RT Journal Article
T1 Chromatin modifiers and recombination factors promote a telomere fold-back structure, that is lost during replicative senescence
A1 Wagner, Tina
A1 Pérez-Martínez, Lara
A1 Schellhaas, René
A1 Barrientos-Moreno, Marta
A1 Öztürk, Merve
A1 Prado, Félix
A1 Butter, Falk
A1 Luke, Brian
K1 Chromatin
K1 Telomere
K1 Chromosomes
K1 Saccharomyces cerevisiae
K1 DNA Damage
K1 Cellular Senescence
K1 Rad52 DNA Repair and Recombination Protein
K1 Cromatina
K1 Telómero
K1 Cromosomas
K1 Daño del ADN
K1 Senescencia celular
K1 Proteína recombinante y reparadora de ADN Rad52
AB 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.
PB Public Library of Science
YR 2020
FD 2020-12-28
LK http://hdl.handle.net/10668/3774
UL http://hdl.handle.net/10668/3774
LA en
NO Wagner T, Pérez-Martínez L, Schellhaas R, Barrientos-Moreno M, Öztürk M, Prado F, et al. Chromatin modifiers and recombination factors promote a telomere fold-back structure, that is lost during replicative senescence. PLoS Genet. 2020 Dec 28;16(12):e1008603
DS RISalud
RD Apr 18, 2025