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Rearrangement of eroded telomeres in quiescent fission yeast cells

Lundi 26 septembre 2016 14:00 - Duree : 1 heure
Lieu : Amphithéâtre Serge Kampf, Grenoble Institut des Neurosciences (GIN) - Bât. Edmond J. Safra, Chemin Fortune Ferrini CHU, La Tronche

Orateur : Vincent GELI (Aix Marseille Université, Institut Paoli-Calmettes)

Telomere length is highly variable between tissues and organs and inversely related to chronological age. While the mechanisms of telomere maintenance have been investigated in dividing cells, little is known about the stability of telomeres in quiescent cells and how dysfunctional telomeres are processed in non-proliferating cells. To tackle this issue we examined the stability of telomeres in quiescent cells using fission yeast cells that can be maintained for weeks in quiescence by nitrogen starvation. We have investigated how eroded telomeres are processed during quiescence and the fate of quiescent cells harboring these short telomeres. By deleting the RNA component of telomerase, we have first monitored the progressive telomere shortening after successive divisions. Then cells with short telomeres were placed under conditions in which they enter into quiescence. While WT telomeres are stable in quiescence, strikingly we observed that short telomeres were highly rearranged. We have determined that these rearrangements depended on homologous recombination and corresponded to the expansion of subtelomeric regions (named STEEx). We have identified an homologous sequence of 226 bp within subtelomeric regions that might be used as a seed to promote recombination. We have further monitored the impact of STEEx on cell mortality during quiescence and at the exit of quiescence. We first observed that the mortality of cells in the absence of telomerase is correlated with the shortening of telomeres and the time spent in quiescence. Second, STEEx were not maintained when cells exit quiescence to re-enter into the cell cycle. We thus describe in fission yeast a new mode of telomere maintenance in the absence of telomerase that is promoted in quiescence. This discovery highlights how non-dividing cells that harbor eroded telomeres may circumvent the lack of a functional telomere protection in the absence of replication.

Contact : sandrine.humbert@univ-grenoble-alpes.fr

Discipline évènement : (Biologie / Chimie)
Entité organisatrice : (GIN)
Nature évènement : (Séminaire)
Evènement répétitif : (Séminaire Grenoblois de Neurosciences)
Site de l'évènement : Pôle Santé / La Tronche

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