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dc.contributor.authorCao, Chuanen
dc.contributor.authorMagwire, Michael Men
dc.contributor.authorBayer, Florianen
dc.contributor.authorJiggins, Francisen
dc.date.accessioned2016-01-08T16:19:52Z
dc.date.available2016-01-08T16:19:52Z
dc.date.issued2016-01-22en
dc.identifier.citationPLOS Pathogens 2016.en
dc.identifier.issn1553-7366
dc.identifier.urihttps://www.repository.cam.ac.uk/handle/1810/253177
dc.description.abstractHosts encounter an ever-changing array of pathogens, so there is continual selection for novel ways to resist infection. A powerful way to understand how hosts evolve resistance is to identify the genes that cause variation in susceptibility to infection. Using high-resolution genetic mapping we have identified a naturally occurring polymorphism in a gene called Ge-1 that makes Drosophila melanogaster highly resistant to its natural pathogen Drosophila melanogaster sigma virus (DMelSV). By modifying the sequence of the gene in transgenic flies, we identified a 26 amino acid deletion in the serine-rich linker region of Ge-1 that is causing the resistance. Knocking down the expression of the susceptible allele leads to a decrease in viral titre in infected flies, indicating that Ge-1 is an existing restriction factor whose antiviral effects have been increased by the deletion. Ge-1 plays a central role in RNA degradation and the formation of processing bodies (P bodies). A key effector in antiviral immunity, the RNAi induced silencing complex (RISC), localises to P bodies, but we found that Ge-1-based resistance is not dependent on the small interfering RNA (siRNA) pathway. However, we found that Decapping protein 1 (DCP1) protects flies against sigma virus. This protein interacts with Ge-1 and commits mRNA for degradation by removing the 5’ cap, suggesting that resistance may rely on this RNA degradation pathway. The serine-rich linker domain of Ge-1 has experienced strong selection during the evolution of Drosophila, suggesting that this gene may be under long-term selection by viruses. These findings demonstrate that studying naturally occurring polymorphisms that increase resistance to infections enables us to identify novel forms of antiviral defence, and support a pattern of major effect polymorphisms controlling resistance to viruses in Drosophila
dc.languageEnglishen
dc.language.isoenen
dc.publisherPLOS
dc.rightsAttribution 2.0 UK: England & Wales*
dc.rights.urihttp://creativecommons.org/licenses/by/2.0/uk/*
dc.titleA Polymorphism in the processing body component Ge-1 Controls Resistance to a Rhabdovirus in Drosophilaen
dc.typeArticle
dc.description.versionThis is the final version of the article. It first appeared from PLOS via http://dx.doi.org/10.1371/journal.ppat.1005387en
prism.numbere1005387en
prism.publicationDate2016en
prism.publicationNamePLOS Pathogensen
prism.volume12en
dcterms.dateAccepted2015-12-17en
rioxxterms.versionofrecord10.1371/journal.ppat.1005387en
rioxxterms.licenseref.urihttp://www.rioxx.net/licenses/all-rights-reserveden
rioxxterms.licenseref.startdate2016-01-22en
dc.contributor.orcidJiggins, Francis [0000-0001-7470-8157]
dc.identifier.eissn1553-7374
rioxxterms.typeJournal Article/Reviewen
pubs.funder-project-idEuropean Research Council (281668)
pubs.funder-project-idWellcome Trust (081279/B/06/Z)
cam.orpheus.successThu Jan 30 12:55:26 GMT 2020 - The item has an open VoR version.*
rioxxterms.freetoread.startdate2100-01-01


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Attribution 2.0 UK: England & Wales
Except where otherwise noted, this item's licence is described as Attribution 2.0 UK: England & Wales