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dc.contributor.authorHalfmann, Randal Arthur
dc.contributor.authorJarosz, Daniel F.
dc.contributor.authorJones, Sandra K.
dc.contributor.authorChang, Amelia
dc.contributor.authorLancaster, Alex K.
dc.contributor.authorLindquist, Susan
dc.date.accessioned2014-02-14T16:18:34Z
dc.date.available2014-02-14T16:18:34Z
dc.date.issued2012-02
dc.identifier.issn0028-0836
dc.identifier.issn1476-4687
dc.identifier.urihttp://hdl.handle.net/1721.1/84950
dc.description.abstractThe self-templating conformations of yeast prion proteins act as epigenetic elements of inheritance. Yeast prions might provide a mechanism for generating heritable phenotypic diversity that promotes survival in fluctuating environments and the evolution of new traits. However, this hypothesis is highly controversial. Prions that create new traits have not been found in wild strains, leading to the perception that they are rare ‘diseases’ of laboratory cultivation. Here we biochemically test approximately 700 wild strains of Saccharomyces for [PSI+] or [MOT3+], and find these prions in many. They conferred diverse phenotypes that were frequently beneficial under selective conditions. Simple meiotic re-assortment of the variation harboured within a strain readily fixed one such trait, making it robust and prion-independent. Finally, we genetically screened for unknown prion elements. Fully one-third of wild strains harboured them. These, too, created diverse, often beneficial phenotypes. Thus, prions broadly govern heritable traits in nature, in a manner that could profoundly expand adaptive opportunities.en_US
dc.description.sponsorshipHoward Hughes Medical Institute (Investigator)en_US
dc.description.sponsorshipG. Harold and Leila Y. Mathers Foundationen_US
dc.description.sponsorshipDamon Runyon Cancer Research Foundation (HHMI fellow, DRG-1964-08)en_US
dc.description.sponsorshipNational Institutes of Health (U.S.) (NIH Pathway to independence award (K99 GM098600))en_US
dc.description.sponsorshipHoward Hughes Medical Institute (Exceptional Research Opportunities Program (EXROP))en_US
dc.language.isoen_US
dc.publisherNature Publishing Groupen_US
dc.relation.isversionofhttp://dx.doi.org/10.1038/nature10875en_US
dc.rightsArticle is made available in accordance with the publisher's policy and may be subject to US copyright law. Please refer to the publisher's site for terms of use.en_US
dc.rights.urien_US
dc.sourcePMCen_US
dc.titlePrions are a common mechanism for phenotypic inheritance in wild yeastsen_US
dc.typeArticleen_US
dc.identifier.citationHalfmann, Randal, Daniel F. Jarosz, Sandra K. Jones, Amelia Chang, Alex K. Lancaster, and Susan Lindquist. “Prions are a common mechanism for phenotypic inheritance in wild yeasts.” Nature 482, no. 7385 (February 15, 2012): 363-368.en_US
dc.contributor.departmentMassachusetts Institute of Technology. Department of Biologyen_US
dc.contributor.departmentWhitehead Institute for Biomedical Researchen_US
dc.contributor.mitauthorHalfmann, Randal Arthuren_US
dc.contributor.mitauthorJarosz, Daniel F.en_US
dc.contributor.mitauthorJones, Sandra K.en_US
dc.contributor.mitauthorChang, Ameliaen_US
dc.contributor.mitauthorLancaster, Alex K.en_US
dc.contributor.mitauthorLindquist, Susanen_US
dc.relation.journalNatureen_US
dc.eprint.versionAuthor's final manuscripten_US
dc.type.urihttp://purl.org/eprint/type/JournalArticleen_US
eprint.statushttp://purl.org/eprint/status/PeerRevieweden_US
dspace.orderedauthorsHalfmann, Randal; Jarosz, Daniel F.; Jones, Sandra K.; Chang, Amelia; Lancaster, Alex K.; Lindquist, Susanen_US
dc.identifier.orcidhttps://orcid.org/0000-0003-1307-882X
dspace.mitauthor.errortrue
mit.licensePUBLISHER_POLICYen_US
mit.metadata.statusComplete


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