[{"month":"01","article_number":"e64543","file":[{"file_size":5604343,"date_created":"2022-02-07T07:14:09Z","creator":"cchlebak","date_updated":"2022-02-07T07:14:09Z","file_id":"10739","success":1,"file_name":"2022_ELife_Lagator.pdf","access_level":"open_access","content_type":"application/pdf","relation":"main_file","checksum":"decdcdf600ff51e9a9703b49ca114170"}],"department":[{"_id":"CaGu"},{"_id":"GaTk"},{"_id":"NiBa"}],"language":[{"iso":"eng"}],"oa":1,"user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","citation":{"ieee":"M. Lagator <i>et al.</i>, “Predicting bacterial promoter function and evolution from random sequences,” <i>eLife</i>, vol. 11. eLife Sciences Publications, 2022.","short":"M. Lagator, S. Sarikas, M. Steinrueck, D. Toledo-Aparicio, J.P. Bollback, C.C. Guet, G. Tkačik, ELife 11 (2022).","ama":"Lagator M, Sarikas S, Steinrueck M, et al. Predicting bacterial promoter function and evolution from random sequences. <i>eLife</i>. 2022;11. doi:<a href=\"https://doi.org/10.7554/eLife.64543\">10.7554/eLife.64543</a>","apa":"Lagator, M., Sarikas, S., Steinrueck, M., Toledo-Aparicio, D., Bollback, J. P., Guet, C. C., &#38; Tkačik, G. (2022). Predicting bacterial promoter function and evolution from random sequences. <i>ELife</i>. eLife Sciences Publications. <a href=\"https://doi.org/10.7554/eLife.64543\">https://doi.org/10.7554/eLife.64543</a>","mla":"Lagator, Mato, et al. “Predicting Bacterial Promoter Function and Evolution from Random Sequences.” <i>ELife</i>, vol. 11, e64543, eLife Sciences Publications, 2022, doi:<a href=\"https://doi.org/10.7554/eLife.64543\">10.7554/eLife.64543</a>.","ista":"Lagator M, Sarikas S, Steinrueck M, Toledo-Aparicio D, Bollback JP, Guet CC, Tkačik G. 2022. Predicting bacterial promoter function and evolution from random sequences. eLife. 11, e64543.","chicago":"Lagator, Mato, Srdjan Sarikas, Magdalena Steinrueck, David Toledo-Aparicio, Jonathan P Bollback, Calin C Guet, and Gašper Tkačik. “Predicting Bacterial Promoter Function and Evolution from Random Sequences.” <i>ELife</i>. eLife Sciences Publications, 2022. <a href=\"https://doi.org/10.7554/eLife.64543\">https://doi.org/10.7554/eLife.64543</a>."},"title":"Predicting bacterial promoter function and evolution from random sequences","oa_version":"Published Version","author":[{"first_name":"Mato","last_name":"Lagator","full_name":"Lagator, Mato","id":"345D25EC-F248-11E8-B48F-1D18A9856A87"},{"last_name":"Sarikas","full_name":"Sarikas, Srdjan","id":"35F0286E-F248-11E8-B48F-1D18A9856A87","first_name":"Srdjan"},{"first_name":"Magdalena","full_name":"Steinrueck, Magdalena","last_name":"Steinrueck"},{"first_name":"David","last_name":"Toledo-Aparicio","full_name":"Toledo-Aparicio, David"},{"first_name":"Jonathan P","orcid":"0000-0002-4624-4612","last_name":"Bollback","full_name":"Bollback, Jonathan P","id":"2C6FA9CC-F248-11E8-B48F-1D18A9856A87"},{"first_name":"Calin C","orcid":"0000-0001-6220-2052","last_name":"Guet","id":"47F8433E-F248-11E8-B48F-1D18A9856A87","full_name":"Guet, Calin C"},{"last_name":"Tkačik","full_name":"Tkačik, Gašper","id":"3D494DCA-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-6699-1455","first_name":"Gašper"}],"scopus_import":"1","day":"26","article_type":"original","date_created":"2022-02-06T23:01:32Z","volume":11,"intvolume":"        11","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","image":"/images/cc_by.png","short":"CC BY (4.0)"},"abstract":[{"lang":"eng","text":"Predicting function from sequence is a central problem of biology. Currently, this is possible only locally in a narrow mutational neighborhood around a wildtype sequence rather than globally from any sequence. Using random mutant libraries, we developed a biophysical model that accounts for multiple features of σ70 binding bacterial promoters to predict constitutive gene expression levels from any sequence. We experimentally and theoretically estimated that 10–20% of random sequences lead to expression and ~80% of non-expressing sequences are one mutation away from a functional promoter. The potential for generating expression from random sequences is so pervasive that selection acts against σ70-RNA polymerase binding sites even within inter-genic, promoter-containing regions. This pervasiveness of σ70-binding sites implies that emergence of promoters is not the limiting step in gene regulatory evolution. Ultimately, the inclusion of novel features of promoter function into a mechanistic model enabled not only more accurate predictions of gene expression levels, but also identified that promoters evolve more rapidly than previously thought."}],"has_accepted_license":"1","publication_identifier":{"eissn":["2050-084X"]},"publication_status":"published","file_date_updated":"2022-02-07T07:14:09Z","external_id":{"isi":["000751104400001"],"pmid":["35080492"]},"isi":1,"year":"2022","project":[{"grant_number":"648440","name":"Selective Barriers to Horizontal Gene Transfer","call_identifier":"H2020","_id":"2578D616-B435-11E9-9278-68D0E5697425"}],"publication":"eLife","status":"public","date_published":"2022-01-26T00:00:00Z","acknowledgement":"We thank Hande Acar, Nicholas H Barton, Rok Grah, Tiago Paixao, Maros Pleska, Anna Staron, and Murat Tugrul for insightful comments and input on the manuscript. This work was supported by: Sir Henry Dale Fellowship jointly funded by the Wellcome Trust and the Royal Society (grant number 216779/Z/19/Z) to ML; IPC Grant from IST Austria to ML and SS; European Research Council Funding Programme 7 (2007–2013, grant agreement number 648440) to JPB.","pmid":1,"ec_funded":1,"publisher":"eLife Sciences Publications","doi":"10.7554/eLife.64543","article_processing_charge":"No","type":"journal_article","date_updated":"2023-08-02T14:09:02Z","_id":"10736","ddc":["576"],"quality_controlled":"1"},{"type":"journal_article","_id":"7652","date_updated":"2024-03-25T23:30:20Z","publisher":"Springer Nature","article_processing_charge":"No","doi":"10.1038/s41559-020-1132-7","quality_controlled":"1","ddc":["570"],"page":"612-625","related_material":{"link":[{"url":"https://ist.ac.at/en/news/how-to-thrive-without-gene-regulation/","description":"News on IST Homepage","relation":"press_release"}],"record":[{"status":"public","relation":"dissertation_contains","id":"8155"},{"relation":"research_data","status":"public","id":"7383"},{"status":"public","relation":"research_data","id":"7016"},{"status":"public","relation":"used_in_publication","id":"8653"}]},"external_id":{"isi":["000519008300005"]},"year":"2020","isi":1,"acknowledgement":"We thank L. Hurst, N. Barton, M. Pleska, M. Steinrück, B. Kavcic and A. Staron for input on the manuscript, and To. Bergmiller and R. Chait for help with microfluidics experiments. I.T. is a recipient the OMV fellowship. R.G. is a recipient of a DOC (Doctoral Fellowship Programme of the Austrian Academy of Sciences) Fellowship of the Austrian Academy of Sciences.","date_published":"2020-04-01T00:00:00Z","status":"public","publication":"Nature Ecology & Evolution","project":[{"_id":"267C84F4-B435-11E9-9278-68D0E5697425","name":"Biophysically realistic genotype-phenotype maps for regulatory networks"}],"date_created":"2020-04-08T15:20:53Z","article_type":"original","volume":4,"title":"Gene amplification as a form of population-level gene expression regulation","oa_version":"Submitted Version","scopus_import":"1","day":"01","author":[{"full_name":"Tomanek, Isabella","id":"3981F020-F248-11E8-B48F-1D18A9856A87","last_name":"Tomanek","first_name":"Isabella","orcid":"0000-0001-6197-363X"},{"first_name":"Rok","orcid":"0000-0003-2539-3560","last_name":"Grah","full_name":"Grah, Rok","id":"483E70DE-F248-11E8-B48F-1D18A9856A87"},{"first_name":"M.","last_name":"Lagator","full_name":"Lagator, M."},{"full_name":"Andersson, A. M. C.","last_name":"Andersson","first_name":"A. M. C."},{"first_name":"Jonathan P","orcid":"0000-0002-4624-4612","full_name":"Bollback, Jonathan P","id":"2C6FA9CC-F248-11E8-B48F-1D18A9856A87","last_name":"Bollback"},{"last_name":"Tkačik","full_name":"Tkačik, Gašper","id":"3D494DCA-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-6699-1455","first_name":"Gašper"},{"full_name":"Guet, Calin C","id":"47F8433E-F248-11E8-B48F-1D18A9856A87","last_name":"Guet","orcid":"0000-0001-6220-2052","first_name":"Calin C"}],"file_date_updated":"2020-10-09T09:56:01Z","publication_identifier":{"issn":["2397-334X"]},"publication_status":"published","intvolume":"         4","abstract":[{"text":"Organisms cope with change by taking advantage of transcriptional regulators. However, when faced with rare environments, the evolution of transcriptional regulators and their promoters may be too slow. Here, we investigate whether the intrinsic instability of gene duplication and amplification provides a generic alternative to canonical gene regulation. Using real-time monitoring of gene-copy-number mutations in Escherichia coli, we show that gene duplications and amplifications enable adaptation to fluctuating environments by rapidly generating copy-number and, therefore, expression-level polymorphisms. This amplification-mediated gene expression tuning (AMGET) occurs on timescales that are similar to canonical gene regulation and can respond to rapid environmental changes. Mathematical modelling shows that amplifications also tune gene expression in stochastic environments in which transcription-factor-based schemes are hard to evolve or maintain. The fleeting nature of gene amplifications gives rise to a generic population-level mechanism that relies on genetic heterogeneity to rapidly tune the expression of any gene, without leaving any genomic signature.","lang":"eng"}],"has_accepted_license":"1","file":[{"creator":"dernst","date_updated":"2020-10-09T09:56:01Z","date_created":"2020-10-09T09:56:01Z","file_size":745242,"file_id":"8640","content_type":"application/pdf","access_level":"open_access","file_name":"2020_NatureEcolEvo_Tomanek.pdf","success":1,"checksum":"ef3bbf42023e30b2c24a6278025d2040","relation":"main_file"}],"department":[{"_id":"GaTk"},{"_id":"CaGu"}],"month":"04","user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","citation":{"ama":"Tomanek I, Grah R, Lagator M, et al. Gene amplification as a form of population-level gene expression regulation. <i>Nature Ecology &#38; Evolution</i>. 2020;4(4):612-625. doi:<a href=\"https://doi.org/10.1038/s41559-020-1132-7\">10.1038/s41559-020-1132-7</a>","short":"I. Tomanek, R. Grah, M. Lagator, A.M.C. Andersson, J.P. Bollback, G. Tkačik, C.C. Guet, Nature Ecology &#38; Evolution 4 (2020) 612–625.","ieee":"I. Tomanek <i>et al.</i>, “Gene amplification as a form of population-level gene expression regulation,” <i>Nature Ecology &#38; Evolution</i>, vol. 4, no. 4. Springer Nature, pp. 612–625, 2020.","chicago":"Tomanek, Isabella, Rok Grah, M. Lagator, A. M. C. Andersson, Jonathan P Bollback, Gašper Tkačik, and Calin C Guet. “Gene Amplification as a Form of Population-Level Gene Expression Regulation.” <i>Nature Ecology &#38; Evolution</i>. Springer Nature, 2020. <a href=\"https://doi.org/10.1038/s41559-020-1132-7\">https://doi.org/10.1038/s41559-020-1132-7</a>.","ista":"Tomanek I, Grah R, Lagator M, Andersson AMC, Bollback JP, Tkačik G, Guet CC. 2020. Gene amplification as a form of population-level gene expression regulation. Nature Ecology &#38; Evolution. 4(4), 612–625.","mla":"Tomanek, Isabella, et al. “Gene Amplification as a Form of Population-Level Gene Expression Regulation.” <i>Nature Ecology &#38; Evolution</i>, vol. 4, no. 4, Springer Nature, 2020, pp. 612–25, doi:<a href=\"https://doi.org/10.1038/s41559-020-1132-7\">10.1038/s41559-020-1132-7</a>.","apa":"Tomanek, I., Grah, R., Lagator, M., Andersson, A. M. C., Bollback, J. P., Tkačik, G., &#38; Guet, C. C. (2020). Gene amplification as a form of population-level gene expression regulation. <i>Nature Ecology &#38; Evolution</i>. Springer Nature. <a href=\"https://doi.org/10.1038/s41559-020-1132-7\">https://doi.org/10.1038/s41559-020-1132-7</a>"},"issue":"4","language":[{"iso":"eng"}],"oa":1},{"language":[{"iso":"eng"}],"oa":1,"user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","issue":"10","citation":{"chicago":"Igler, Claudia, Mato Lagator, Gašper Tkačik, Jonathan P Bollback, and Calin C Guet. “Evolutionary Potential of Transcription Factors for Gene Regulatory Rewiring.” <i>Nature Ecology and Evolution</i>. Nature Publishing Group, 2018. <a href=\"https://doi.org/10.1038/s41559-018-0651-y\">https://doi.org/10.1038/s41559-018-0651-y</a>.","ista":"Igler C, Lagator M, Tkačik G, Bollback JP, Guet CC. 2018. Evolutionary potential of transcription factors for gene regulatory rewiring. Nature Ecology and Evolution. 2(10), 1633–1643.","apa":"Igler, C., Lagator, M., Tkačik, G., Bollback, J. P., &#38; Guet, C. C. (2018). Evolutionary potential of transcription factors for gene regulatory rewiring. <i>Nature Ecology and Evolution</i>. Nature Publishing Group. <a href=\"https://doi.org/10.1038/s41559-018-0651-y\">https://doi.org/10.1038/s41559-018-0651-y</a>","mla":"Igler, Claudia, et al. “Evolutionary Potential of Transcription Factors for Gene Regulatory Rewiring.” <i>Nature Ecology and Evolution</i>, vol. 2, no. 10, Nature Publishing Group, 2018, pp. 1633–43, doi:<a href=\"https://doi.org/10.1038/s41559-018-0651-y\">10.1038/s41559-018-0651-y</a>.","ama":"Igler C, Lagator M, Tkačik G, Bollback JP, Guet CC. Evolutionary potential of transcription factors for gene regulatory rewiring. <i>Nature Ecology and Evolution</i>. 2018;2(10):1633-1643. doi:<a href=\"https://doi.org/10.1038/s41559-018-0651-y\">10.1038/s41559-018-0651-y</a>","ieee":"C. Igler, M. Lagator, G. Tkačik, J. P. Bollback, and C. C. Guet, “Evolutionary potential of transcription factors for gene regulatory rewiring,” <i>Nature Ecology and Evolution</i>, vol. 2, no. 10. Nature Publishing Group, pp. 1633–1643, 2018.","short":"C. Igler, M. Lagator, G. Tkačik, J.P. Bollback, C.C. Guet, Nature Ecology and Evolution 2 (2018) 1633–1643."},"month":"09","file":[{"content_type":"application/pdf","access_level":"open_access","file_name":"2018_NatureEcology_Igler.pdf","checksum":"383a2e2c944a856e2e821ec8e7bf71b6","relation":"main_file","date_updated":"2020-07-14T12:47:37Z","creator":"dernst","file_size":1135973,"date_created":"2020-05-14T11:28:52Z","file_id":"7830"}],"department":[{"_id":"CaGu"},{"_id":"GaTk"},{"_id":"JoBo"}],"intvolume":"         2","abstract":[{"lang":"eng","text":"Gene regulatory networks evolve through rewiring of individual components—that is, through changes in regulatory connections. However, the mechanistic basis of regulatory rewiring is poorly understood. Using a canonical gene regulatory system, we quantify the properties of transcription factors that determine the evolutionary potential for rewiring of regulatory connections: robustness, tunability and evolvability. In vivo repression measurements of two repressors at mutated operator sites reveal their contrasting evolutionary potential: while robustness and evolvability were positively correlated, both were in trade-off with tunability. Epistatic interactions between adjacent operators alleviated this trade-off. A thermodynamic model explains how the differences in robustness, tunability and evolvability arise from biophysical characteristics of repressor–DNA binding. The model also uncovers that the energy matrix, which describes how mutations affect repressor–DNA binding, encodes crucial information about the evolutionary potential of a repressor. The biophysical determinants of evolutionary potential for regulatory rewiring constitute a mechanistic framework for understanding network evolution."}],"has_accepted_license":"1","publication_status":"published","file_date_updated":"2020-07-14T12:47:37Z","oa_version":"Submitted Version","title":"Evolutionary potential of transcription factors for gene regulatory rewiring","author":[{"last_name":"Igler","full_name":"Igler, Claudia","id":"46613666-F248-11E8-B48F-1D18A9856A87","first_name":"Claudia"},{"last_name":"Lagator","id":"345D25EC-F248-11E8-B48F-1D18A9856A87","full_name":"Lagator, Mato","first_name":"Mato"},{"full_name":"Tkacik, Gasper","id":"3D494DCA-F248-11E8-B48F-1D18A9856A87","last_name":"Tkacik","orcid":"0000-0002-6699-1455","first_name":"Gasper"},{"full_name":"Bollback, Jonathan P","id":"2C6FA9CC-F248-11E8-B48F-1D18A9856A87","last_name":"Bollback","first_name":"Jonathan P","orcid":"0000-0002-4624-4612"},{"last_name":"Guet","id":"47F8433E-F248-11E8-B48F-1D18A9856A87","full_name":"Guet, Calin C","orcid":"0000-0001-6220-2052","first_name":"Calin C"}],"day":"10","scopus_import":"1","article_type":"original","date_created":"2018-12-11T11:44:27Z","volume":2,"project":[{"call_identifier":"FP7","grant_number":"291734","name":"International IST Postdoc Fellowship Programme","_id":"25681D80-B435-11E9-9278-68D0E5697425"},{"call_identifier":"H2020","grant_number":"648440","name":"Selective Barriers to Horizontal Gene Transfer","_id":"2578D616-B435-11E9-9278-68D0E5697425"},{"_id":"251EE76E-B435-11E9-9278-68D0E5697425","grant_number":"24573","name":"Design principles underlying genetic switch architecture (DOC Fellowship)"}],"publication":"Nature Ecology and Evolution","status":"public","date_published":"2018-09-10T00:00:00Z","ec_funded":1,"external_id":{"isi":["000447947600021"]},"related_material":{"record":[{"id":"5585","status":"public","relation":"popular_science"},{"relation":"dissertation_contains","status":"public","id":"6371"}]},"year":"2018","isi":1,"publist_id":"7987","ddc":["570"],"page":"1633 - 1643","quality_controlled":"1","publisher":"Nature Publishing Group","doi":"10.1038/s41559-018-0651-y","article_processing_charge":"No","type":"journal_article","date_updated":"2024-03-25T23:30:27Z","_id":"67"},{"file_date_updated":"2020-07-14T12:47:07Z","has_accepted_license":"1","ddc":["576"],"license":"https://creativecommons.org/publicdomain/zero/1.0/","tmp":{"name":"Creative Commons Public Domain Dedication (CC0 1.0)","legal_code_url":"https://creativecommons.org/publicdomain/zero/1.0/legalcode","image":"/images/cc_0.png","short":"CC0 (1.0)"},"abstract":[{"lang":"eng","text":"Mean repression values and standard error of the mean are given for all operator mutant libraries."}],"_id":"5585","date_updated":"2024-03-25T23:30:27Z","date_created":"2018-12-12T12:31:40Z","type":"research_data","day":"20","article_processing_charge":"No","doi":"10.15479/AT:ISTA:108","author":[{"last_name":"Igler","full_name":"Igler, Claudia","id":"46613666-F248-11E8-B48F-1D18A9856A87","first_name":"Claudia"},{"last_name":"Lagator","id":"345D25EC-F248-11E8-B48F-1D18A9856A87","full_name":"Lagator, Mato","first_name":"Mato"},{"first_name":"Gasper","orcid":"0000-0002-6699-1455","id":"3D494DCA-F248-11E8-B48F-1D18A9856A87","full_name":"Tkacik, Gasper","last_name":"Tkacik"},{"first_name":"Jonathan P","orcid":"0000-0002-4624-4612","id":"2C6FA9CC-F248-11E8-B48F-1D18A9856A87","full_name":"Bollback, Jonathan P","last_name":"Bollback"},{"first_name":"Calin C","orcid":"0000-0001-6220-2052","full_name":"Guet, Calin C","id":"47F8433E-F248-11E8-B48F-1D18A9856A87","last_name":"Guet"}],"title":"Data for the paper Evolutionary potential of transcription factors for gene regulatory rewiring","publisher":"Institute of Science and Technology Austria","oa_version":"Published Version","ec_funded":1,"citation":{"chicago":"Igler, Claudia, Mato Lagator, Gašper Tkačik, Jonathan P Bollback, and Calin C Guet. “Data for the Paper Evolutionary Potential of Transcription Factors for Gene Regulatory Rewiring.” Institute of Science and Technology Austria, 2018. <a href=\"https://doi.org/10.15479/AT:ISTA:108\">https://doi.org/10.15479/AT:ISTA:108</a>.","ista":"Igler C, Lagator M, Tkačik G, Bollback JP, Guet CC. 2018. Data for the paper Evolutionary potential of transcription factors for gene regulatory rewiring, Institute of Science and Technology Austria, <a href=\"https://doi.org/10.15479/AT:ISTA:108\">10.15479/AT:ISTA:108</a>.","mla":"Igler, Claudia, et al. <i>Data for the Paper Evolutionary Potential of Transcription Factors for Gene Regulatory Rewiring</i>. Institute of Science and Technology Austria, 2018, doi:<a href=\"https://doi.org/10.15479/AT:ISTA:108\">10.15479/AT:ISTA:108</a>.","apa":"Igler, C., Lagator, M., Tkačik, G., Bollback, J. P., &#38; Guet, C. C. (2018). Data for the paper Evolutionary potential of transcription factors for gene regulatory rewiring. Institute of Science and Technology Austria. <a href=\"https://doi.org/10.15479/AT:ISTA:108\">https://doi.org/10.15479/AT:ISTA:108</a>","ama":"Igler C, Lagator M, Tkačik G, Bollback JP, Guet CC. Data for the paper Evolutionary potential of transcription factors for gene regulatory rewiring. 2018. doi:<a href=\"https://doi.org/10.15479/AT:ISTA:108\">10.15479/AT:ISTA:108</a>","short":"C. Igler, M. Lagator, G. Tkačik, J.P. Bollback, C.C. Guet, (2018).","ieee":"C. Igler, M. Lagator, G. Tkačik, J. P. Bollback, and C. C. Guet, “Data for the paper Evolutionary potential of transcription factors for gene regulatory rewiring.” Institute of Science and Technology Austria, 2018."},"datarep_id":"108","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","date_published":"2018-07-20T00:00:00Z","oa":1,"status":"public","project":[{"_id":"25681D80-B435-11E9-9278-68D0E5697425","name":"International IST Postdoc Fellowship Programme","grant_number":"291734","call_identifier":"FP7"},{"call_identifier":"H2020","name":"Selective Barriers to Horizontal Gene Transfer","grant_number":"648440","_id":"2578D616-B435-11E9-9278-68D0E5697425"},{"_id":"251EE76E-B435-11E9-9278-68D0E5697425","name":"Design principles underlying genetic switch architecture (DOC Fellowship)","grant_number":"24573"}],"department":[{"_id":"CaGu"},{"_id":"GaTk"}],"file":[{"checksum":"1435781526c77413802adee0d4583cce","relation":"main_file","content_type":"application/vnd.openxmlformats-officedocument.spreadsheetml.sheet","access_level":"open_access","file_name":"IST-2018-108-v1+1_data_figures.xlsx","file_id":"5611","creator":"system","date_updated":"2020-07-14T12:47:07Z","date_created":"2018-12-12T13:02:45Z","file_size":16507}],"year":"2018","month":"07","related_material":{"record":[{"status":"public","relation":"research_paper","id":"67"},{"id":"6371","relation":"research_paper","status":"public"}]}},{"department":[{"_id":"NiBa"},{"_id":"JoBo"}],"month":"03","related_material":{"record":[{"id":"423","status":"public","relation":"used_in_publication"}]},"year":"2018","user_id":"6785fbc1-c503-11eb-8a32-93094b40e1cf","date_published":"2018-03-12T00:00:00Z","citation":{"short":"P. Payne, L. Geyrhofer, N.H. Barton, J.P. Bollback, (2018).","ieee":"P. Payne, L. Geyrhofer, N. H. Barton, and J. P. Bollback, “Data from: CRISPR-based herd immunity limits phage epidemics in bacterial populations.” Dryad, 2018.","ama":"Payne P, Geyrhofer L, Barton NH, Bollback JP. Data from: CRISPR-based herd immunity limits phage epidemics in bacterial populations. 2018. doi:<a href=\"https://doi.org/10.5061/dryad.42n44\">10.5061/dryad.42n44</a>","mla":"Payne, Pavel, et al. <i>Data from: CRISPR-Based Herd Immunity Limits Phage Epidemics in Bacterial Populations</i>. Dryad, 2018, doi:<a href=\"https://doi.org/10.5061/dryad.42n44\">10.5061/dryad.42n44</a>.","apa":"Payne, P., Geyrhofer, L., Barton, N. H., &#38; Bollback, J. P. (2018). Data from: CRISPR-based herd immunity limits phage epidemics in bacterial populations. Dryad. <a href=\"https://doi.org/10.5061/dryad.42n44\">https://doi.org/10.5061/dryad.42n44</a>","chicago":"Payne, Pavel, Lukas Geyrhofer, Nicholas H Barton, and Jonathan P Bollback. “Data from: CRISPR-Based Herd Immunity Limits Phage Epidemics in Bacterial Populations.” Dryad, 2018. <a href=\"https://doi.org/10.5061/dryad.42n44\">https://doi.org/10.5061/dryad.42n44</a>.","ista":"Payne P, Geyrhofer L, Barton NH, Bollback JP. 2018. Data from: CRISPR-based herd immunity limits phage epidemics in bacterial populations, Dryad, <a href=\"https://doi.org/10.5061/dryad.42n44\">10.5061/dryad.42n44</a>."},"status":"public","oa":1,"date_created":"2021-08-09T13:10:02Z","type":"research_data_reference","_id":"9840","date_updated":"2023-09-11T12:49:17Z","publisher":"Dryad","title":"Data from: CRISPR-based herd immunity limits phage epidemics in bacterial populations","oa_version":"Published Version","day":"12","article_processing_charge":"No","doi":"10.5061/dryad.42n44","author":[{"last_name":"Payne","full_name":"Payne, Pavel","id":"35F78294-F248-11E8-B48F-1D18A9856A87","first_name":"Pavel","orcid":"0000-0002-2711-9453"},{"full_name":"Geyrhofer, Lukas","last_name":"Geyrhofer","first_name":"Lukas"},{"first_name":"Nicholas H","orcid":"0000-0002-8548-5240","last_name":"Barton","id":"4880FE40-F248-11E8-B48F-1D18A9856A87","full_name":"Barton, Nicholas H"},{"orcid":"0000-0002-4624-4612","first_name":"Jonathan P","id":"2C6FA9CC-F248-11E8-B48F-1D18A9856A87","full_name":"Bollback, Jonathan P","last_name":"Bollback"}],"main_file_link":[{"open_access":"1","url":"https://doi.org/10.5061/dryad.42n44"}],"abstract":[{"text":"Herd immunity, a process in which resistant individuals limit the spread of a pathogen among susceptible hosts has been extensively studied in eukaryotes. Even though bacteria have evolved multiple immune systems against their phage pathogens, herd immunity in bacteria remains unexplored. Here we experimentally demonstrate that herd immunity arises during phage epidemics in structured and unstructured Escherichia coli populations consisting of differing frequencies of susceptible and resistant cells harboring CRISPR immunity. In addition, we develop a mathematical model that quantifies how herd immunity is affected by spatial population structure, bacterial growth rate, and phage replication rate. Using our model we infer a general epidemiological rule describing the relative speed of an epidemic in partially resistant spatially structured populations. Our experimental and theoretical findings indicate that herd immunity may be important in bacterial communities, allowing for stable coexistence of bacteria and their phages and the maintenance of polymorphism in bacterial immunity.","lang":"eng"}]},{"date_published":"2018-03-09T00:00:00Z","acknowledgement":"We are grateful to Remy Chait for his help and assistance with establishing our experimental setups and to Tobias Bergmiller for valuable insights into some specific experimental details. We thank Luciano Marraffini for donating us the pCas9 plasmid used in this study. We also want to express our gratitude to Seth Barribeau, Andrea Betancourt, Călin Guet, Mato Lagator, Tiago Paixão and Maroš Pleška for valuable discussions on the manuscript. Finally, we would like to thank the \r\neditors and reviewers for their helpful comments and suggestions.","ec_funded":1,"publication":"eLife","status":"public","project":[{"_id":"2578D616-B435-11E9-9278-68D0E5697425","grant_number":"648440","name":"Selective Barriers to Horizontal Gene Transfer","call_identifier":"H2020"}],"publist_id":"7400","related_material":{"record":[{"id":"9840","status":"public","relation":"research_data"}]},"external_id":{"isi":["000431035800001"]},"year":"2018","isi":1,"quality_controlled":"1","ddc":["576"],"type":"journal_article","_id":"423","date_updated":"2023-09-11T12:49:17Z","publisher":"eLife Sciences Publications","article_processing_charge":"No","doi":"10.7554/eLife.32035","user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","citation":{"short":"P. Payne, L. Geyrhofer, N.H. Barton, J.P. Bollback, ELife 7 (2018).","ieee":"P. Payne, L. Geyrhofer, N. H. Barton, and J. P. Bollback, “CRISPR-based herd immunity can limit phage epidemics in bacterial populations,” <i>eLife</i>, vol. 7. eLife Sciences Publications, 2018.","ama":"Payne P, Geyrhofer L, Barton NH, Bollback JP. CRISPR-based herd immunity can limit phage epidemics in bacterial populations. <i>eLife</i>. 2018;7. doi:<a href=\"https://doi.org/10.7554/eLife.32035\">10.7554/eLife.32035</a>","mla":"Payne, Pavel, et al. “CRISPR-Based Herd Immunity Can Limit Phage Epidemics in Bacterial Populations.” <i>ELife</i>, vol. 7, e32035, eLife Sciences Publications, 2018, doi:<a href=\"https://doi.org/10.7554/eLife.32035\">10.7554/eLife.32035</a>.","apa":"Payne, P., Geyrhofer, L., Barton, N. H., &#38; Bollback, J. P. (2018). CRISPR-based herd immunity can limit phage epidemics in bacterial populations. <i>ELife</i>. eLife Sciences Publications. <a href=\"https://doi.org/10.7554/eLife.32035\">https://doi.org/10.7554/eLife.32035</a>","chicago":"Payne, Pavel, Lukas Geyrhofer, Nicholas H Barton, and Jonathan P Bollback. “CRISPR-Based Herd Immunity Can Limit Phage Epidemics in Bacterial Populations.” <i>ELife</i>. eLife Sciences Publications, 2018. <a href=\"https://doi.org/10.7554/eLife.32035\">https://doi.org/10.7554/eLife.32035</a>.","ista":"Payne P, Geyrhofer L, Barton NH, Bollback JP. 2018. CRISPR-based herd immunity can limit phage epidemics in bacterial populations. eLife. 7, e32035."},"language":[{"iso":"eng"}],"oa":1,"file":[{"file_id":"5689","date_created":"2018-12-17T10:36:07Z","file_size":3533881,"creator":"dernst","date_updated":"2020-07-14T12:46:25Z","relation":"main_file","checksum":"447cf6e680bdc3c01062a8737d876569","file_name":"2018_eLife_Payne.pdf","content_type":"application/pdf","access_level":"open_access"}],"article_number":"e32035","department":[{"_id":"NiBa"},{"_id":"JoBo"}],"month":"03","file_date_updated":"2020-07-14T12:46:25Z","publication_status":"published","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","image":"/images/cc_by.png","short":"CC BY (4.0)"},"abstract":[{"lang":"eng","text":"Herd immunity, a process in which resistant individuals limit the spread of a pathogen among susceptible hosts has been extensively studied in eukaryotes. Even though bacteria have evolved multiple immune systems against their phage pathogens, herd immunity in bacteria remains unexplored. Here we experimentally demonstrate that herd immunity arises during phage epidemics in structured and unstructured Escherichia coli populations consisting of differing frequencies of susceptible and resistant cells harboring CRISPR immunity. In addition, we develop a mathematical model that quantifies how herd immunity is affected by spatial population structure, bacterial growth rate, and phage replication rate. Using our model we infer a general epidemiological rule describing the relative speed of an epidemic in partially resistant spatially structured populations. Our experimental and theoretical findings indicate that herd immunity may be important in bacterial communities, allowing for stable coexistence of bacteria and their phages and the maintenance of polymorphism in bacterial immunity."}],"intvolume":"         7","has_accepted_license":"1","date_created":"2018-12-11T11:46:23Z","volume":7,"oa_version":"Published Version","title":"CRISPR-based herd immunity can limit phage epidemics in bacterial populations","scopus_import":"1","day":"09","author":[{"orcid":"0000-0002-2711-9453","first_name":"Pavel","last_name":"Payne","full_name":"Payne, Pavel","id":"35F78294-F248-11E8-B48F-1D18A9856A87"},{"first_name":"Lukas","last_name":"Geyrhofer","full_name":"Geyrhofer, Lukas"},{"full_name":"Barton, Nicholas H","id":"4880FE40-F248-11E8-B48F-1D18A9856A87","last_name":"Barton","orcid":"0000-0002-8548-5240","first_name":"Nicholas H"},{"full_name":"Bollback, Jonathan P","id":"2C6FA9CC-F248-11E8-B48F-1D18A9856A87","last_name":"Bollback","first_name":"Jonathan P","orcid":"0000-0002-4624-4612"}]},{"date_updated":"2025-05-28T11:42:51Z","_id":"1077","type":"journal_article","doi":"10.1098/rsif.2016.0139","article_processing_charge":"Yes (in subscription journal)","publisher":"Royal Society of London","quality_controlled":"1","ddc":["570"],"publist_id":"6303","isi":1,"year":"2017","external_id":{"isi":["000393380400001"]},"related_material":{"record":[{"id":"9864","relation":"research_data","status":"public"}]},"ec_funded":1,"date_published":"2017-01-04T00:00:00Z","project":[{"_id":"25B07788-B435-11E9-9278-68D0E5697425","name":"Limits to selection in biology and in evolutionary computation","grant_number":"250152","call_identifier":"FP7"},{"_id":"2578D616-B435-11E9-9278-68D0E5697425","name":"Selective Barriers to Horizontal Gene Transfer","grant_number":"648440","call_identifier":"H2020"}],"status":"public","publication":"Journal of the Royal Society Interface","volume":14,"date_created":"2018-12-11T11:50:01Z","author":[{"first_name":"Rodrigo A","orcid":"0000-0002-5837-2793","last_name":"Fernandes Redondo","full_name":"Fernandes Redondo, Rodrigo A","id":"409D5C96-F248-11E8-B48F-1D18A9856A87"},{"first_name":"Harold","orcid":"0000-0002-5985-7653","last_name":"Vladar","id":"2A181218-F248-11E8-B48F-1D18A9856A87","full_name":"Vladar, Harold"},{"full_name":"Włodarski, Tomasz","last_name":"Włodarski","first_name":"Tomasz"},{"last_name":"Bollback","id":"2C6FA9CC-F248-11E8-B48F-1D18A9856A87","full_name":"Bollback, Jonathan P","orcid":"0000-0002-4624-4612","first_name":"Jonathan P"}],"day":"04","scopus_import":"1","oa_version":"Published Version","title":"Evolutionary interplay between structure, energy and epistasis in the coat protein of the ϕX174 phage family","publication_identifier":{"issn":["17425689"]},"publication_status":"published","file_date_updated":"2019-01-18T09:14:02Z","has_accepted_license":"1","intvolume":"        14","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","image":"/images/cc_by.png","short":"CC BY (4.0)"},"abstract":[{"text":"Viral capsids are structurally constrained by interactions among the amino acids (AAs) of their constituent proteins. Therefore, epistasis is expected to evolve among physically interacting sites and to influence the rates of substitution. To study the evolution of epistasis, we focused on the major structural protein of the fX174 phage family by first reconstructing the ancestral protein sequences of 18 species using a Bayesian statistical framework. The inferred ancestral reconstruction differed at eight AAs, for a total of 256 possible ancestral haplotypes. For each ancestral haplotype and the extant species, we estimated, in silico, the distribution of free energies and epistasis of the capsid structure. We found that free energy has not significantly increased but epistasis has. We decomposed epistasis up to fifth order and found that higher-order epistasis sometimes compensates pairwise interactions making the free energy seem additive. The dN/dS ratio is low, suggesting strong purifying selection, and that structure is under stabilizing selection. We synthesized phages carrying ancestral haplotypes of the coat protein gene and measured their fitness experimentally. Our findings indicate that stabilizing mutations can have higher fitness, and that fitness optima do not necessarily coincide with energy minima.","lang":"eng"}],"department":[{"_id":"NiBa"},{"_id":"JoBo"}],"article_number":"20160139","file":[{"relation":"main_file","success":1,"file_name":"2017_JRSI_Redondo.pdf","access_level":"open_access","content_type":"application/pdf","file_id":"5843","file_size":1092015,"date_created":"2019-01-18T09:14:02Z","date_updated":"2019-01-18T09:14:02Z","creator":"dernst"}],"month":"01","issue":"126","citation":{"ieee":"R. A. Fernandes Redondo, H. de Vladar, T. Włodarski, and J. P. Bollback, “Evolutionary interplay between structure, energy and epistasis in the coat protein of the ϕX174 phage family,” <i>Journal of the Royal Society Interface</i>, vol. 14, no. 126. Royal Society of London, 2017.","short":"R.A. Fernandes Redondo, H. de Vladar, T. Włodarski, J.P. Bollback, Journal of the Royal Society Interface 14 (2017).","ama":"Fernandes Redondo RA, de Vladar H, Włodarski T, Bollback JP. Evolutionary interplay between structure, energy and epistasis in the coat protein of the ϕX174 phage family. <i>Journal of the Royal Society Interface</i>. 2017;14(126). doi:<a href=\"https://doi.org/10.1098/rsif.2016.0139\">10.1098/rsif.2016.0139</a>","apa":"Fernandes Redondo, R. A., de Vladar, H., Włodarski, T., &#38; Bollback, J. P. (2017). Evolutionary interplay between structure, energy and epistasis in the coat protein of the ϕX174 phage family. <i>Journal of the Royal Society Interface</i>. Royal Society of London. <a href=\"https://doi.org/10.1098/rsif.2016.0139\">https://doi.org/10.1098/rsif.2016.0139</a>","mla":"Fernandes Redondo, Rodrigo A., et al. “Evolutionary Interplay between Structure, Energy and Epistasis in the Coat Protein of the ΦX174 Phage Family.” <i>Journal of the Royal Society Interface</i>, vol. 14, no. 126, 20160139, Royal Society of London, 2017, doi:<a href=\"https://doi.org/10.1098/rsif.2016.0139\">10.1098/rsif.2016.0139</a>.","chicago":"Fernandes Redondo, Rodrigo A, Harold de Vladar, Tomasz Włodarski, and Jonathan P Bollback. “Evolutionary Interplay between Structure, Energy and Epistasis in the Coat Protein of the ΦX174 Phage Family.” <i>Journal of the Royal Society Interface</i>. Royal Society of London, 2017. <a href=\"https://doi.org/10.1098/rsif.2016.0139\">https://doi.org/10.1098/rsif.2016.0139</a>.","ista":"Fernandes Redondo RA, de Vladar H, Włodarski T, Bollback JP. 2017. Evolutionary interplay between structure, energy and epistasis in the coat protein of the ϕX174 phage family. Journal of the Royal Society Interface. 14(126), 20160139."},"user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","oa":1,"language":[{"iso":"eng"}]},{"type":"journal_article","date_updated":"2021-01-12T08:03:15Z","_id":"570","publisher":"eLife Sciences Publications","doi":"10.7554/eLife.28921","quality_controlled":"1","ddc":["576"],"publist_id":"7244","year":"2017","date_published":"2017-11-13T00:00:00Z","ec_funded":1,"project":[{"_id":"25681D80-B435-11E9-9278-68D0E5697425","call_identifier":"FP7","name":"International IST Postdoc Fellowship Programme","grant_number":"291734"},{"grant_number":"648440","name":"Selective Barriers to Horizontal Gene Transfer","call_identifier":"H2020","_id":"2578D616-B435-11E9-9278-68D0E5697425"}],"publication":"eLife","status":"public","date_created":"2018-12-11T11:47:14Z","volume":6,"title":"Regulatory network structure determines patterns of intermolecular epistasis","oa_version":"Published Version","author":[{"full_name":"Lagator, Mato","id":"345D25EC-F248-11E8-B48F-1D18A9856A87","last_name":"Lagator","first_name":"Mato"},{"id":"35F0286E-F248-11E8-B48F-1D18A9856A87","full_name":"Sarikas, Srdjan","last_name":"Sarikas","first_name":"Srdjan"},{"last_name":"Acar","id":"2DDF136A-F248-11E8-B48F-1D18A9856A87","full_name":"Acar, Hande","orcid":"0000-0003-1986-9753","first_name":"Hande"},{"last_name":"Bollback","full_name":"Bollback, Jonathan P","id":"2C6FA9CC-F248-11E8-B48F-1D18A9856A87","first_name":"Jonathan P","orcid":"0000-0002-4624-4612"},{"last_name":"Guet","full_name":"Guet, Calin C","id":"47F8433E-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0001-6220-2052","first_name":"Calin C"}],"scopus_import":1,"day":"13","publication_identifier":{"issn":["2050084X"]},"publication_status":"published","file_date_updated":"2020-07-14T12:47:10Z","abstract":[{"text":"Most phenotypes are determined by molecular systems composed of specifically interacting molecules. However, unlike for individual components, little is known about the distributions of mutational effects of molecular systems as a whole. We ask how the distribution of mutational effects of a transcriptional regulatory system differs from the distributions of its components, by first independently, and then simultaneously, mutating a transcription factor and the associated promoter it represses. We find that the system distribution exhibits increased phenotypic variation compared to individual component distributions - an effect arising from intermolecular epistasis between the transcription factor and its DNA-binding site. In large part, this epistasis can be qualitatively attributed to the structure of the transcriptional regulatory system and could therefore be a common feature in prokaryotes. Counter-intuitively, intermolecular epistasis can alleviate the constraints of individual components, thereby increasing phenotypic variation that selection could act on and facilitating adaptive evolution. ","lang":"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","image":"/images/cc_by.png","short":"CC BY (4.0)"},"intvolume":"         6","has_accepted_license":"1","file":[{"date_created":"2018-12-12T10:14:42Z","file_size":8453470,"creator":"system","date_updated":"2020-07-14T12:47:10Z","file_id":"5096","file_name":"IST-2017-918-v1+1_elife-28921-figures-v3.pdf","access_level":"open_access","content_type":"application/pdf","relation":"main_file","checksum":"273ab17f33305e4eaafd911ff88e7c5b"},{"access_level":"open_access","content_type":"application/pdf","file_name":"IST-2017-918-v1+2_elife-28921-v3.pdf","checksum":"b433f90576c7be597cd43367946f8e7f","relation":"main_file","creator":"system","date_updated":"2020-07-14T12:47:10Z","file_size":1953221,"date_created":"2018-12-12T10:14:43Z","file_id":"5097"}],"article_number":"e28921","department":[{"_id":"CaGu"},{"_id":"JoBo"},{"_id":"NiBa"}],"month":"11","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","citation":{"short":"M. Lagator, S. Sarikas, H. Acar, J.P. Bollback, C.C. Guet, ELife 6 (2017).","ieee":"M. Lagator, S. Sarikas, H. Acar, J. P. Bollback, and C. C. Guet, “Regulatory network structure determines patterns of intermolecular epistasis,” <i>eLife</i>, vol. 6. eLife Sciences Publications, 2017.","ama":"Lagator M, Sarikas S, Acar H, Bollback JP, Guet CC. Regulatory network structure determines patterns of intermolecular epistasis. <i>eLife</i>. 2017;6. doi:<a href=\"https://doi.org/10.7554/eLife.28921\">10.7554/eLife.28921</a>","mla":"Lagator, Mato, et al. “Regulatory Network Structure Determines Patterns of Intermolecular Epistasis.” <i>ELife</i>, vol. 6, e28921, eLife Sciences Publications, 2017, doi:<a href=\"https://doi.org/10.7554/eLife.28921\">10.7554/eLife.28921</a>.","apa":"Lagator, M., Sarikas, S., Acar, H., Bollback, J. P., &#38; Guet, C. C. (2017). Regulatory network structure determines patterns of intermolecular epistasis. <i>ELife</i>. eLife Sciences Publications. <a href=\"https://doi.org/10.7554/eLife.28921\">https://doi.org/10.7554/eLife.28921</a>","chicago":"Lagator, Mato, Srdjan Sarikas, Hande Acar, Jonathan P Bollback, and Calin C Guet. “Regulatory Network Structure Determines Patterns of Intermolecular Epistasis.” <i>ELife</i>. eLife Sciences Publications, 2017. <a href=\"https://doi.org/10.7554/eLife.28921\">https://doi.org/10.7554/eLife.28921</a>.","ista":"Lagator M, Sarikas S, Acar H, Bollback JP, Guet CC. 2017. Regulatory network structure determines patterns of intermolecular epistasis. eLife. 6, e28921."},"language":[{"iso":"eng"}],"pubrep_id":"918","oa":1},{"isi":1,"year":"2017","external_id":{"isi":["000404024800001"]},"publist_id":"6460","status":"public","publication":"eLife","project":[{"call_identifier":"FP7","name":"Speed of Adaptation in Population Genetics and Evolutionary Computation","grant_number":"618091","_id":"25B1EC9E-B435-11E9-9278-68D0E5697425"},{"_id":"25681D80-B435-11E9-9278-68D0E5697425","grant_number":"291734","name":"International IST Postdoc Fellowship Programme","call_identifier":"FP7"},{"grant_number":"648440","name":"Selective Barriers to Horizontal Gene Transfer","call_identifier":"H2020","_id":"2578D616-B435-11E9-9278-68D0E5697425"}],"ec_funded":1,"date_published":"2017-05-18T00:00:00Z","article_processing_charge":"Yes","doi":"10.7554/eLife.25192","publisher":"eLife Sciences Publications","_id":"954","date_updated":"2023-09-22T10:01:17Z","type":"journal_article","ddc":["576"],"quality_controlled":"1","month":"05","department":[{"_id":"CaGu"},{"_id":"NiBa"},{"_id":"JoBo"}],"file":[{"file_name":"IST-2017-841-v1+1_elife-25192-v2.pdf","access_level":"open_access","content_type":"application/pdf","relation":"main_file","checksum":"59cdd4400fb41280122d414fea971546","file_size":2441529,"date_created":"2018-12-12T10:17:49Z","creator":"system","date_updated":"2020-07-14T12:48:16Z","file_id":"5306"},{"file_id":"5307","creator":"system","date_updated":"2020-07-14T12:48:16Z","file_size":3752660,"date_created":"2018-12-12T10:17:50Z","checksum":"b69024880558b858eb8c5d47a92b6377","relation":"main_file","access_level":"open_access","content_type":"application/pdf","file_name":"IST-2017-841-v1+2_elife-25192-figures-v2.pdf"}],"article_number":"e25192","oa":1,"language":[{"iso":"eng"}],"pubrep_id":"841","citation":{"ista":"Lagator M, Paixao T, Barton NH, Bollback JP, Guet CC. 2017. On the mechanistic nature of epistasis in a canonical cis-regulatory element. eLife. 6, e25192.","chicago":"Lagator, Mato, Tiago Paixao, Nicholas H Barton, Jonathan P Bollback, and Calin C Guet. “On the Mechanistic Nature of Epistasis in a Canonical Cis-Regulatory Element.” <i>ELife</i>. eLife Sciences Publications, 2017. <a href=\"https://doi.org/10.7554/eLife.25192\">https://doi.org/10.7554/eLife.25192</a>.","mla":"Lagator, Mato, et al. “On the Mechanistic Nature of Epistasis in a Canonical Cis-Regulatory Element.” <i>ELife</i>, vol. 6, e25192, eLife Sciences Publications, 2017, doi:<a href=\"https://doi.org/10.7554/eLife.25192\">10.7554/eLife.25192</a>.","apa":"Lagator, M., Paixao, T., Barton, N. H., Bollback, J. P., &#38; Guet, C. C. (2017). On the mechanistic nature of epistasis in a canonical cis-regulatory element. <i>ELife</i>. eLife Sciences Publications. <a href=\"https://doi.org/10.7554/eLife.25192\">https://doi.org/10.7554/eLife.25192</a>","ama":"Lagator M, Paixao T, Barton NH, Bollback JP, Guet CC. On the mechanistic nature of epistasis in a canonical cis-regulatory element. <i>eLife</i>. 2017;6. doi:<a href=\"https://doi.org/10.7554/eLife.25192\">10.7554/eLife.25192</a>","short":"M. Lagator, T. Paixao, N.H. Barton, J.P. Bollback, C.C. Guet, ELife 6 (2017).","ieee":"M. Lagator, T. Paixao, N. H. Barton, J. P. Bollback, and C. C. Guet, “On the mechanistic nature of epistasis in a canonical cis-regulatory element,” <i>eLife</i>, vol. 6. eLife Sciences Publications, 2017."},"user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","day":"18","scopus_import":"1","author":[{"full_name":"Lagator, Mato","id":"345D25EC-F248-11E8-B48F-1D18A9856A87","last_name":"Lagator","first_name":"Mato"},{"last_name":"Paixao","full_name":"Paixao, Tiago","id":"2C5658E6-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0003-2361-3953","first_name":"Tiago"},{"id":"4880FE40-F248-11E8-B48F-1D18A9856A87","full_name":"Barton, Nicholas H","last_name":"Barton","orcid":"0000-0002-8548-5240","first_name":"Nicholas H"},{"last_name":"Bollback","id":"2C6FA9CC-F248-11E8-B48F-1D18A9856A87","full_name":"Bollback, Jonathan P","orcid":"0000-0002-4624-4612","first_name":"Jonathan P"},{"id":"47F8433E-F248-11E8-B48F-1D18A9856A87","full_name":"Guet, Calin C","last_name":"Guet","orcid":"0000-0001-6220-2052","first_name":"Calin C"}],"oa_version":"Published Version","title":"On the mechanistic nature of epistasis in a canonical cis-regulatory element","volume":6,"date_created":"2018-12-11T11:49:23Z","has_accepted_license":"1","abstract":[{"text":"Understanding the relation between genotype and phenotype remains a major challenge. The difficulty of predicting individual mutation effects, and particularly the interactions between them, has prevented the development of a comprehensive theory that links genotypic changes to their phenotypic effects. We show that a general thermodynamic framework for gene regulation, based on a biophysical understanding of protein-DNA binding, accurately predicts the sign of epistasis in a canonical cis-regulatory element consisting of overlapping RNA polymerase and repressor binding sites. Sign and magnitude of individual mutation effects are sufficient to predict the sign of epistasis and its environmental dependence. Thus, the thermodynamic model offers the correct null prediction for epistasis between mutations across DNA-binding sites. Our results indicate that a predictive theory for the effects of cis-regulatory mutations is possible from first principles, as long as the essential molecular mechanisms and the constraints these impose on a biological system are accounted for.","lang":"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","image":"/images/cc_by.png","short":"CC BY (4.0)"},"intvolume":"         6","file_date_updated":"2020-07-14T12:48:16Z","publication_identifier":{"issn":["2050084X"]},"publication_status":"published"},{"pubrep_id":"588","language":[{"iso":"eng"}],"oa":1,"user_id":"3E5EF7F0-F248-11E8-B48F-1D18A9856A87","issue":"3","citation":{"chicago":"Lagator, Mato, Claudia Igler, Anaisa Moreno, Calin C Guet, and Jonathan P Bollback. “Epistatic Interactions in the Arabinose Cis-Regulatory Element.” <i>Molecular Biology and Evolution</i>. Oxford University Press, 2016. <a href=\"https://doi.org/10.1093/molbev/msv269\">https://doi.org/10.1093/molbev/msv269</a>.","ista":"Lagator M, Igler C, Moreno A, Guet CC, Bollback JP. 2016. Epistatic interactions in the arabinose cis-regulatory element. Molecular Biology and Evolution. 33(3), 761–769.","mla":"Lagator, Mato, et al. “Epistatic Interactions in the Arabinose Cis-Regulatory Element.” <i>Molecular Biology and Evolution</i>, vol. 33, no. 3, Oxford University Press, 2016, pp. 761–69, doi:<a href=\"https://doi.org/10.1093/molbev/msv269\">10.1093/molbev/msv269</a>.","apa":"Lagator, M., Igler, C., Moreno, A., Guet, C. C., &#38; Bollback, J. P. (2016). Epistatic interactions in the arabinose cis-regulatory element. <i>Molecular Biology and Evolution</i>. Oxford University Press. <a href=\"https://doi.org/10.1093/molbev/msv269\">https://doi.org/10.1093/molbev/msv269</a>","ama":"Lagator M, Igler C, Moreno A, Guet CC, Bollback JP. Epistatic interactions in the arabinose cis-regulatory element. <i>Molecular Biology and Evolution</i>. 2016;33(3):761-769. doi:<a href=\"https://doi.org/10.1093/molbev/msv269\">10.1093/molbev/msv269</a>","short":"M. Lagator, C. Igler, A. Moreno, C.C. Guet, J.P. Bollback, Molecular Biology and Evolution 33 (2016) 761–769.","ieee":"M. Lagator, C. Igler, A. Moreno, C. C. Guet, and J. P. Bollback, “Epistatic interactions in the arabinose cis-regulatory element,” <i>Molecular Biology and Evolution</i>, vol. 33, no. 3. Oxford University Press, pp. 761–769, 2016."},"month":"03","file":[{"access_level":"open_access","content_type":"application/pdf","file_name":"IST-2016-588-v1+1_Mol_Biol_Evol-2016-Lagator-761-9.pdf","checksum":"1f456ce1d2aa2f67176a1709f9702ecf","relation":"main_file","date_updated":"2020-07-14T12:44:53Z","creator":"system","file_size":648115,"date_created":"2018-12-12T10:09:27Z","file_id":"4751"}],"department":[{"_id":"CaGu"},{"_id":"JoBo"}],"intvolume":"        33","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","image":"/images/cc_by.png","short":"CC BY (4.0)"},"abstract":[{"text":"Changes in gene expression are an important mode of evolution; however, the proximate mechanism of these changes is poorly understood. In particular, little is known about the effects of mutations within cis binding sites for transcription factors, or the nature of epistatic interactions between these mutations. Here, we tested the effects of single and double mutants in two cis binding sites involved in the transcriptional regulation of the Escherichia coli araBAD operon, a component of arabinose metabolism, using a synthetic system. This system decouples transcriptional control from any posttranslational effects on fitness, allowing a precise estimate of the effect of single and double mutations, and hence epistasis, on gene expression. We found that epistatic interactions between mutations in the araBAD cis-regulatory element are common, and that the predominant form of epistasis is negative. The magnitude of the interactions depended on whether the mutations are located in the same or in different operator sites. Importantly, these epistatic interactions were dependent on the presence of arabinose, a native inducer of the araBAD operon in vivo, with some interactions changing in sign (e.g., from negative to positive) in its presence. This study thus reveals that mutations in even relatively simple cis-regulatory elements interact in complex ways such that selection on the level of gene expression in one environment might perturb regulation in the other environment in an unpredictable and uncorrelated manner.","lang":"eng"}],"has_accepted_license":"1","publication_status":"published","file_date_updated":"2020-07-14T12:44:53Z","title":"Epistatic interactions in the arabinose cis-regulatory element","oa_version":"Published Version","author":[{"full_name":"Lagator, Mato","id":"345D25EC-F248-11E8-B48F-1D18A9856A87","last_name":"Lagator","first_name":"Mato"},{"first_name":"Claudia","last_name":"Igler","full_name":"Igler, Claudia","id":"46613666-F248-11E8-B48F-1D18A9856A87"},{"last_name":"Moreno","full_name":"Moreno, Anaisa","first_name":"Anaisa"},{"orcid":"0000-0001-6220-2052","first_name":"Calin C","id":"47F8433E-F248-11E8-B48F-1D18A9856A87","full_name":"Guet, Calin C","last_name":"Guet"},{"orcid":"0000-0002-4624-4612","first_name":"Jonathan P","last_name":"Bollback","full_name":"Bollback, Jonathan P","id":"2C6FA9CC-F248-11E8-B48F-1D18A9856A87"}],"scopus_import":1,"day":"01","date_created":"2018-12-11T11:51:57Z","volume":33,"project":[{"grant_number":"291734","name":"International IST Postdoc Fellowship Programme","call_identifier":"FP7","_id":"25681D80-B435-11E9-9278-68D0E5697425"}],"publication":"Molecular Biology and Evolution","status":"public","date_published":"2016-03-01T00:00:00Z","ec_funded":1,"year":"2016","publist_id":"5772","ddc":["570","576"],"page":"761 - 769","quality_controlled":"1","publisher":"Oxford University Press","doi":"10.1093/molbev/msv269","type":"journal_article","date_updated":"2021-01-12T06:50:39Z","_id":"1427"},{"year":"2016","month":"12","related_material":{"record":[{"id":"1077","relation":"used_in_publication","status":"public"}]},"department":[{"_id":"NiBa"},{"_id":"JoBo"}],"oa":1,"status":"public","citation":{"mla":"Fernandes Redondo, Rodrigo A., et al. <i>Data from Evolutionary Interplay between Structure, Energy and Epistasis in the Coat Protein of the ΦX174 Phage Family</i>. The Royal Society, 2016, doi:<a href=\"https://doi.org/10.6084/m9.figshare.4315652.v1\">10.6084/m9.figshare.4315652.v1</a>.","apa":"Fernandes Redondo, R. A., de Vladar, H., Włodarski, T., &#38; Bollback, J. P. (2016). Data from evolutionary interplay between structure, energy and epistasis in the coat protein of the ϕX174 phage family. The Royal Society. <a href=\"https://doi.org/10.6084/m9.figshare.4315652.v1\">https://doi.org/10.6084/m9.figshare.4315652.v1</a>","chicago":"Fernandes Redondo, Rodrigo A, Harold de Vladar, Tomasz Włodarski, and Jonathan P Bollback. “Data from Evolutionary Interplay between Structure, Energy and Epistasis in the Coat Protein of the ΦX174 Phage Family.” The Royal Society, 2016. <a href=\"https://doi.org/10.6084/m9.figshare.4315652.v1\">https://doi.org/10.6084/m9.figshare.4315652.v1</a>.","ista":"Fernandes Redondo RA, de Vladar H, Włodarski T, Bollback JP. 2016. Data from evolutionary interplay between structure, energy and epistasis in the coat protein of the ϕX174 phage family, The Royal Society, <a href=\"https://doi.org/10.6084/m9.figshare.4315652.v1\">10.6084/m9.figshare.4315652.v1</a>.","short":"R.A. Fernandes Redondo, H. de Vladar, T. Włodarski, J.P. Bollback, (2016).","ieee":"R. A. Fernandes Redondo, H. de Vladar, T. Włodarski, and J. P. Bollback, “Data from evolutionary interplay between structure, energy and epistasis in the coat protein of the ϕX174 phage family.” The Royal Society, 2016.","ama":"Fernandes Redondo RA, de Vladar H, Włodarski T, Bollback JP. Data from evolutionary interplay between structure, energy and epistasis in the coat protein of the ϕX174 phage family. 2016. doi:<a href=\"https://doi.org/10.6084/m9.figshare.4315652.v1\">10.6084/m9.figshare.4315652.v1</a>"},"date_published":"2016-12-14T00:00:00Z","user_id":"6785fbc1-c503-11eb-8a32-93094b40e1cf","author":[{"first_name":"Rodrigo A","orcid":"0000-0002-5837-2793","last_name":"Fernandes Redondo","full_name":"Fernandes Redondo, Rodrigo A","id":"409D5C96-F248-11E8-B48F-1D18A9856A87"},{"first_name":"Harold","orcid":"0000-0002-5985-7653","full_name":"de Vladar, Harold","id":"2A181218-F248-11E8-B48F-1D18A9856A87","last_name":"de Vladar"},{"first_name":"Tomasz","last_name":"Włodarski","full_name":"Włodarski, Tomasz"},{"orcid":"0000-0002-4624-4612","first_name":"Jonathan P","last_name":"Bollback","id":"2C6FA9CC-F248-11E8-B48F-1D18A9856A87","full_name":"Bollback, Jonathan P"}],"doi":"10.6084/m9.figshare.4315652.v1","day":"14","article_processing_charge":"No","title":"Data from evolutionary interplay between structure, energy and epistasis in the coat protein of the ϕX174 phage family","oa_version":"Published Version","publisher":"The Royal Society","date_updated":"2025-05-28T11:57:06Z","_id":"9864","type":"research_data_reference","date_created":"2021-08-10T08:29:47Z","abstract":[{"lang":"eng","text":"Viral capsids are structurally constrained by interactions among the amino acids (AAs) of their constituent proteins. Therefore, epistasis is expected to evolve among physically interacting sites and to influence the rates of substitution. To study the evolution of epistasis, we focused on the major structural protein of the ϕX174 phage family by, first, reconstructing the ancestral protein sequences of 18 species using a Bayesian statistical framework. The inferred ancestral reconstruction differed at eight AAs, for a total of 256 possible ancestral haplotypes. For each ancestral haplotype and the extant species, we estimated, in silico, the distribution of free energies and epistasis of the capsid structure. We found that free energy has not significantly increased but epistasis has. We decomposed epistasis up to fifth order and found that higher-order epistasis sometimes compensates pairwise interactions making the free energy seem additive. The dN/dS ratio is low, suggesting strong purifying selection, and that structure is under stabilizing selection. We synthesized phages carrying ancestral haplotypes of the coat protein gene and measured their fitness experimentally. Our findings indicate that stabilizing mutations can have higher fitness, and that fitness optima do not necessarily coincide with energy minima."}],"main_file_link":[{"open_access":"1","url":"https://doi.org/10.6084/m9.figshare.4315652.v1"}]},{"user_id":"4435EBFC-F248-11E8-B48F-1D18A9856A87","citation":{"mla":"Kupczok, Anne, and Jonathan P. Bollback. “Motif Depletion in Bacteriophages Infecting Hosts with CRISPR Systems.” <i>BMC Genomics</i>, vol. 15, no. 1, 663, BioMed Central, 2014, doi:<a href=\"https://doi.org/10.1186/1471-2164-15-663\">10.1186/1471-2164-15-663</a>.","apa":"Kupczok, A., &#38; Bollback, J. P. (2014). Motif depletion in bacteriophages infecting hosts with CRISPR systems. <i>BMC Genomics</i>. BioMed Central. <a href=\"https://doi.org/10.1186/1471-2164-15-663\">https://doi.org/10.1186/1471-2164-15-663</a>","chicago":"Kupczok, Anne, and Jonathan P Bollback. “Motif Depletion in Bacteriophages Infecting Hosts with CRISPR Systems.” <i>BMC Genomics</i>. BioMed Central, 2014. <a href=\"https://doi.org/10.1186/1471-2164-15-663\">https://doi.org/10.1186/1471-2164-15-663</a>.","ista":"Kupczok A, Bollback JP. 2014. Motif depletion in bacteriophages infecting hosts with CRISPR systems. BMC Genomics. 15(1), 663.","short":"A. Kupczok, J.P. Bollback, BMC Genomics 15 (2014).","ieee":"A. Kupczok and J. P. Bollback, “Motif depletion in bacteriophages infecting hosts with CRISPR systems,” <i>BMC Genomics</i>, vol. 15, no. 1. BioMed Central, 2014.","ama":"Kupczok A, Bollback JP. Motif depletion in bacteriophages infecting hosts with CRISPR systems. <i>BMC Genomics</i>. 2014;15(1). doi:<a href=\"https://doi.org/10.1186/1471-2164-15-663\">10.1186/1471-2164-15-663</a>"},"issue":"1","language":[{"iso":"eng"}],"pubrep_id":"396","oa":1,"file":[{"file_id":"4878","file_size":1489769,"date_created":"2018-12-12T10:11:24Z","date_updated":"2020-07-14T12:45:26Z","creator":"system","relation":"main_file","checksum":"3f6d2776b90a842a28359cc957d3d04b","file_name":"IST-2015-396-v1+1_1471-2164-15-663.pdf","access_level":"open_access","content_type":"application/pdf"}],"article_number":"663","department":[{"_id":"JoBo"}],"month":"08","file_date_updated":"2020-07-14T12:45:26Z","publication_status":"published","tmp":{"name":"Creative Commons Public Domain Dedication (CC0 1.0)","legal_code_url":"https://creativecommons.org/publicdomain/zero/1.0/legalcode","image":"/images/cc_0.png","short":"CC0 (1.0)"},"intvolume":"        15","abstract":[{"lang":"eng","text":"Background: CRISPR is a microbial immune system likely to be involved in host-parasite coevolution. It functions using target sequences encoded by the bacterial genome, which interfere with invading nucleic acids using a homology-dependent system. The system also requires protospacer associated motifs (PAMs), short motifs close to the target sequence that are required for interference in CRISPR types I and II. Here, we investigate whether PAMs are depleted in phage genomes due to selection pressure to escape recognition.Results: To this end, we analyzed two data sets. Phages infecting all bacterial hosts were analyzed first, followed by a detailed analysis of phages infecting the genus Streptococcus, where PAMs are best understood. We use two different measures of motif underrepresentation that control for codon bias and the frequency of submotifs. We compare phages infecting species with a particular CRISPR type to those infecting species without that type. Since only known PAMs were investigated, the analysis is restricted to CRISPR types I-C and I-E and in Streptococcus to types I-C and II. We found evidence for PAM depletion in Streptococcus phages infecting hosts with CRISPR type I-C, in Vibrio phages infecting hosts with CRISPR type I-E and in Streptococcus thermopilus phages infecting hosts with type II-A, known as CRISPR3.Conclusions: The observed motif depletion in phages with hosts having CRISPR can be attributed to selection rather than to mutational bias, as mutational bias should affect the phages of all hosts. This observation implies that the CRISPR system has been efficient in the groups discussed here."}],"has_accepted_license":"1","date_created":"2018-12-11T11:55:23Z","volume":15,"title":"Motif depletion in bacteriophages infecting hosts with CRISPR systems","oa_version":"Published Version","scopus_import":1,"day":"08","author":[{"full_name":"Kupczok, Anne","id":"2BB22BC2-F248-11E8-B48F-1D18A9856A87","last_name":"Kupczok","first_name":"Anne"},{"id":"2C6FA9CC-F248-11E8-B48F-1D18A9856A87","full_name":"Bollback, Jonathan P","last_name":"Bollback","first_name":"Jonathan P","orcid":"0000-0002-4624-4612"}],"date_published":"2014-08-08T00:00:00Z","publication":"BMC Genomics","status":"public","publist_id":"5009","year":"2014","quality_controlled":"1","ddc":["570"],"type":"journal_article","_id":"2042","date_updated":"2021-01-12T06:54:56Z","publisher":"BioMed Central","doi":"10.1186/1471-2164-15-663"},{"volume":1,"date_created":"2018-12-11T11:57:30Z","scopus_import":1,"day":"13","author":[{"orcid":"0000-0002-5837-2793","first_name":"Rodrigo A","id":"409D5C96-F248-11E8-B48F-1D18A9856A87","full_name":"Fernandes Redondo, Rodrigo A","last_name":"Fernandes Redondo"},{"last_name":"Kupczok","full_name":"Kupczok, Anne","id":"2BB22BC2-F248-11E8-B48F-1D18A9856A87","first_name":"Anne"},{"first_name":"Gertraud","last_name":"Stift","full_name":"Stift, Gertraud","id":"2DB195CA-F248-11E8-B48F-1D18A9856A87"},{"orcid":"0000-0002-4624-4612","first_name":"Jonathan P","id":"2C6FA9CC-F248-11E8-B48F-1D18A9856A87","full_name":"Bollback, Jonathan P","last_name":"Bollback"}],"oa_version":"Published Version","title":"Complete genome sequence of the novel phage MG-B1 infecting bacillus weihenstephanensis","file_date_updated":"2020-07-14T12:45:40Z","publication_status":"published","has_accepted_license":"1","abstract":[{"text":"Here, we describe a novel virulent bacteriophage that infects Bacillus weihenstephanensis, isolated from soil in Austria. It is the first phage to be discovered that infects this species. Here, we present the complete genome sequence of this podovirus. ","lang":"eng"}],"intvolume":"         1","department":[{"_id":"JoBo"},{"_id":"LifeSc"}],"file":[{"checksum":"0751ec74b695567e0cdf02aaf9c26829","relation":"main_file","access_level":"open_access","content_type":"application/pdf","file_name":"IST-2015-398-v1+1_Genome_Announc.-2013-Redondo-.pdf","file_id":"5291","creator":"system","date_updated":"2020-07-14T12:45:40Z","date_created":"2018-12-12T10:17:36Z","file_size":130026}],"month":"06","citation":{"ieee":"R. A. Fernandes Redondo, A. Kupczok, G. Stift, and J. P. Bollback, “Complete genome sequence of the novel phage MG-B1 infecting bacillus weihenstephanensis,” <i>Genome Announcements</i>, vol. 1, no. 3. American Society for Microbiology, 2013.","short":"R.A. Fernandes Redondo, A. Kupczok, G. Stift, J.P. Bollback, Genome Announcements 1 (2013).","ama":"Fernandes Redondo RA, Kupczok A, Stift G, Bollback JP. Complete genome sequence of the novel phage MG-B1 infecting bacillus weihenstephanensis. <i>Genome Announcements</i>. 2013;1(3). doi:<a href=\"https://doi.org/10.1128/genomeA.00216-13\">10.1128/genomeA.00216-13</a>","apa":"Fernandes Redondo, R. A., Kupczok, A., Stift, G., &#38; Bollback, J. P. (2013). Complete genome sequence of the novel phage MG-B1 infecting bacillus weihenstephanensis. <i>Genome Announcements</i>. American Society for Microbiology. <a href=\"https://doi.org/10.1128/genomeA.00216-13\">https://doi.org/10.1128/genomeA.00216-13</a>","mla":"Fernandes Redondo, Rodrigo A., et al. “Complete Genome Sequence of the Novel Phage MG-B1 Infecting Bacillus Weihenstephanensis.” <i>Genome Announcements</i>, vol. 1, no. 3, American Society for Microbiology, 2013, doi:<a href=\"https://doi.org/10.1128/genomeA.00216-13\">10.1128/genomeA.00216-13</a>.","chicago":"Fernandes Redondo, Rodrigo A, Anne Kupczok, Gertraud Stift, and Jonathan P Bollback. “Complete Genome Sequence of the Novel Phage MG-B1 Infecting Bacillus Weihenstephanensis.” <i>Genome Announcements</i>. American Society for Microbiology, 2013. <a href=\"https://doi.org/10.1128/genomeA.00216-13\">https://doi.org/10.1128/genomeA.00216-13</a>.","ista":"Fernandes Redondo RA, Kupczok A, Stift G, Bollback JP. 2013. Complete genome sequence of the novel phage MG-B1 infecting bacillus weihenstephanensis. Genome Announcements. 1(3)."},"issue":"3","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","oa":1,"pubrep_id":"398","language":[{"iso":"eng"}],"_id":"2410","date_updated":"2021-01-12T06:57:19Z","type":"journal_article","doi":"10.1128/genomeA.00216-13","publisher":"American Society for Microbiology","quality_controlled":"1","ddc":["576"],"publist_id":"4516","year":"2013","date_published":"2013-06-13T00:00:00Z","publication":"Genome Announcements","status":"public"},{"year":"2013","publist_id":"4514","publication":"BMC Evolutionary Biology","status":"public","date_published":"2013-02-26T00:00:00Z","doi":"10.1186/1471-2148-13-54","publisher":"BioMed Central","date_updated":"2021-01-12T06:57:20Z","_id":"2412","type":"journal_article","page":"54 - 54","ddc":["576"],"quality_controlled":"1","month":"02","department":[{"_id":"JoBo"}],"file":[{"file_size":518729,"date_created":"2018-12-12T10:17:15Z","date_updated":"2020-07-14T12:45:40Z","creator":"system","file_id":"5268","file_name":"IST-2015-397-v1+1_1471-2148-13-54.pdf","access_level":"open_access","content_type":"application/pdf","relation":"main_file","checksum":"029c7e0b198c19312b66ecce3cabb22f"}],"oa":1,"pubrep_id":"397","language":[{"iso":"eng"}],"issue":"1","citation":{"ama":"Kupczok A, Bollback JP. Probabilistic models for CRISPR spacer content evolution . <i>BMC Evolutionary Biology</i>. 2013;13(1):54-54. doi:<a href=\"https://doi.org/10.1186/1471-2148-13-54\">10.1186/1471-2148-13-54</a>","short":"A. Kupczok, J.P. Bollback, BMC Evolutionary Biology 13 (2013) 54–54.","ieee":"A. Kupczok and J. P. Bollback, “Probabilistic models for CRISPR spacer content evolution ,” <i>BMC Evolutionary Biology</i>, vol. 13, no. 1. BioMed Central, pp. 54–54, 2013.","chicago":"Kupczok, Anne, and Jonathan P Bollback. “Probabilistic Models for CRISPR Spacer Content Evolution .” <i>BMC Evolutionary Biology</i>. BioMed Central, 2013. <a href=\"https://doi.org/10.1186/1471-2148-13-54\">https://doi.org/10.1186/1471-2148-13-54</a>.","ista":"Kupczok A, Bollback JP. 2013. Probabilistic models for CRISPR spacer content evolution . BMC Evolutionary Biology. 13(1), 54–54.","mla":"Kupczok, Anne, and Jonathan P. Bollback. “Probabilistic Models for CRISPR Spacer Content Evolution .” <i>BMC Evolutionary Biology</i>, vol. 13, no. 1, BioMed Central, 2013, pp. 54–54, doi:<a href=\"https://doi.org/10.1186/1471-2148-13-54\">10.1186/1471-2148-13-54</a>.","apa":"Kupczok, A., &#38; Bollback, J. P. (2013). Probabilistic models for CRISPR spacer content evolution . <i>BMC Evolutionary Biology</i>. BioMed Central. <a href=\"https://doi.org/10.1186/1471-2148-13-54\">https://doi.org/10.1186/1471-2148-13-54</a>"},"user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","author":[{"first_name":"Anne","last_name":"Kupczok","full_name":"Kupczok, Anne","id":"2BB22BC2-F248-11E8-B48F-1D18A9856A87"},{"orcid":"0000-0002-4624-4612","first_name":"Jonathan P","last_name":"Bollback","id":"2C6FA9CC-F248-11E8-B48F-1D18A9856A87","full_name":"Bollback, Jonathan P"}],"day":"26","scopus_import":1,"title":"Probabilistic models for CRISPR spacer content evolution ","oa_version":"Published Version","volume":13,"date_created":"2018-12-11T11:57:31Z","has_accepted_license":"1","abstract":[{"text":"Background: The CRISPR/Cas system is known to act as an adaptive and heritable immune system in Eubacteria and Archaea. Immunity is encoded in an array of spacer sequences. Each spacer can provide specific immunity to invasive elements that carry the same or a similar sequence. Even in closely related strains, spacer content is very dynamic and evolves quickly. Standard models of nucleotide evolutioncannot be applied to quantify its rate of change since processes other than single nucleotide changes determine its evolution.Methods We present probabilistic models that are specific for spacer content evolution. They account for the different processes of insertion and deletion. Insertions can be constrained to occur on one end only or are allowed to occur throughout the array. One deletion event can affect one spacer or a whole fragment of adjacent spacers. Parameters of the underlying models are estimated for a pair of arrays by maximum likelihood using explicit ancestor enumeration.Results Simulations show that parameters are well estimated on average under the models presented here. There is a bias in the rate estimation when including fragment deletions. The models also estimate times between pairs of strains. But with increasing time, spacer overlap goes to zero, and thus there is an upper bound on the distance that can be estimated. Spacer content similarities are displayed in a distance based phylogeny using the estimated times.We use the presented models to analyze different Yersinia pestis data sets and find that the results among them are largely congruent. The models also capture the variation in diversity of spacers among the data sets. A comparison of spacer-based phylogenies and Cas gene phylogenies shows that they resolve very different time scales for this data set.Conclusions The simulations and data analyses show that the presented models are useful for quantifying spacer content evolution and for displaying spacer content similarities of closely related strains in a phylogeny. This allows for comparisons of different CRISPR arrays or for comparisons between CRISPR arrays and nucleotide substitution rates.","lang":"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","image":"/images/cc_by.png","short":"CC BY (4.0)"},"intvolume":"        13","publication_status":"published","file_date_updated":"2020-07-14T12:45:40Z"},{"scopus_import":1,"day":"09","author":[{"first_name":"Melissa","last_name":"Ward","full_name":"Ward, Melissa"},{"full_name":"Lycett, Samantha","last_name":"Lycett","first_name":"Samantha"},{"full_name":"Avila, Dorita","last_name":"Avila","first_name":"Dorita"},{"last_name":"Bollback","id":"2C6FA9CC-F248-11E8-B48F-1D18A9856A87","full_name":"Bollback, Jonathan P","orcid":"0000-0002-4624-4612","first_name":"Jonathan P"},{"first_name":"Andrew","last_name":"Leigh Brown","full_name":"Leigh Brown, Andrew"}],"oa_version":"Published Version","title":"Evolutionary interactions between haemagglutinin and neuraminidase in avian influenza","volume":13,"date_created":"2018-12-11T11:46:49Z","has_accepted_license":"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","image":"/images/cc_by.png","short":"CC BY (4.0)"},"abstract":[{"lang":"eng","text":"Background: Reassortment between the RNA segments encoding haemagglutinin (HA) and neuraminidase (NA), the major antigenic influenza proteins, produces viruses with novel HA and NA subtype combinations and has preceded the emergence of pandemic strains. It has been suggested that productive viral infection requires a balance in the level of functional activity of HA and NA, arising from their closely interacting roles in the viral life cycle, and that this functional balance could be mediated by genetic changes in the HA and NA. Here, we investigate how the selective pressure varies for H7 avian influenza HA on different NA subtype backgrounds. Results: By extending Bayesian stochastic mutational mapping methods to calculate the ratio of the rate of non-synonymous change to the rate of synonymous change (d N/d S), we found the average d N/d S across the avian influenza H7 HA1 region to be significantly greater on an N2 NA subtype background than on an N1, N3 or N7 background. Observed differences in evolutionary rates of H7 HA on different NA subtype backgrounds could not be attributed to underlying differences between avian host species or virus pathogenicity. Examination of d N/d S values for each subtype on a site-by-site basis indicated that the elevated d N/d S on the N2 NA background was a result of increased selection, rather than a relaxation of selective constraint. Conclusions: Our results are consistent with the hypothesis that reassortment exposes influenza HA to significant changes in selective pressure through genetic interactions with NA. Such epistatic effects might be explicitly accounted for in future models of influenza evolution."}],"intvolume":"        13","file_date_updated":"2020-07-14T12:46:36Z","publication_status":"published","month":"10","department":[{"_id":"JoBo"}],"article_number":"222","file":[{"access_level":"open_access","content_type":"application/pdf","file_name":"IST-2018-941-v1+1_2013_Bollback_Evolutionary_interactionspdf.pdf","checksum":"52cf48a7c1794676ae8b0029573a84a9","relation":"main_file","date_updated":"2020-07-14T12:46:36Z","creator":"system","file_size":1150052,"date_created":"2018-12-12T10:08:59Z","file_id":"4722"}],"oa":1,"pubrep_id":"941","language":[{"iso":"eng"}],"citation":{"ama":"Ward M, Lycett S, Avila D, Bollback JP, Leigh Brown A. Evolutionary interactions between haemagglutinin and neuraminidase in avian influenza. <i>BMC Evolutionary Biology</i>. 2013;13(1). doi:<a href=\"https://doi.org/10.1186/1471-2148-13-222\">10.1186/1471-2148-13-222</a>","short":"M. Ward, S. Lycett, D. Avila, J.P. Bollback, A. Leigh Brown, BMC Evolutionary Biology 13 (2013).","ieee":"M. Ward, S. Lycett, D. Avila, J. P. Bollback, and A. Leigh Brown, “Evolutionary interactions between haemagglutinin and neuraminidase in avian influenza,” <i>BMC Evolutionary Biology</i>, vol. 13, no. 1. BioMed Central, 2013.","ista":"Ward M, Lycett S, Avila D, Bollback JP, Leigh Brown A. 2013. Evolutionary interactions between haemagglutinin and neuraminidase in avian influenza. BMC Evolutionary Biology. 13(1), 222.","chicago":"Ward, Melissa, Samantha Lycett, Dorita Avila, Jonathan P Bollback, and Andrew Leigh Brown. “Evolutionary Interactions between Haemagglutinin and Neuraminidase in Avian Influenza.” <i>BMC Evolutionary Biology</i>. BioMed Central, 2013. <a href=\"https://doi.org/10.1186/1471-2148-13-222\">https://doi.org/10.1186/1471-2148-13-222</a>.","mla":"Ward, Melissa, et al. “Evolutionary Interactions between Haemagglutinin and Neuraminidase in Avian Influenza.” <i>BMC Evolutionary Biology</i>, vol. 13, no. 1, 222, BioMed Central, 2013, doi:<a href=\"https://doi.org/10.1186/1471-2148-13-222\">10.1186/1471-2148-13-222</a>.","apa":"Ward, M., Lycett, S., Avila, D., Bollback, J. P., &#38; Leigh Brown, A. (2013). Evolutionary interactions between haemagglutinin and neuraminidase in avian influenza. <i>BMC Evolutionary Biology</i>. BioMed Central. <a href=\"https://doi.org/10.1186/1471-2148-13-222\">https://doi.org/10.1186/1471-2148-13-222</a>"},"issue":"1","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","doi":"10.1186/1471-2148-13-222","publisher":"BioMed Central","_id":"500","date_updated":"2021-01-12T08:01:08Z","type":"journal_article","ddc":["576"],"quality_controlled":"1","year":"2013","publist_id":"7320","status":"public","publication":"BMC Evolutionary Biology","acknowledgement":"This work was supported by the Biotechnology and Biological Sciences Research Council, the Government of the Republic of Panama, the Interdisciplinary Centre for Human and Avian Influenza Research (www.ichair-flu.org) funded by the Scottish Funding Council, and the Institute for Science and Technology Austria.\r\nCC BY 2.0\r\n","date_published":"2013-10-09T00:00:00Z"},{"type":"journal_article","date_created":"2018-12-11T12:08:27Z","date_updated":"2021-01-12T07:56:23Z","_id":"4358","volume":2,"title":"Evolutionary genomics of Staphylococcus aureus reveals insights into the origin and molecular basis of ruminant host adaptation","publisher":"Oxford University Press","author":[{"first_name":"Caitriona","last_name":"Guinane","full_name":"Guinane, Caitriona M"},{"last_name":"Ben Zakour","full_name":"Ben Zakour, Nouri L","first_name":"Nouri"},{"last_name":"Tormo Mas","full_name":"Tormo-Mas, Maria A","first_name":"Maria"},{"first_name":"Lucy","full_name":"Weinert, Lucy A","last_name":"Weinert"},{"first_name":"Bethan","full_name":"Lowder, Bethan V","last_name":"Lowder"},{"last_name":"Cartwright","full_name":"Cartwright, Robyn A","first_name":"Robyn"},{"first_name":"Davida","last_name":"Smyth","full_name":"Smyth, Davida S"},{"last_name":"Smyth","full_name":"Smyth, Cyril J","first_name":"Cyril"},{"first_name":"Jodi","last_name":"Lindsay","full_name":"Lindsay, Jodi A"},{"last_name":"Gould","full_name":"Gould, Katherine A","first_name":"Katherine"},{"first_name":"Adam","full_name":"Witney, Adam","last_name":"Witney"},{"full_name":"Hinds, Jason","last_name":"Hinds","first_name":"Jason"},{"orcid":"0000-0002-4624-4612","first_name":"Jonathan P","last_name":"Bollback","id":"2C6FA9CC-F248-11E8-B48F-1D18A9856A87","full_name":"Jonathan Bollback"},{"last_name":"Rambaut","full_name":"Rambaut, Andrew","first_name":"Andrew"},{"last_name":"Penades","full_name":"Penades, Jose R","first_name":"Jose"},{"first_name":"J Ross","full_name":"Fitzgerald, J Ross","last_name":"Fitzgerald"}],"doi":"10.1093/gbe/evq031","day":"09","quality_controlled":0,"publication_status":"published","intvolume":"         2","abstract":[{"text":"Phenotypic biotyping has traditionally been used to differentiate bacteria occupying distinct ecological niches such as host species. For example, the capacity of Staphylococcus aureus from sheep to coagulate ruminant plasma, reported over 60 years ago, led to the description of small ruminant and bovine S. aureus ecovars. The great majority of small ruminant isolates are represented by a single, widespread clonal complex (CC133) of S. aureus, but its evolutionary origin and the molecular basis for its host tropism remain unknown. Here, we provide evidence that the CC133 clone evolved as the result of a human to ruminant host jump followed by adaptive genome diversification. Comparative whole-genome sequencing revealed molecular evidence for host adaptation including gene decay and diversification of proteins involved in host-pathogen interactions. Importantly, several novel mobile genetic elements encoding virulence proteins with attenuated or enhanced activity in ruminants were widely distributed in CC133 isolates, suggesting a key role in its host-specific interactions. To investigate this further, we examined the activity of a novel staphylococcal pathogenicity island (SaPIov2) found in the great majority of CC133 isolates which encodes a variant of the chromosomally encoded von Willebrand-binding protein (vWbp(Sov2)), previously demonstrated to have coagulase activity for human plasma. Remarkably, we discovered that SaPIov2 confers the ability to coagulate ruminant plasma suggesting an important role in ruminant disease pathogenesis and revealing the origin of a defining phenotype of the classical S. aureus biotyping scheme. Taken together, these data provide broad new insights into the origin and molecular basis of S. aureus ruminant host specificity.","lang":"eng"}],"page":"454 - 466","publist_id":"1100","month":"06","year":"2010","date_published":"2010-06-09T00:00:00Z","citation":{"mla":"Guinane, Caitriona, et al. “Evolutionary Genomics of Staphylococcus Aureus Reveals Insights into the Origin and Molecular Basis of Ruminant Host Adaptation.” <i>Genome Biology and Evolution</i>, vol. 2, Oxford University Press, 2010, pp. 454–66, doi:<a href=\"https://doi.org/10.1093/gbe/evq031\">10.1093/gbe/evq031</a>.","apa":"Guinane, C., Ben Zakour, N., Tormo Mas, M., Weinert, L., Lowder, B., Cartwright, R., … Fitzgerald, J. R. (2010). Evolutionary genomics of Staphylococcus aureus reveals insights into the origin and molecular basis of ruminant host adaptation. <i>Genome Biology and Evolution</i>. Oxford University Press. <a href=\"https://doi.org/10.1093/gbe/evq031\">https://doi.org/10.1093/gbe/evq031</a>","chicago":"Guinane, Caitriona, Nouri Ben Zakour, Maria Tormo Mas, Lucy Weinert, Bethan Lowder, Robyn Cartwright, Davida Smyth, et al. “Evolutionary Genomics of Staphylococcus Aureus Reveals Insights into the Origin and Molecular Basis of Ruminant Host Adaptation.” <i>Genome Biology and Evolution</i>. Oxford University Press, 2010. <a href=\"https://doi.org/10.1093/gbe/evq031\">https://doi.org/10.1093/gbe/evq031</a>.","ista":"Guinane C, Ben Zakour N, Tormo Mas M, Weinert L, Lowder B, Cartwright R, Smyth D, Smyth C, Lindsay J, Gould K, Witney A, Hinds J, Bollback JP, Rambaut A, Penades J, Fitzgerald JR. 2010. Evolutionary genomics of Staphylococcus aureus reveals insights into the origin and molecular basis of ruminant host adaptation. Genome Biology and Evolution. 2, 454–466.","short":"C. Guinane, N. Ben Zakour, M. Tormo Mas, L. Weinert, B. Lowder, R. Cartwright, D. Smyth, C. Smyth, J. Lindsay, K. Gould, A. Witney, J. Hinds, J.P. Bollback, A. Rambaut, J. Penades, J.R. Fitzgerald, Genome Biology and Evolution 2 (2010) 454–466.","ieee":"C. Guinane <i>et al.</i>, “Evolutionary genomics of Staphylococcus aureus reveals insights into the origin and molecular basis of ruminant host adaptation,” <i>Genome Biology and Evolution</i>, vol. 2. Oxford University Press, pp. 454–466, 2010.","ama":"Guinane C, Ben Zakour N, Tormo Mas M, et al. Evolutionary genomics of Staphylococcus aureus reveals insights into the origin and molecular basis of ruminant host adaptation. <i>Genome Biology and Evolution</i>. 2010;2:454-466. doi:<a href=\"https://doi.org/10.1093/gbe/evq031\">10.1093/gbe/evq031</a>"},"extern":1,"publication":"Genome Biology and Evolution","status":"public"},{"day":"01","doi":"10.1534/genetics.107.085225","author":[{"orcid":"0000-0002-4624-4612","first_name":"Jonathan P","last_name":"Bollback","id":"2C6FA9CC-F248-11E8-B48F-1D18A9856A87","full_name":"Jonathan Bollback"},{"last_name":"Huelsenbeck","full_name":"Huelsenbeck, John P","first_name":"John"}],"title":"Parallel genetic evolution within and between bacteriophage species of varying degrees of divergence","publisher":"Genetics Society of America","volume":181,"_id":"4357","date_updated":"2021-01-12T07:56:22Z","date_created":"2018-12-11T12:08:26Z","type":"journal_article","page":"225 - 234","intvolume":"       181","abstract":[{"text":"Parallel evolution is the acquisition of identical adaptive traits in independently evolving populations. Understanding whether the genetic changes underlying adaptation to a common selective environment are parallel within and between species is interesting because it sheds light on the degree of evolutionary constraints. If parallel evolution is perfect, then the implication is that forces such as functional constraints, epistasis, and pleiotropy play an important role in shaping the outcomes of adaptive evolution. In addition, population genetic theory predicts that the probability of parallel evolution will decline with an increase in the number of adaptive solutions-if a single adaptive solution exists, then parallel evolution will be observed among highly divergent species. For this reason, it is predicted that close relatives-which likely overlap more in the details of their adaptive solutions-will show more parallel evolution. By adapting three related bacteriophage species to a novel environment we find (1) a high rate of parallel genetic evolution at orthologous nucleotide and amino acid residues within species, (2) parallel beneficial mutations do not occur in a common order in which they fix or appear in an evolving population, (3) low rates of parallel evolution and convergent evolution between species, and (4) the probability of parallel and convergent evolution between species is strongly effected by divergence.","lang":"eng"}],"publication_status":"published","quality_controlled":0,"year":"2009","month":"01","publist_id":"1101","extern":1,"publication":"Genetics","status":"public","citation":{"ieee":"J. P. Bollback and J. Huelsenbeck, “Parallel genetic evolution within and between bacteriophage species of varying degrees of divergence,” <i>Genetics</i>, vol. 181, no. 1. Genetics Society of America, pp. 225–234, 2009.","short":"J.P. Bollback, J. Huelsenbeck, Genetics 181 (2009) 225–234.","ama":"Bollback JP, Huelsenbeck J. Parallel genetic evolution within and between bacteriophage species of varying degrees of divergence. <i>Genetics</i>. 2009;181(1):225-234. doi:<a href=\"https://doi.org/10.1534/genetics.107.085225\">10.1534/genetics.107.085225</a>","apa":"Bollback, J. P., &#38; Huelsenbeck, J. (2009). Parallel genetic evolution within and between bacteriophage species of varying degrees of divergence. <i>Genetics</i>. Genetics Society of America. <a href=\"https://doi.org/10.1534/genetics.107.085225\">https://doi.org/10.1534/genetics.107.085225</a>","mla":"Bollback, Jonathan P., and John Huelsenbeck. “Parallel Genetic Evolution within and between Bacteriophage Species of Varying Degrees of Divergence.” <i>Genetics</i>, vol. 181, no. 1, Genetics Society of America, 2009, pp. 225–34, doi:<a href=\"https://doi.org/10.1534/genetics.107.085225\">10.1534/genetics.107.085225</a>.","chicago":"Bollback, Jonathan P, and John Huelsenbeck. “Parallel Genetic Evolution within and between Bacteriophage Species of Varying Degrees of Divergence.” <i>Genetics</i>. Genetics Society of America, 2009. <a href=\"https://doi.org/10.1534/genetics.107.085225\">https://doi.org/10.1534/genetics.107.085225</a>.","ista":"Bollback JP, Huelsenbeck J. 2009. Parallel genetic evolution within and between bacteriophage species of varying degrees of divergence. Genetics. 181(1), 225–234."},"issue":"1","date_published":"2009-01-01T00:00:00Z"},{"citation":{"short":"J.P. Bollback, T. York, R. Nielsen, Genetics 179 (2008) 497–502.","ieee":"J. P. Bollback, T. York, and R. Nielsen, “Estimation of 2Nes From Temporal Allele Frequency Data,” <i>Genetics</i>, vol. 179, no. 1. Genetics Society of America, pp. 497–502, 2008.","ama":"Bollback JP, York T, Nielsen R. Estimation of 2Nes From Temporal Allele Frequency Data. <i>Genetics</i>. 2008;179(1):497-502. doi:<a href=\"https://doi.org/10.1534/genetics.107.085019\">10.1534/genetics.107.085019</a>","mla":"Bollback, Jonathan P., et al. “Estimation of 2Nes From Temporal Allele Frequency Data.” <i>Genetics</i>, vol. 179, no. 1, Genetics Society of America, 2008, pp. 497–502, doi:<a href=\"https://doi.org/10.1534/genetics.107.085019\">10.1534/genetics.107.085019</a>.","apa":"Bollback, J. P., York, T., &#38; Nielsen, R. (2008). Estimation of 2Nes From Temporal Allele Frequency Data. <i>Genetics</i>. Genetics Society of America. <a href=\"https://doi.org/10.1534/genetics.107.085019\">https://doi.org/10.1534/genetics.107.085019</a>","chicago":"Bollback, Jonathan P, Thomas York, and Rasmus Nielsen. “Estimation of 2Nes From Temporal Allele Frequency Data.” <i>Genetics</i>. Genetics Society of America, 2008. <a href=\"https://doi.org/10.1534/genetics.107.085019\">https://doi.org/10.1534/genetics.107.085019</a>.","ista":"Bollback JP, York T, Nielsen R. 2008. Estimation of 2Nes From Temporal Allele Frequency Data. Genetics. 179(1), 497–502."},"issue":"1","date_published":"2008-05-01T00:00:00Z","oa":1,"status":"public","extern":1,"publication":"Genetics","publist_id":"2965","year":"2008","month":"05","main_file_link":[{"url":"http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2390626","open_access":"1"}],"publication_status":"published","quality_controlled":0,"page":"497 - 502","abstract":[{"text":"We develop a new method for estimating effective population sizes, Ne, and selection coefficients, s, from time-series data of allele frequencies sampled from a single diallelic locus. The method is based on calculating transition probabilities, using a numerical solution of the diffusion process, and assuming independent binomial sampling from this diffusion process at each time point. We apply the method in two example applications. First, we estimate selection coefficients acting on the CCR5-Δ32 mutation on the basis of published samples of contemporary and ancient human DNA. We show that the data are compatible with the assumption of s = 0, although moderate amounts of selection acting on this mutation cannot be excluded. In our second example, we estimate the selection coefficient acting on a mutation segregating in an experimental phage population. We show that the selection coefficient acting on this mutation is ~0.43.","lang":"eng"}],"intvolume":"       179","volume":179,"_id":"3435","date_updated":"2021-01-12T07:43:27Z","date_created":"2018-12-11T12:03:19Z","type":"journal_article","day":"01","doi":"10.1534/genetics.107.085019","author":[{"first_name":"Jonathan P","orcid":"0000-0002-4624-4612","full_name":"Jonathan Bollback","id":"2C6FA9CC-F248-11E8-B48F-1D18A9856A87","last_name":"Bollback"},{"full_name":"York, Thomas L","last_name":"York","first_name":"Thomas"},{"last_name":"Nielsen","full_name":"Nielsen, Rasmus","first_name":"Rasmus"}],"title":"Estimation of 2Nes From Temporal Allele Frequency Data","publisher":"Genetics Society of America"},{"status":"public","extern":1,"publication":"Ancestral Sequence Reconstruction","date_published":"2007-01-01T00:00:00Z","citation":{"chicago":"Bollback, Jonathan P, Paul Gardner, and Rasmus Nielsen. “Estimating the History of Mutations on a Phylogeny.” In <i>Ancestral Sequence Reconstruction</i>, edited by David Liberles, 69–79. Oxford University Press, 2007. <a href=\"https://doi.org/10.1093/acprof:oso/9780199299188.003.0006\">https://doi.org/10.1093/acprof:oso/9780199299188.003.0006</a>.","ista":"Bollback JP, Gardner P, Nielsen R. 2007.Estimating the history of mutations on a phylogeny. In: Ancestral Sequence Reconstruction. , 69–79.","apa":"Bollback, J. P., Gardner, P., &#38; Nielsen, R. (2007). Estimating the history of mutations on a phylogeny. In D. Liberles (Ed.), <i>Ancestral Sequence Reconstruction</i> (pp. 69–79). Oxford University Press. <a href=\"https://doi.org/10.1093/acprof:oso/9780199299188.003.0006\">https://doi.org/10.1093/acprof:oso/9780199299188.003.0006</a>","mla":"Bollback, Jonathan P., et al. “Estimating the History of Mutations on a Phylogeny.” <i>Ancestral Sequence Reconstruction</i>, edited by David Liberles, Oxford University Press, 2007, pp. 69–79, doi:<a href=\"https://doi.org/10.1093/acprof:oso/9780199299188.003.0006\">10.1093/acprof:oso/9780199299188.003.0006</a>.","ama":"Bollback JP, Gardner P, Nielsen R. Estimating the history of mutations on a phylogeny. In: Liberles D, ed. <i>Ancestral Sequence Reconstruction</i>. Oxford University Press; 2007:69-79. doi:<a href=\"https://doi.org/10.1093/acprof:oso/9780199299188.003.0006\">10.1093/acprof:oso/9780199299188.003.0006</a>","ieee":"J. P. Bollback, P. Gardner, and R. Nielsen, “Estimating the history of mutations on a phylogeny,” in <i>Ancestral Sequence Reconstruction</i>, D. Liberles, Ed. Oxford University Press, 2007, pp. 69–79.","short":"J.P. Bollback, P. Gardner, R. Nielsen, in:, D. Liberles (Ed.), Ancestral Sequence Reconstruction, Oxford University Press, 2007, pp. 69–79."},"month":"01","year":"2007","publist_id":"2968","abstract":[{"text":"Evolution has left its signature on the molecules and morphology of living organisms. Ancestral reconstruction offers an excellent tool for understanding the process of evolution using comparative information. Methods for ancestral reconstruction have generally focused on reconstructing the ancestral states at the internal nodes of a phylogeny. Often, we are not interested in particular nodes of the phylogeny but the whole history of a character. This chapter focuses on a Bayesian method for estimating these histories, or mutational paths, on phylogenies. Mutational path methods differ most notably from other approaches in their ability to estimate not only the ancestral states at the internal nodes of a phylogeny, but also the order and timing of mutational changes across the phylogeny. The chapter provides a concise introduction to the statistical tools needed for sampling mutational paths on a phylogeny.","lang":"eng"}],"page":"69 - 79","quality_controlled":0,"publication_status":"published","editor":[{"first_name":"David","full_name":"Liberles, David A","last_name":"Liberles"}],"title":"Estimating the history of mutations on a phylogeny","publisher":"Oxford University Press","doi":"10.1093/acprof:oso/9780199299188.003.0006","author":[{"first_name":"Jonathan P","orcid":"0000-0002-4624-4612","last_name":"Bollback","id":"2C6FA9CC-F248-11E8-B48F-1D18A9856A87","full_name":"Jonathan Bollback"},{"full_name":"Gardner, Paul P","last_name":"Gardner","first_name":"Paul"},{"full_name":"Nielsen, Rasmus","last_name":"Nielsen","first_name":"Rasmus"}],"day":"01","type":"book_chapter","date_created":"2018-12-11T12:03:18Z","date_updated":"2021-01-12T07:43:26Z","_id":"3432"},{"publication_status":"published","quality_controlled":0,"abstract":[{"text":"he potential for di? erences between genetic paternity and paternity inferred from behavioral observation has long been recognized. These di? erences are associated with the challenge for females of seeking both genetic and material bene? ts; this challenge is less severe in species with polygynous, non-resource-based mating systems (such as leks) than in those with resource-based systems. We pres- ent the ? rst study of paternity patt erns in a non-resource-based species that does not form true leks. We compared paternity inferred from observed mating behavior to genetically assigned paternity in the Satin Bowerbird (Ptilonorhynchus violaceus) using eight microsatellite markers. Mating behavior was observed and recorded via automated video-cameras positioned at all bowers (29?34 bowers each year) in the study site throughout each mating season. We obtained blood samples and identi- ? ed mothers for 11 chicks in 9 nests. For all chicks, the most likely genetic father had been observed to mate with the mother in the year the chick was sampled. All most likely genetic fathers were assigned with high con? dence and all were bower- holding males. These results demonstrate that genetic paternity can be inferred from observed mating behavior with reasonable con? dence in Satin Bowerbirds. Observed male mating-success is therefore a reliable predictor of reproductive success, and this suggests that high skew in observed male mating-success translates directly to high skew in reproductive success. ","lang":"eng"}],"intvolume":"       124","page":"857 - 867","type":"journal_article","date_created":"2018-12-11T12:03:19Z","date_updated":"2021-01-12T07:43:27Z","volume":124,"_id":"3436","title":"Behavioral paternity predicts genetic paternity in satin bowerbirds, a species with a non-resource-based mating system","publisher":"University of California Press","author":[{"first_name":"Sheila","last_name":"Reynolds","full_name":"Reynolds, Sheila M"},{"first_name":"Katie","full_name":"Dryer, Katie","last_name":"Dryer"},{"full_name":"Jonathan Bollback","id":"2C6FA9CC-F248-11E8-B48F-1D18A9856A87","last_name":"Bollback","first_name":"Jonathan P","orcid":"0000-0002-4624-4612"},{"first_name":"J Albert","full_name":"Uy, J Albert","last_name":"Uy"},{"first_name":"Gail","full_name":"Patricelli, Gail L","last_name":"Patricelli"},{"full_name":"Robson, Timothy","last_name":"Robson","first_name":"Timothy"},{"first_name":"Gerald","last_name":"Borgia","full_name":"Borgia, Gerald"},{"full_name":"Braun, Michael J","last_name":"Braun","first_name":"Michael"}],"doi":"10.1642/0004-8038(2007)124[857:BPPGPI]2.0.CO;2","day":"01","date_published":"2007-01-01T00:00:00Z","issue":"3","citation":{"chicago":"Reynolds, Sheila, Katie Dryer, Jonathan P Bollback, J Albert Uy, Gail Patricelli, Timothy Robson, Gerald Borgia, and Michael Braun. “Behavioral Paternity Predicts Genetic Paternity in Satin Bowerbirds, a Species with a Non-Resource-Based Mating System.” <i>The Auk</i>. University of California Press, 2007. <a href=\"https://doi.org/10.1642/0004-8038(2007)124[857:BPPGPI]2.0.CO;2\">https://doi.org/10.1642/0004-8038(2007)124[857:BPPGPI]2.0.CO;2</a>.","ista":"Reynolds S, Dryer K, Bollback JP, Uy JA, Patricelli G, Robson T, Borgia G, Braun M. 2007. Behavioral paternity predicts genetic paternity in satin bowerbirds, a species with a non-resource-based mating system. The Auk. 124(3), 857–867.","apa":"Reynolds, S., Dryer, K., Bollback, J. P., Uy, J. A., Patricelli, G., Robson, T., … Braun, M. (2007). Behavioral paternity predicts genetic paternity in satin bowerbirds, a species with a non-resource-based mating system. <i>The Auk</i>. University of California Press. <a href=\"https://doi.org/10.1642/0004-8038(2007)124[857:BPPGPI]2.0.CO;2\">https://doi.org/10.1642/0004-8038(2007)124[857:BPPGPI]2.0.CO;2</a>","mla":"Reynolds, Sheila, et al. “Behavioral Paternity Predicts Genetic Paternity in Satin Bowerbirds, a Species with a Non-Resource-Based Mating System.” <i>The Auk</i>, vol. 124, no. 3, University of California Press, 2007, pp. 857–67, doi:<a href=\"https://doi.org/10.1642/0004-8038(2007)124[857:BPPGPI]2.0.CO;2\">10.1642/0004-8038(2007)124[857:BPPGPI]2.0.CO;2</a>.","ama":"Reynolds S, Dryer K, Bollback JP, et al. Behavioral paternity predicts genetic paternity in satin bowerbirds, a species with a non-resource-based mating system. <i>The Auk</i>. 2007;124(3):857-867. doi:<a href=\"https://doi.org/10.1642/0004-8038(2007)124[857:BPPGPI]2.0.CO;2\">10.1642/0004-8038(2007)124[857:BPPGPI]2.0.CO;2</a>","ieee":"S. Reynolds <i>et al.</i>, “Behavioral paternity predicts genetic paternity in satin bowerbirds, a species with a non-resource-based mating system,” <i>The Auk</i>, vol. 124, no. 3. University of California Press, pp. 857–867, 2007.","short":"S. Reynolds, K. Dryer, J.P. Bollback, J.A. Uy, G. Patricelli, T. Robson, G. Borgia, M. Braun, The Auk 124 (2007) 857–867."},"status":"public","publication":"The Auk","extern":1,"publist_id":"2964","month":"01","year":"2007"}]