Gutenberg Open Science: Chromatin modifiers and recombination factors promote a telomere fold-back structure, that is lost during replicative senescence

Please use this identifier to cite or link to this item: http://doi.org/10.25358/openscience-6495

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DC Field	Value	Language
dc.contributor.author	Wagner, Tina	-
dc.contributor.author	Pérez-Martínez, Lara	-
dc.contributor.author	Schellhaas, René	-
dc.contributor.author	Barrientos-Moreno, Marta	-
dc.contributor.author	Öztürk, Merve	-
dc.contributor.author	Prado, Félix	-
dc.contributor.author	Butter, Falk	-
dc.contributor.author	Luke, Brian	-
dc.date.accessioned	2021-11-12T12:03:46Z	-
dc.date.available	2021-11-12T12:03:46Z	-
dc.date.issued	2021	-
dc.identifier.uri	https://openscience.ub.uni-mainz.de/handle/20.500.12030/6505	-
dc.description.abstract	Telomeres 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.sponsorship	Open Access-Publizieren Universität Mainz / Universitätsmedizin Mainz	de
dc.language.iso	eng	de
dc.rights	CC BY	*
dc.rights.uri	https://creativecommons.org/licenses/by/4.0/	*
dc.subject.ddc	570 Biowissenschaften	de_DE
dc.subject.ddc	570 Life sciences	en_GB
dc.title	Chromatin modifiers and recombination factors promote a telomere fold-back structure, that is lost during replicative senescence	en_GB
dc.type	Zeitschriftenaufsatz	de
dc.identifier.doi	http://doi.org/10.25358/openscience-6495	-
jgu.type.dinitype	article	en_GB
jgu.type.version	Published version	de
jgu.type.resource	Text	de
jgu.organisation.department	FB 10 Biologie	de
jgu.organisation.number	7970	-
jgu.organisation.name	Johannes Gutenberg-Universität Mainz	-
jgu.rights.accessrights	openAccess	-
jgu.journal.title	PLoS Genetics	de
jgu.journal.volume	16	de
jgu.journal.issue	12	de
jgu.pages.alternative	e1008603	de
jgu.publisher.year	2021	-
jgu.publisher.name	Public Library of Science	de
jgu.publisher.place	San Francisco, Calif.	de
jgu.publisher.uri	https://doi.org/10.1371/journal.pgen.1008603	de
jgu.publisher.issn	1553-7404	de
jgu.organisation.place	Mainz	-
jgu.subject.ddccode	570	de
jgu.publisher.doi	10.1371/journal.pgen.1008603
jgu.organisation.ror	https://ror.org/023b0x485
Appears in collections:	JGU-Publikationen

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