichia coli to determine the effects of past and present exposure to parasitic viruses (phages) on the spread of mutator alleles, resistance, and bacterial competitive fitness. We found that mutator alleles spread rapidly during adaptation to any of four different phage species, and this pattern was even more pronounced with multiple phages present simultaneously. However, hypermutability did not detectably accelerate adaptation in the absence of phages and recovery of fitness costs associated with resistance. Several lineages evolved phage resistance through elevated mucoidy, and during subsequent evolution in phage-free conditions they rapidly reverted to nonmucoid, phage-susceptible phenotypes. Genome sequencing revealed that this phenotypic reversion was achieved by additional genetic changes rather than by genotypic reversion of the initial resistance mutations. Insertion sequence (IS) elements played a key role in both the acquisition of resistance and adaptation in the absence of parasites; unlike single nucleotide polymorphisms, IS insertions were not more frequent in mutator lineages. Our results provide a genetic explanation for rapid reversion of mucoidy, a phenotype observed in other bacterial species including human pathogens. Moreover, this demonstrates that the types of genetic change underlying adaptation to fitness costs, and consequently the impact of evolvability mechanisms such as increased point-mutation rates, depend critically on the mechanism of resistance. acknowledgement: The authors thank three anonymous reviewers and the editor for helpful comments on the manuscript, as well as Dominique Schneider for feedback on an earlier draft, Jenna Gallie for lytic λ and Julien Capelle for T5 and T6. This work was supported by the Swiss National Science Foundation (PZ00P3_148255 to A.H.) and an EU Marie Curie PEOPLE Postdoctoral Fellowship for Career Development (FP7-PEOPLE-2012-IEF-331824 to S.W.). article_processing_charge: No author: - first_name: Sébastien full_name: Wielgoss, Sébastien last_name: Wielgoss - first_name: Tobias full_name: Bergmiller, Tobias id: 2C471CFA-F248-11E8-B48F-1D18A9856A87 last_name: Bergmiller orcid: 0000-0001-5396-4346 - first_name: Anna M. full_name: Bischofberger, Anna M. last_name: Bischofberger - first_name: Alex R. full_name: Hall, Alex R. last_name: Hall citation: ama: Wielgoss S, Bergmiller T, Bischofberger AM, Hall AR. Adaptation to parasites and costs of parasite resistance in mutator and nonmutator bacteria. Molecular Biology and Evolution. 2016;33(3):770-782. doi:10.1093/molbev/msv270 apa: Wielgoss, S., Bergmiller, T., Bischofberger, A. M., & Hall, A. R. (2016). Adaptation to parasites and costs of parasite resistance in mutator and nonmutator bacteria. Molecular Biology and Evolution. Oxford University Press. https://doi.org/10.1093/molbev/msv270 chicago: Wielgoss, Sébastien, Tobias Bergmiller, Anna M. Bischofberger, and Alex R. Hall. “Adaptation to Parasites and Costs of Parasite Resistance in Mutator and Nonmutator Bacteria.” Molecular Biology and Evolution. Oxford University Press, 2016. https://doi.org/10.1093/molbev/msv270. ieee: S. Wielgoss, T. Bergmiller, A. M. Bischofberger, and A. R. Hall, “Adaptation to parasites and costs of parasite resistance in mutator and nonmutator bacteria,” Molecular Biology and Evolution, vol. 33, no. 3. Oxford University Press, pp. 770–782, 2016. ista: Wielgoss S, Bergmiller T, Bischofberger AM, Hall AR. 2016. Adaptation to parasites and costs of parasite resistance in mutator and nonmutator bacteria. Molecular Biology and Evolution. 33(3), 770–782. mla: Wielgoss, Sébastien, et al. “Adaptation to Parasites and Costs of Parasite Resistance in Mutator and Nonmutator Bacteria.” Molecular Biology and Evolution, vol. 33, no. 3, Oxford University Press, 2016, pp. 770–82, doi:10.1093/molbev/msv270. short: S. Wielgoss, T. Bergmiller, A.M. Bischofberger, A.R. Hall, Molecular Biology and Evolution 33 (2016) 770–782. date_created: 2018-12-18T13:18:10Z date_published: 2016-03-01T00:00:00Z date_updated: 2023-09-05T13:46:05Z day: '01' ddc: - '576' department: - _id: CaGu doi: 10.1093/molbev/msv270 external_id: pmid: - '26609077' file: - access_level: open_access checksum: 47d9010690b6c5c17f2ac830cc63ac5c content_type: application/pdf creator: dernst date_created: 2018-12-18T13:21:45Z date_updated: 2020-07-14T12:47:10Z file_id: '5750' file_name: 2016_MolBiolEvol_Wielgoss.pdf file_size: 634037 relation: main_file file_date_updated: 2020-07-14T12:47:10Z has_accepted_license: '1' intvolume: ' 33' issue: '3' language: - iso: eng license: https://creativecommons.org/licenses/by-nc/4.0/ month: '03' oa: 1 oa_version: Published Version page: 770-782 pmid: 1 publication: Molecular Biology and Evolution publication_identifier: eissn: - 1537-1719 issn: - 0737-4038 publication_status: published publisher: Oxford University Press pubrep_id: '587' quality_controlled: '1' related_material: record: - id: '9719' relation: research_data status: public scopus_import: '1' status: public title: Adaptation to parasites and costs of parasite resistance in mutator and nonmutator bacteria tmp: image: /images/cc_by_nc.png legal_code_url: https://creativecommons.org/licenses/by-nc/4.0/legalcode name: Creative Commons Attribution-NonCommercial 4.0 International (CC BY-NC 4.0) short: CC BY-NC (4.0) type: journal_article user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1 volume: 33 year: '2016' ... --- _id: '1243' abstract: - lang: eng text: Restriction-modification (RM) systems represent a minimal and ubiquitous biological system of self/non-self discrimination in prokaryotes [1], which protects hosts from exogenous DNA [2]. The mechanism is based on the balance between methyltransferase (M) and cognate restriction endonuclease (R). M tags endogenous DNA as self by methylating short specific DNA sequences called restriction sites, whereas R recognizes unmethylated restriction sites as non-self and introduces a double-stranded DNA break [3]. Restriction sites are significantly underrepresented in prokaryotic genomes [4-7], suggesting that the discrimination mechanism is imperfect and occasionally leads to autoimmunity due to self-DNA cleavage (self-restriction) [8]. Furthermore, RM systems can promote DNA recombination [9] and contribute to genetic variation in microbial populations, thus facilitating adaptive evolution [10]. However, cleavage of self-DNA by RM systems as elements shaping prokaryotic genomes has not been directly detected, and its cause, frequency, and outcome are unknown. We quantify self-restriction caused by two RM systems of Escherichia coli and find that, in agreement with levels of restriction site avoidance, EcoRI, but not EcoRV, cleaves self-DNA at a measurable rate. Self-restriction is a stochastic process, which temporarily induces the SOS response, and is followed by DNA repair, maintaining cell viability. We find that RM systems with higher restriction efficiency against bacteriophage infections exhibit a higher rate of self-restriction, and that this rate can be further increased by stochastic imbalance between R and M. Our results identify molecular noise in RM systems as a factor shaping prokaryotic genomes. acknowledgement: This work was funded by an HFSP Young Investigators’ grant. M.P. is a recipient of a DOC Fellowship of the Austrian Academy of Science at the Institute of Science and Technology Austria. R.O. and Y.W. were supported by the Platform for Dynamic Approaches to Living System from MEXT, Japan. We wish to thank I. Kobayashi for providing us with the EcoRI and EcoRV plasmids, and A. Campbell for providing us with the λ vir phage. We thank D. Siekhaus and C. Uhler and members of the C.C.G. and J.P. Bollback laboratories for in-depth discussions. We thank B. Stern for comments on an earlier version of the manuscript. We especially thank B.R. Levin for advice and comments, and the anonymous reviewers for significantly improving the manuscript. author: - first_name: Maros full_name: Pleska, Maros id: 4569785E-F248-11E8-B48F-1D18A9856A87 last_name: Pleska orcid: 0000-0001-7460-7479 - first_name: Long full_name: Qian, Long last_name: Qian - first_name: Reiko full_name: Okura, Reiko last_name: Okura - first_name: Tobias full_name: Bergmiller, Tobias id: 2C471CFA-F248-11E8-B48F-1D18A9856A87 last_name: Bergmiller orcid: 0000-0001-5396-4346 - first_name: Yuichi full_name: Wakamoto, Yuichi last_name: Wakamoto - first_name: Edo full_name: Kussell, Edo last_name: Kussell - first_name: Calin C full_name: Guet, Calin C id: 47F8433E-F248-11E8-B48F-1D18A9856A87 last_name: Guet orcid: 0000-0001-6220-2052 citation: ama: Pleska M, Qian L, Okura R, et al. Bacterial autoimmunity due to a restriction-modification system. Current Biology. 2016;26(3):404-409. doi:10.1016/j.cub.2015.12.041 apa: Pleska, M., Qian, L., Okura, R., Bergmiller, T., Wakamoto, Y., Kussell, E., & Guet, C. C. (2016). Bacterial autoimmunity due to a restriction-modification system. Current Biology. Cell Press. https://doi.org/10.1016/j.cub.2015.12.041 chicago: Pleska, Maros, Long Qian, Reiko Okura, Tobias Bergmiller, Yuichi Wakamoto, Edo Kussell, and Calin C Guet. “Bacterial Autoimmunity Due to a Restriction-Modification System.” Current Biology. Cell Press, 2016. https://doi.org/10.1016/j.cub.2015.12.041. ieee: M. Pleska et al., “Bacterial autoimmunity due to a restriction-modification system,” Current Biology, vol. 26, no. 3. Cell Press, pp. 404–409, 2016. ista: Pleska M, Qian L, Okura R, Bergmiller T, Wakamoto Y, Kussell E, Guet CC. 2016. Bacterial autoimmunity due to a restriction-modification system. Current Biology. 26(3), 404–409. mla: Pleska, Maros, et al. “Bacterial Autoimmunity Due to a Restriction-Modification System.” Current Biology, vol. 26, no. 3, Cell Press, 2016, pp. 404–09, doi:10.1016/j.cub.2015.12.041. short: M. Pleska, L. Qian, R. Okura, T. Bergmiller, Y. Wakamoto, E. Kussell, C.C. Guet, Current Biology 26 (2016) 404–409. date_created: 2018-12-11T11:50:54Z date_published: 2016-02-08T00:00:00Z date_updated: 2023-09-07T11:59:32Z day: '08' department: - _id: CaGu doi: 10.1016/j.cub.2015.12.041 intvolume: ' 26' issue: '3' language: - iso: eng month: '02' oa_version: None page: 404 - 409 project: - _id: 251D65D8-B435-11E9-9278-68D0E5697425 grant_number: '24210' name: Effects of Stochasticity on the Function of Restriction-Modi cation Systems at the Single-Cell Level (DOC Fellowship) publication: Current Biology publication_status: published publisher: Cell Press publist_id: '6087' quality_controlled: '1' related_material: record: - id: '202' relation: dissertation_contains status: public scopus_import: 1 status: public title: Bacterial autoimmunity due to a restriction-modification system type: journal_article user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87 volume: 26 year: '2016' ... --- _id: '9719' abstract: - lang: eng text: Parasitism creates selection for resistance mechanisms in host populations and is hypothesized to promote increased host evolvability. However, the influence of these traits on host evolution when parasites are no longer present is unclear. We used experimental evolution and whole-genome sequencing of Escherichia coli to determine the effects of past and present exposure to parasitic viruses (phages) on the spread of mutator alleles, resistance, and bacterial competitive fitness. We found that mutator alleles spread rapidly during adaptation to any of four different phage species, and this pattern was even more pronounced with multiple phages present simultaneously. However, hypermutability did not detectably accelerate adaptation in the absence of phages and recovery of fitness costs associated with resistance. Several lineages evolved phage resistance through elevated mucoidy, and during subsequent evolution in phage-free conditions they rapidly reverted to nonmucoid, phage-susceptible phenotypes. Genome sequencing revealed that this phenotypic reversion was achieved by additional genetic changes rather than by genotypic reversion of the initial resistance mutations. Insertion sequence (IS) elements played a key role in both the acquisition of resistance and adaptation in the absence of parasites; unlike single nucleotide polymorphisms, IS insertions were not more frequent in mutator lineages. Our results provide a genetic explanation for rapid reversion of mucoidy, a phenotype observed in other bacterial species including human pathogens. Moreover, this demonstrates that the types of genetic change underlying adaptation to fitness costs, and consequently the impact of evolvability mechanisms such as increased point-mutation rates, depend critically on the mechanism of resistance. article_processing_charge: No author: - first_name: Sébastien full_name: Wielgoss, Sébastien last_name: Wielgoss - first_name: Tobias full_name: Bergmiller, Tobias id: 2C471CFA-F248-11E8-B48F-1D18A9856A87 last_name: Bergmiller orcid: 0000-0001-5396-4346 - first_name: Anna M. full_name: Bischofberger, Anna M. last_name: Bischofberger - first_name: Alex R. full_name: Hall, Alex R. last_name: Hall citation: ama: 'Wielgoss S, Bergmiller T, Bischofberger AM, Hall AR. Data from: Adaptation to parasites and costs of parasite resistance in mutator and non-mutator bacteria. 2015. doi:10.5061/dryad.cj910' apa: 'Wielgoss, S., Bergmiller, T., Bischofberger, A. M., & Hall, A. R. (2015). Data from: Adaptation to parasites and costs of parasite resistance in mutator and non-mutator bacteria. Dryad. https://doi.org/10.5061/dryad.cj910' chicago: 'Wielgoss, Sébastien, Tobias Bergmiller, Anna M. Bischofberger, and Alex R. Hall. “Data from: Adaptation to Parasites and Costs of Parasite Resistance in Mutator and Non-Mutator Bacteria.” Dryad, 2015. https://doi.org/10.5061/dryad.cj910.' ieee: 'S. Wielgoss, T. Bergmiller, A. M. Bischofberger, and A. R. Hall, “Data from: Adaptation to parasites and costs of parasite resistance in mutator and non-mutator bacteria.” Dryad, 2015.' ista: 'Wielgoss S, Bergmiller T, Bischofberger AM, Hall AR. 2015. Data from: Adaptation to parasites and costs of parasite resistance in mutator and non-mutator bacteria, Dryad, 10.5061/dryad.cj910.' mla: 'Wielgoss, Sébastien, et al. Data from: Adaptation to Parasites and Costs of Parasite Resistance in Mutator and Non-Mutator Bacteria. Dryad, 2015, doi:10.5061/dryad.cj910.' short: S. Wielgoss, T. Bergmiller, A.M. Bischofberger, A.R. Hall, (2015). date_created: 2021-07-26T08:44:04Z date_published: 2015-12-21T00:00:00Z date_updated: 2023-09-05T13:46:04Z day: '21' department: - _id: CaGu doi: 10.5061/dryad.cj910 main_file_link: - open_access: '1' url: https://doi.org/10.5061/dryad.cj910 month: '12' oa: 1 oa_version: Published Version publisher: Dryad related_material: record: - id: '5749' relation: used_in_publication status: public status: public title: 'Data from: Adaptation to parasites and costs of parasite resistance in mutator and non-mutator bacteria' type: research_data_reference user_id: 6785fbc1-c503-11eb-8a32-93094b40e1cf year: '2015' ... --- _id: '9931' abstract: - lang: eng text: Gene duplication is important in evolution, because it provides new raw material for evolutionary adaptations. Several existing hypotheses about the causes of duplicate retention and diversification differ in their emphasis on gene dosage, subfunctionalization, and neofunctionalization. Little experimental data exist on the relative importance of gene expression changes and changes in coding regions for the evolution of duplicate genes. Furthermore, we do not know how strongly the environment could affect this importance. To address these questions, we performed evolution experiments with the TEM-1 beta lactamase gene in Escherichia coli to study the initial stages of duplicate gene evolution in the laboratory. We mimicked tandem duplication by inserting two copies of the TEM-1 gene on the same plasmid. We then subjected these copies to repeated cycles of mutagenesis and selection in various environments that contained antibiotics in different combinations and concentrations. Our experiments showed that gene dosage is the most important factor in the initial stages of duplicate gene evolution, and overshadows the importance of point mutations in the coding region. acknowledgement: We thank the Functional Genomics Center Zurich for its service in generating sequencing data, M. Ackermann and E. Hayden for helpful discussions, A. de Visser for comments on earlier versions of this manuscript, and M. Moser for help with quantitative PCR. This work was supported by Swiss National Science Foundation (grant 315230–129708), as well as through the YeastX project of SystemsX.ch, and the University Priority Research Program in Systems Biology at the University of Zurich. RD acknowledges support from the Forschungskredit program of the University of Zurich. The authors declare no conflict of interest. article_processing_charge: No article_type: original author: - first_name: Riddhiman full_name: Dhar, Riddhiman last_name: Dhar - first_name: Tobias full_name: Bergmiller, Tobias id: 2C471CFA-F248-11E8-B48F-1D18A9856A87 last_name: Bergmiller orcid: 0000-0001-5396-4346 - first_name: Andreas full_name: Wagner, Andreas last_name: Wagner citation: ama: Dhar R, Bergmiller T, Wagner A. Increased gene dosage plays a predominant role in the initial stages of evolution of duplicate TEM-1 beta lactamase genes. Evolution. 2014;68(6):1775-1791. doi:10.1111/evo.12373 apa: Dhar, R., Bergmiller, T., & Wagner, A. (2014). Increased gene dosage plays a predominant role in the initial stages of evolution of duplicate TEM-1 beta lactamase genes. Evolution. Wiley. https://doi.org/10.1111/evo.12373 chicago: Dhar, Riddhiman, Tobias Bergmiller, and Andreas Wagner. “Increased Gene Dosage Plays a Predominant Role in the Initial Stages of Evolution of Duplicate TEM-1 Beta Lactamase Genes.” Evolution. Wiley, 2014. https://doi.org/10.1111/evo.12373. ieee: R. Dhar, T. Bergmiller, and A. Wagner, “Increased gene dosage plays a predominant role in the initial stages of evolution of duplicate TEM-1 beta lactamase genes,” Evolution, vol. 68, no. 6. Wiley, pp. 1775–1791, 2014. ista: Dhar R, Bergmiller T, Wagner A. 2014. Increased gene dosage plays a predominant role in the initial stages of evolution of duplicate TEM-1 beta lactamase genes. Evolution. 68(6), 1775–1791. mla: Dhar, Riddhiman, et al. “Increased Gene Dosage Plays a Predominant Role in the Initial Stages of Evolution of Duplicate TEM-1 Beta Lactamase Genes.” Evolution, vol. 68, no. 6, Wiley, 2014, pp. 1775–91, doi:10.1111/evo.12373. short: R. Dhar, T. Bergmiller, A. Wagner, Evolution 68 (2014) 1775–1791. date_created: 2021-08-17T09:03:09Z date_published: 2014-06-03T00:00:00Z date_updated: 2023-02-23T14:13:27Z day: '03' department: - _id: CaGu doi: 10.1111/evo.12373 external_id: pmid: - '24495000' intvolume: ' 68' issue: '6' language: - iso: eng month: '06' oa_version: None page: 1775-1791 pmid: 1 publication: Evolution publication_identifier: eissn: - 1558-5646 issn: - 0014-3820 publication_status: published publisher: Wiley quality_controlled: '1' related_material: record: - id: '9932' relation: research_data status: public scopus_import: '1' status: public title: Increased gene dosage plays a predominant role in the initial stages of evolution of duplicate TEM-1 beta lactamase genes type: journal_article user_id: 6785fbc1-c503-11eb-8a32-93094b40e1cf volume: 68 year: '2014' ... --- _id: '9932' abstract: - lang: eng text: Gene duplication is important in evolution, because it provides new raw material for evolutionary adaptations. Several existing hypotheses about the causes of duplicate retention and diversification differ in their emphasis on gene dosage, sub-functionalization, and neo-functionalization. Little experimental data exists on the relative importance of gene expression changes and changes in coding regions for the evolution of duplicate genes. Furthermore, we do not know how strongly the environment could affect this importance. To address these questions, we performed evolution experiments with the TEM-1 beta lactamase gene in E. coli to study the initial stages of duplicate gene evolution in the laboratory. We mimicked tandem duplication by inserting two copies of the TEM-1 gene on the same plasmid. We then subjected these copies to repeated cycles of mutagenesis and selection in various environments that contained antibiotics in different combinations and concentrations. Our experiments showed that gene dosage is the most important factor in the initial stages of duplicate gene evolution, and overshadows the importance of point mutations in the coding region. article_processing_charge: No author: - first_name: Riddhiman full_name: Dhar, Riddhiman last_name: Dhar - first_name: Tobias full_name: Bergmiller, Tobias id: 2C471CFA-F248-11E8-B48F-1D18A9856A87 last_name: Bergmiller orcid: 0000-0001-5396-4346 - first_name: Andreas full_name: Wagner, Andreas last_name: Wagner citation: ama: 'Dhar R, Bergmiller T, Wagner A. Data from: Increased gene dosage plays a predominant role in the initial stages of evolution of duplicate TEM-1 beta lactamase genes. 2014. doi:10.5061/dryad.jc402' apa: 'Dhar, R., Bergmiller, T., & Wagner, A. (2014). Data from: Increased gene dosage plays a predominant role in the initial stages of evolution of duplicate TEM-1 beta lactamase genes. Dryad. https://doi.org/10.5061/dryad.jc402' chicago: 'Dhar, Riddhiman, Tobias Bergmiller, and Andreas Wagner. “Data from: Increased Gene Dosage Plays a Predominant Role in the Initial Stages of Evolution of Duplicate TEM-1 Beta Lactamase Genes.” Dryad, 2014. https://doi.org/10.5061/dryad.jc402.' ieee: 'R. Dhar, T. Bergmiller, and A. Wagner, “Data from: Increased gene dosage plays a predominant role in the initial stages of evolution of duplicate TEM-1 beta lactamase genes.” Dryad, 2014.' ista: 'Dhar R, Bergmiller T, Wagner A. 2014. Data from: Increased gene dosage plays a predominant role in the initial stages of evolution of duplicate TEM-1 beta lactamase genes, Dryad, 10.5061/dryad.jc402.' mla: 'Dhar, Riddhiman, et al. Data from: Increased Gene Dosage Plays a Predominant Role in the Initial Stages of Evolution of Duplicate TEM-1 Beta Lactamase Genes. Dryad, 2014, doi:10.5061/dryad.jc402.' short: R. Dhar, T. Bergmiller, A. Wagner, (2014). date_created: 2021-08-17T09:11:40Z date_published: 2014-01-27T00:00:00Z date_updated: 2023-02-23T14:13:24Z day: '27' department: - _id: CaGu doi: 10.5061/dryad.jc402 main_file_link: - open_access: '1' url: https://doi.org/10.5061/dryad.jc402 month: '01' oa: 1 oa_version: Published Version publisher: Dryad related_material: record: - id: '9931' relation: used_in_publication status: public status: public title: 'Data from: Increased gene dosage plays a predominant role in the initial stages of evolution of duplicate TEM-1 beta lactamase genes' type: research_data_reference user_id: 6785fbc1-c503-11eb-8a32-93094b40e1cf year: '2014' ... --- _id: '2853' abstract: - lang: eng text: High relatedness among interacting individuals has generally been considered a precondition for the evolution of altruism. However, kin-selection theory also predicts the evolution of altruism when relatedness is low, as long as the cost of the altruistic act is minor compared with its benefit. Here, we demonstrate evidence for a low-cost altruistic act in bacteria. We investigated Escherichia coli responding to the attack of an obligately lytic phage by committing suicide in order to prevent parasite transmission to nearby relatives. We found that bacterial suicide provides large benefits to survivors at marginal costs to committers. The cost of suicide was low, because infected cells are moribund, rapidly dying upon phage infection, such that no more opportunity for reproduction remains. As a consequence of its marginal cost, host suicide was selectively favoured even when relatedness between committers and survivors approached zero. Altogether, our findings demonstrate that low-cost suicide can evolve with ease, represents an effective host-defence strategy, and seems to be widespread among microbes. Moreover, low-cost suicide might also occur in higher organisms as exemplified by infected social insect workers leaving the colony to die in isolation. article_processing_charge: No article_type: original author: - first_name: Dominik full_name: Refardt, Dominik last_name: Refardt - first_name: Tobias full_name: Bergmiller, Tobias id: 2C471CFA-F248-11E8-B48F-1D18A9856A87 last_name: Bergmiller orcid: 0000-0001-5396-4346 - first_name: Rolf full_name: Kümmerli, Rolf last_name: Kümmerli citation: ama: 'Refardt D, Bergmiller T, Kümmerli R. Altruism can evolve when relatedness is low: Evidence from bacteria committing suicide upon phage infection. Proceedings of the Royal Society of London Series B Biological Sciences. 2013;280(1759). doi:10.1098/rspb.2012.3035' apa: 'Refardt, D., Bergmiller, T., & Kümmerli, R. (2013). Altruism can evolve when relatedness is low: Evidence from bacteria committing suicide upon phage infection. Proceedings of the Royal Society of London Series B Biological Sciences. The Royal Society. https://doi.org/10.1098/rspb.2012.3035' chicago: 'Refardt, Dominik, Tobias Bergmiller, and Rolf Kümmerli. “Altruism Can Evolve When Relatedness Is Low: Evidence from Bacteria Committing Suicide upon Phage Infection.” Proceedings of the Royal Society of London Series B Biological Sciences. The Royal Society, 2013. https://doi.org/10.1098/rspb.2012.3035.' ieee: 'D. Refardt, T. Bergmiller, and R. Kümmerli, “Altruism can evolve when relatedness is low: Evidence from bacteria committing suicide upon phage infection,” Proceedings of the Royal Society of London Series B Biological Sciences, vol. 280, no. 1759. The Royal Society, 2013.' ista: 'Refardt D, Bergmiller T, Kümmerli R. 2013. Altruism can evolve when relatedness is low: Evidence from bacteria committing suicide upon phage infection. Proceedings of the Royal Society of London Series B Biological Sciences. 280(1759).' mla: 'Refardt, Dominik, et al. “Altruism Can Evolve When Relatedness Is Low: Evidence from Bacteria Committing Suicide upon Phage Infection.” Proceedings of the Royal Society of London Series B Biological Sciences, vol. 280, no. 1759, The Royal Society, 2013, doi:10.1098/rspb.2012.3035.' short: D. Refardt, T. Bergmiller, R. Kümmerli, Proceedings of the Royal Society of London Series B Biological Sciences 280 (2013). date_created: 2018-12-11T11:59:56Z date_published: 2013-05-22T00:00:00Z date_updated: 2023-10-18T06:43:23Z day: '22' department: - _id: CaGu doi: 10.1098/rspb.2012.3035 external_id: pmid: - '23516238' intvolume: ' 280' issue: '1759' language: - iso: eng main_file_link: - open_access: '1' url: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3619501/ month: '05' oa: 1 oa_version: Submitted Version pmid: 1 publication: Proceedings of the Royal Society of London Series B Biological Sciences publication_identifier: eissn: - 1471-2954 publication_status: published publisher: The Royal Society publist_id: '3939' quality_controlled: '1' related_material: record: - id: '9751' relation: research_data status: public scopus_import: '1' status: public title: 'Altruism can evolve when relatedness is low: Evidence from bacteria committing suicide upon phage infection' type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 280 year: '2013' ...