Journal
SCIENTIFIC REPORTS
Volume 9, Issue -, Pages -Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/s41598-018-38000-9
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Funding
- European Research Council [ERC-2010-StG 260906-D-END]
- Mairie de Paris (Programme Emergences)
- Fondation de la Recherche Medicale (equipe labellisee)
- French National Research Agency (ANR) as part of the Investissements d'Avenir Program (LabEx Dynamo) [ANR-11-LABX-0011-01, ANR-16-CE12-0026]
- CancerTelSys in the E: med program of the German Federal Ministry of Education and Research (BMBF) [01ZX1302]
- Hartmut Hoffmann-Berling International Graduate School PhD fellowship
- Lebanese National Council for Scientific Research
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In eukaryotes, telomeres determine cell proliferation potential by triggering replicative senescence in the absence of telomerase. In Saccharomyces cerevisiae, senescence is mainly dictated by the first telomere that reaches a critically short length, activating a DNA-damage-like response. How the corresponding signaling is modulated by the telomeric structure and context is largely unknown. Here we investigated how subtelomeric elements of the shortest telomere in a telomerase-negative cell influence the onset of senescence. We found that a 15 kb truncation of the 7L subtelomere widely used in studies of telomere biology affects cell growth when combined with telomerase inactivation. This effect is likely not explained by (i) elimination of sequence homology at chromosome ends that would compromise homology-directed DNA repair mechanisms; (ii) elimination of the conserved subtelomeric X-element; (iii) elimination of a gene that would become essential in the absence of telomerase; and (iv) heterochromatinization of inner genes, causing the silencing of an essential gene in replicative senescent cells. This works contributes to better delineate subtelomere functions and their impact on telomere biology.
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