dc.contributor.author | Landsberger, M | |
dc.contributor.author | Gandon, S | |
dc.contributor.author | Meaden, S | |
dc.contributor.author | Rollie, C | |
dc.contributor.author | Chevallereau, A | |
dc.contributor.author | Chabas, H | |
dc.contributor.author | Buckling, A | |
dc.contributor.author | Westra, ER | |
dc.contributor.author | van Houte, S | |
dc.date.accessioned | 2018-09-28T14:13:26Z | |
dc.date.issued | 2018-07-19 | |
dc.description.abstract | Some phages encode anti-CRISPR (acr) genes, which antagonize bacterial CRISPR-Cas immune systems by binding components of its machinery, but it is less clear how deployment of these acr genes impacts phage replication and epidemiology. Here, we demonstrate that bacteria with CRISPR-Cas resistance are still partially immune to Acr-encoding phage. As a consequence, Acr-phages often need to cooperate in order to overcome CRISPR resistance, with a first phage blocking the host CRISPR-Cas immune system to allow a second Acr-phage to successfully replicate. This cooperation leads to epidemiological tipping points in which the initial density of Acr-phage tips the balance from phage extinction to a phage epidemic. Furthermore, both higher levels of CRISPR-Cas immunity and weaker Acr activities shift the tipping points toward higher initial phage densities. Collectively, these data help elucidate how interactions between phage-encoded immune suppressors and the CRISPR systems they target shape bacteria-phage population dynamics. | en_GB |
dc.description.sponsorship | M.L. was supported by funding from the Wellcome Trust (https://wellcome.ac.uk) (109776/Z/15/Z), which was awarded to E.R.W. E.R.W. further acknowledges the Natural Environment Research Council (https://nerc.ukri.org) (NE/M018350/1), the BBSRC (BB/N017412/1), and the European Research Council (https://erc.europa.eu) (ERC-STG-2016-714478 - EVOIMMECH) for funding. S.v.H. acknowledges funding from the People Programme (Marie Curie Actions; https://ec.europa.eu/research/mariecurieactions/) of the European Union’s Horizon 2020 (REA grant agreement no. 660039) and from the BBSRC (BB/R010781/1). S.G. acknowledges funding (Visiting Professorship) from the Leverhulme Trust. A.B. acknowledges funding from the Royal Society. The authors thank Olivier Fradet for experimental contributions and Adair Borges and Joe Bondy-Denomy (UCSF) for providing DMS3mvir-AcrIF4 and phage JBD26. | en_GB |
dc.identifier.citation | Vol. 174 (4), pp. 908 - 916.e12 | en_GB |
dc.identifier.doi | 10.1016/j.cell.2018.05.058 | |
dc.identifier.uri | http://hdl.handle.net/10871/34137 | |
dc.language.iso | en | en_GB |
dc.publisher | Elsevier (Cell Press) | en_GB |
dc.relation.url | https://www.ncbi.nlm.nih.gov/pubmed/30033365 | en_GB |
dc.rights | © 2018 The Author(s). Published by Elsevier Inc. This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/). | en_GB |
dc.subject | Allee effect | en_GB |
dc.subject | CRISPR-Cas | en_GB |
dc.subject | anti-CRISPR | en_GB |
dc.subject | bacteria | en_GB |
dc.subject | bifurcation | en_GB |
dc.subject | epidemiology | en_GB |
dc.subject | immunosuppression | en_GB |
dc.subject | partial resistance | en_GB |
dc.subject | phage | en_GB |
dc.subject | tipping points | en_GB |
dc.title | Anti-CRISPR Phages Cooperate to Overcome CRISPR-Cas Immunity | en_GB |
dc.type | Article | en_GB |
dc.date.available | 2018-09-28T14:13:26Z | |
exeter.place-of-publication | United States | en_GB |
dc.description | This is the final version of the article. Available from Elsevier via the DOI in this record. | en_GB |
dc.identifier.journal | Cell | en_GB |