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dc.contributor.authorErdmann, Susanneeng
dc.contributor.authorLe Moine Bauer, Sveneng
dc.contributor.authorGarrett, Roger A.eng
dc.description.abstractInfection of Sulfolobus islandicus REY15A with mixtures of different Sulfolobus viruses, including STSV2, did not induce spacer acquisition by the host CRISPR immune system. However, coinfection with the tailed fusiform viruses SMV1 and STSV2 generated hyperactive spacer acquisition in both CRISPR loci, exclusively from STSV2, with the resultant loss of STSV2 but not SMV1. SMV1 was shown to activate adaptation while itself being resistant to CRISPR-mediated adaptation and DNA interference. Exceptionally, a single clone S-1 isolated from an SMV1 + STSV2-infected culture, that carried STSV2-specific spacers and had lost STSV2 but not SMV1, acquired spacers from SMV1. This effect was also reproducible on reinfecting wild-type host cells with a variant SMV1 isolated from the S-1 culture. The SMV1 variant lacked a virion protein ORF114 that was shown to bind DNA. This study also provided evidence for: (i) limits on the maximum sizes of CRISPR loci; (ii) spacer uptake strongly retarding growth of infected cultures; (iii) protospacer selection being essentially random and non-directional, and (iv) the reversible uptake of spacers from STSV2 and SMV1. A hypothesis is presented to explain the interactive conflicts between SMV1 and the host CRISPR immune system.en_US
dc.publisherJohn Wiley & Sons Ltd.en_US
dc.rightsAttribution-NonCommercial-NoDerivs CC BY-NC-NDeng
dc.titleInter-viral conflicts that exploit host CRISPR immune systems of Sulfolobusen_US
dc.typePeer reviewed
dc.typeJournal article
dc.rights.holderCopyright 2013 The Authors. Molecular Microbiology published by John Wiley & Sons Ltd. This is an open access article under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.en_US
dc.source.journalMolecular Microbiology
dc.subject.nsiVDP::Mathematics and natural scienses: 400::Basic biosciences: 470::General immunology: 478en_US
dc.subject.nsiVDP::Matematikk og naturvitenskap: 400::Basale biofag: 470::Generell immunologi: 478nob

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