Related Experiment Video
Updated: Aug 13, 2026
12:08
Telomere Length and Telomerase Activity; A Yin and Yang of Cell Senescence
Published on: May 22, 2013
Esc1-mediated anchoring regulates telomere clustering in response to metabolic changes
Myriam Ruault1, Isabelle Loïodice1, Bradley D Keister2
1UMR 3664 Nuclear Dynamics, CNRS, Institut Curie, Université Paris Sciences et Lettres, Sorbonne University , Paris, France.
The Journal of Cell Biology
|August 12, 2026
Summary
Budding yeast telomeres reorganize during quiescence. Two redundant anchoring pathways, one PKA-dependent and another involving Esc1, are inactivated, releasing telomeres to form a central hypercluster for long-term viability.
Area of Science:
- Cellular Biology
- Molecular Biology
- Genetics
Background:
- Telomere organization in budding yeast is dynamic and influenced by growth conditions.
- In rich medium, telomeres form perinuclear foci, while in quiescent cells, they form a central hypercluster, enhancing viability.
Purpose of the Study:
- To investigate the mechanisms behind telomere hypercluster formation in quiescent yeast cells.
- To determine the role of telomere anchoring and specific proteins in this reorganization.
Main Methods:
- Ruled out Sir3-mediated telomere interactions.
- Utilized physical modeling to predict the role of telomere anchoring.
- Performed genetic analyses to identify anchoring pathways.
Main Results:
- Telomere anchoring antagonizes clustering.
- Two redundant telomere anchoring pathways exist: one PKA-dependent, rapidly inactivated upon glucose depletion.
- A second pathway involves Esc1 dephosphorylation, progressively lost during quiescence entry.
Conclusions:
- Inactivation of both anchoring pathways releases telomeres from the nuclear envelope.
- This release leads to specific hypercluster formation in quiescent cells, contributing to their viability.
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