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dc.contributor.authorGjuvsland, Arne Bjørke
dc.contributor.authorZörgö, Enikö Beatrix
dc.contributor.authorAntony Samy, Jeevan Karloss
dc.contributor.authorStenberg, Simon
dc.contributor.authorDemirsoy, Ibrahim H
dc.contributor.authorRoque, Francisco
dc.contributor.authorMaciaszczyk-Dziubinska, Ewa
dc.contributor.authorMigocka, Magdalena
dc.contributor.authorAlonso-Perez, Elisa
dc.contributor.authorZackrisson, Martin
dc.contributor.authorWysocki, Robert
dc.contributor.authorTamas, Markus J
dc.contributor.authorJonassen, Inge
dc.contributor.authorOmholt, Stig William
dc.contributor.authorWarringer, Jonas
dc.PublishedGjuvsland AB, Zörgö EB, Antony Samy SJK, Stenberg S, Demirsoy, Roque F, Maciaszczyk-Dziubinska, Migocka, Alonso-Perez, Zackrisson M, Wysocki, Tamas, Jonassen I, Omholt SW, Warringer J. Disentangling genetic and epigenetic determinants of ultrafast adaptation. Molecular Systems Biology. 2016;12:892eng
dc.description.abstractA major rationale for the advocacy of epigenetically mediated adaptive responses is that they facilitate faster adaptation to environmental challenges. This motivated us to develop a theoretical–experimental framework for disclosing the presence of such adaptation‐speeding mechanisms in an experimental evolution setting circumventing the need for pursuing costly mutation–accumulation experiments. To this end, we exposed clonal populations of budding yeast to a whole range of stressors. By growth phenotyping, we found that almost complete adaptation to arsenic emerged after a few mitotic cell divisions without involving any phenotypic plasticity. Causative mutations were identified by deep sequencing of the arsenic‐adapted populations and reconstructed for validation. Mutation effects on growth phenotypes, and the associated mutational target sizes were quantified and embedded in data‐driven individual‐based evolutionary population models. We found that the experimentally observed homogeneity of adaptation speed and heterogeneity of molecular solutions could only be accounted for if the mutation rate had been near estimates of the basal mutation rate. The ultrafast adaptation could be fully explained by extensive positive pleiotropy such that all beneficial mutations dramatically enhanced multiple fitness components in concert. As our approach can be exploited across a range of model organisms exposed to a variety of environmental challenges, it may be used for determining the importance of epigenetic adaptation‐speeding mechanisms in general.en_US
dc.publisherEMBO Pressen_US
dc.rightsAttribution CC BYeng
dc.subjectpopulation geneticseng
dc.titleDisentangling genetic and epigenetic determinants of ultrafast adaptationen_US
dc.typePeer reviewed
dc.typeJournal article
dc.rights.holderCopyright 2016 The Author(s)en_US
dc.source.journalMolecular Systems Biology
dc.relation.projectNorges forskningsråd: 222364
dc.relation.projectNotur/NorStore: NN4653K
dc.relation.projectNorges forskningsråd: 223257

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