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dc.contributor.authorPrikrylova, Terezia
dc.contributor.authorRobertson, Julia
dc.contributor.authorFerrucci, Francesca
dc.contributor.authorKonorska, Dorota Joanna
dc.contributor.authorAanes, Håvard
dc.contributor.authorManaf, Adeel
dc.contributor.authorZhang, Beibei
dc.contributor.authorVågbø, Cathrine Broberg
dc.contributor.authorKusnierczyk, Anna
dc.contributor.authorGilljam, Karin Margaretha
dc.contributor.authorLøvkvam-Køster, Caroline
dc.contributor.authorOtterlei, Marit
dc.contributor.authorDahl, John Arne
dc.contributor.authorEnserink, Jorrit
dc.contributor.authorKlungland, Arne
dc.contributor.authorRobertson, Adam Brian
dc.identifier.citationScientific Reports. 2019, 9:11065 1-16.nb_NO
dc.description.abstractIn most mammalian cells, DNA replication occurs once, and only once between cell divisions. Replication initiation is a highly regulated process with redundant mechanisms that prevent errant initiation events. In lower eukaryotes, replication is initiated from a defined consensus sequence, whereas a consensus sequence delineating mammalian origin of replication has not been identified. Here we show that 5-hydroxymethylcytosine (5hmC) is present at mammalian replication origins. Our data support the hypothesis that 5hmC has a role in cell cycle regulation. We show that 5hmC level is inversely proportional to proliferation; indeed, 5hmC negatively influences cell division by increasing the time a cell resides in G1. Our data suggest that 5hmC recruits replication-licensing factors, then is removed prior to or during origin firing. Later we propose that TET2, the enzyme catalyzing 5mC to 5hmC conversion, acts as barrier to rereplication. In a broader context, our results significantly advance the understating of 5hmC involvement in cell proliferation and disease states.nb_NO
dc.publisherNature Researchnb_NO
dc.rightsNavngivelse 4.0 Internasjonal*
dc.title5-hydroxymethylcytosine marks mammalian origins acting as a barrier to replicationnb_NO
dc.typeJournal articlenb_NO
dc.typePeer reviewednb_NO
dc.source.journalScientific Reportsnb_NO
dc.description.localcode© The Author(s) 2019. This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (
cristin.unitnameInstitutt for klinisk og molekylær medisin

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Navngivelse 4.0 Internasjonal
Except where otherwise noted, this item's license is described as Navngivelse 4.0 Internasjonal