Please use this identifier to cite or link to this item: http://doi.org/10.25358/openscience-6495
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dc.contributor.authorWagner, Tina-
dc.contributor.authorPérez-Martínez, Lara-
dc.contributor.authorSchellhaas, René-
dc.contributor.authorBarrientos-Moreno, Marta-
dc.contributor.authorÖztürk, Merve-
dc.contributor.authorPrado, Félix-
dc.contributor.authorButter, Falk-
dc.contributor.authorLuke, Brian-
dc.date.accessioned2021-11-12T12:03:46Z-
dc.date.available2021-11-12T12:03:46Z-
dc.date.issued2021-
dc.identifier.urihttps://openscience.ub.uni-mainz.de/handle/20.500.12030/6505-
dc.description.abstractTelomeres have the ability to adopt a lariat conformation and hence, engage in long and short distance intra-chromosome interactions. Budding yeast telomeres were proposed to fold back into subtelomeric regions, but a robust assay to quantitatively characterize this structure has been lacking. Therefore, it is not well understood how the interactions between telomeres and non-telomeric regions are established and regulated. We employ a telomere chromosome conformation capture (Telo-3C) approach to directly analyze telomere folding and its maintenance in S. cerevisiae. We identify the histone modifiers Sir2, Sin3 and Set2 as critical regulators for telomere folding, which suggests that a distinct telomeric chromatin environment is a major requirement for the folding of yeast telomeres. We demonstrate that telomeres are not folded when cells enter replicative senescence, which occurs independently of short telomere length. Indeed, Sir2, Sin3 and Set2 protein levels are decreased during senescence and their absence may thereby prevent telomere folding. Additionally, we show that the homologous recombination machinery, including the Rad51 and Rad52 proteins, as well as the checkpoint component Rad53 are essential for establishing the telomere fold-back structure. This study outlines a method to interrogate telomere-subtelomere interactions at a single unmodified yeast telomere. Using this method, we provide insights into how the spatial arrangement of the chromosome end structure is established and demonstrate that telomere folding is compromised throughout replicative senescence.en_GB
dc.description.sponsorshipOpen Access-Publizieren Universität Mainz / Universitätsmedizin Mainzde
dc.language.isoengde
dc.rightsCC BY*
dc.rights.urihttps://creativecommons.org/licenses/by/4.0/*
dc.subject.ddc570 Biowissenschaftende_DE
dc.subject.ddc570 Life sciencesen_GB
dc.titleChromatin modifiers and recombination factors promote a telomere fold-back structure, that is lost during replicative senescenceen_GB
dc.typeZeitschriftenaufsatzde
dc.identifier.doihttp://doi.org/10.25358/openscience-6495-
jgu.type.dinitypearticleen_GB
jgu.type.versionPublished versionde
jgu.type.resourceTextde
jgu.organisation.departmentFB 10 Biologiede
jgu.organisation.number7970-
jgu.organisation.nameJohannes Gutenberg-Universität Mainz-
jgu.rights.accessrightsopenAccess-
jgu.journal.titlePLoS Geneticsde
jgu.journal.volume16de
jgu.journal.issue12de
jgu.pages.alternativee1008603de
jgu.publisher.year2021-
jgu.publisher.namePublic Library of Sciencede
jgu.publisher.placeSan Francisco, Calif.de
jgu.publisher.urihttps://doi.org/10.1371/journal.pgen.1008603de
jgu.publisher.issn1553-7404de
jgu.organisation.placeMainz-
jgu.subject.ddccode570de
jgu.publisher.doi10.1371/journal.pgen.1008603
Appears in collections:JGU-Publikationen

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