Marked Variability in the Extent of Protein Disorder within and between Viral Families

DC FieldValueLanguage
dc.contributor.authorPushker, Ravindra-
dc.contributor.authorMooney, Catherine-
dc.contributor.authorDavey, Norman E.-
dc.contributor.authorJacqué, Jean-Marc-
dc.contributor.authorShields, Denis C.-
dc.contributor.editorSticht, Heinrich-
dc.date.accessioned2019-04-23T10:37:50Z-
dc.date.available2019-04-23T10:37:50Z-
dc.date.copyright2013 the Authorsen_US
dc.date.issued2013-04-19-
dc.identifier.citationPLoS ONEen_US
dc.identifier.issn1932-6203-
dc.identifier.urihttp://hdl.handle.net/10197/10072-
dc.description.abstractIntrinsically disordered regions in eukaryotic proteomes contain key signaling and regulatory modules and mediate interactions with many proteins. Many viral proteomes encode disordered proteins and modulate host factors through the use of short linear motifs (SLiMs) embedded within disordered regions. However, the degree of viral protein disorder across different viruses is not well understood, so we set out to establish the constraints acting on viruses, in terms of their use of disordered protein regions. We surveyed predicted disorder across 2,278 available viral genomes in 41 families, and correlated the extent of disorder with genome size and other factors. Protein disorder varies strikingly between viral families (from 2.9% to 23.1% of residues), and also within families. However, this substantial variation did not follow the established trend among their hosts, with increasing disorder seen across eubacterial, archaebacterial, protists, and multicellular eukaryotes. For example, among large mammalian viruses, poxviruses and herpesviruses showed markedly differing disorder (5.6% and 17.9%, respectively). Viral families with smaller genome sizes have more disorder within each of five main viral types (ssDNA, dsDNA, ssRNA+, dsRNA, retroviruses), except for negative single-stranded RNA viruses, where disorder increased with genome size. However, surveying over all viruses, which compares tiny and enormous viruses over a much bigger range of genome sizes, there is no strong association of genome size with protein disorder. We conclude that there is extensive variation in the disorder content of viral proteomes. While a proportion of this may relate to base composition, to extent of gene overlap, and to genome size within viral types, there remain important additional family and virus-specific effects. Differing disorder strategies are likely to impact on how different viruses modulate host factors, and on how rapidly viruses can evolve novel instances of SLiMs subverting host functions, such as innate and acquired immunity.en_US
dc.description.sponsorshipScience Foundation Irelanden_US
dc.format.mediumElectronic-Print-
dc.language.isoenen_US
dc.publisherPLoSen_US
dc.rightsThis is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.en_US
dc.subjectEukaryotic proteomesen_US
dc.subjectDisordered proteinsen_US
dc.subjectShort linear motifs (SLiMs)en_US
dc.subjectViral protein disorderen_US
dc.subjectVirusesen_US
dc.subjectGenome sizeen_US
dc.subjectViral proteomesen_US
dc.subjectImmunityen_US
dc.titleMarked Variability in the Extent of Protein Disorder within and between Viral Familiesen_US
dc.typeJournal Articleen_US
dc.internal.authorcontactothercatherine.mooney@ucd.ieen_US
dc.statusPeer revieweden_US
dc.identifier.volume8en_US
dc.identifier.issue4en_US
dc.identifier.startpagee60724en_US
dc.identifier.doi10.1371/journal.pone.0060724-
dc.neeo.contributorPushker|Ravindra|aut|-
dc.neeo.contributorMooney|Catherine|aut|-
dc.neeo.contributorDavey|Norman E.|aut|-
dc.neeo.contributorJacqué|Jean-Marc|aut|-
dc.neeo.contributorShields|Denis C.|aut|-
dc.neeo.contributorSticht|Heinrich|edt|-
dc.date.updated2018-07-21T22:33:48Z-
dc.identifier.grantid8/IN.1/B1864-
item.fulltextWith Fulltext-
item.grantfulltextopen-
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