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Related Concept Videos

Replicative Cell Senescence02:15

Replicative Cell Senescence

Replicative cell senescence is a property of cells that allows them to divide a finite number of times throughout the organism's lifespan while preventing excessive proliferation. Replicative senescence is associated with the gradual loss of the telomere — short, repetitive DNA sequences found at the end of the chromosomes. Telomeres are bound by a group of proteins to form a protective cap on the ends of chromosomes. Embryonic stem cells express telomerase — an enzyme that adds the telomeric...
Replicative Cell Senescence02:15

Replicative Cell Senescence

Replicative cell senescence is a property of cells that allows them to divide a finite number of times throughout the organism's lifespan while preventing excessive proliferation. Replicative senescence is associated with the gradual loss of the telomere — short, repetitive DNA sequences found at the end of the chromosomes. Telomeres are bound by a group of proteins to form a protective cap on the ends of chromosomes. Embryonic stem cells express telomerase — an enzyme that adds the telomeric...
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Positive regulators allow a cell to advance through cell cycle checkpoints. Negative regulators have an equally important role as they terminate a cell’s progression through the cell cycle—or pause it—until the cell meets specific criteria.
Telomeres and Telomerase02:41

Telomeres and Telomerase

In eukaryotic DNA replication, a single-stranded DNA fragment remains at the end of a chromosome after the removal of the final primer. This section of DNA cannot be replicated in the same manner as the rest of the strand because there is no 3’ end to which the newly synthesized DNA can attach. This non-replicated fragment results in gradual loss of the chromosomal DNA during each cell duplication. Additionally, it can induce a DNA damage response by enzymes that recognize single-stranded DNA.
Telomeres and Telomerase02:41

Telomeres and Telomerase

In eukaryotic DNA replication, a single-stranded DNA fragment remains at the end of a chromosome after the removal of the final primer. This section of DNA cannot be replicated in the same manner as the rest of the strand because there is no 3’ end to which the newly synthesized DNA can attach. This non-replicated fragment results in gradual loss of the chromosomal DNA during each cell duplication. Additionally, it can induce a DNA damage response by enzymes that recognize single-stranded DNA.
The Cell Cycle Control System01:28

The Cell Cycle Control System

The cell cycle regulation directs how a cell proceeds from one phase to the next and begins mitosis. The cell cycle control system includes intracellular regulatory molecules and external triggers. They provide "stop" or "advance" signals and operate at specific cell cycle stages termed checkpoints to ensure that a particular process is completed before the cell advances to the next phase.
Cyclins and cyclin-dependent kinases (Cdks) are the primary cell cycle regulators and function at the cell...

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Manipulation and Analysis of Cell Cycle-Dependent Processes in Budding Yeast
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Published on: September 26, 2025

TOR regulates cell death induced by telomere dysfunction in budding yeast.

Haiyan Qi1, Yongjie Chen, Xuan Fu

  • 1Department of Pharmacology, UMDNJ-Robert Wood Johnson Medical School, Piscataway, NJ, USA. qiha@umdnj.edu

Plos One
|October 25, 2008
PubMed
Summary

Target of Rapamycin (TOR) inhibition prevents cell death from telomere dysfunction in yeast, but not growth arrest. This novel role is independent of telomere length and G-tail amounts, suggesting TOR

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Area of Science:

  • Cellular senescence
  • Molecular biology
  • Genetics

Background:

  • Telomere dysfunction triggers cellular senescence and death, yet the underlying regulatory mechanisms remain unclear.
  • Understanding the senescence-death pathway is crucial for comprehending aging and disease.
  • The Target of Rapamycin (TOR) pathway is a key regulator of cell growth and metabolism.

Purpose of the Study:

  • To investigate the role of TOR signaling in regulating cell death induced by telomere dysfunction.
  • To determine if TOR inhibition affects senescence or cell death in a yeast model of telomere dysfunction.
  • To explore the specificity of TOR's involvement in telomere dysfunction-induced cell death.

Main Methods:

  • Utilized a yeast model (cdc13-1) with temperature-sensitive telomere dysfunction.
  • Administered rapamycin to inhibit the Target of Rapamycin (TOR) pathway.
  • Assessed cell death and growth arrest in response to TOR inhibition and telomere dysfunction.
  • Examined telomere length, G-tail amounts, and telomere position effect (TPE).
  • Investigated the effects of antioxidants and other DNA damaging agents.

Main Results:

  • TOR inhibition prevented cell death but not growth arrest in yeast with dysfunctional telomeres.
  • This TOR function was distinct from its known G1 inhibition role and did not alter telomere length or TPE.
  • Antioxidants also mitigated cell death caused by telomere dysfunction.
  • TOR inhibition also prevented cell death in telomerase-deficient yeast (est1 mutant).
  • Rapamycin did not protect against cell death induced by etoposide or UV radiation.

Conclusions:

  • The Target of Rapamycin (TOR) signaling pathway is specifically implicated in regulating cell death triggered by telomere dysfunction.
  • TOR's role in preventing telomere dysfunction-induced death is separable from its effects on cell cycle progression and telomere maintenance.
  • These findings highlight a novel mechanism linking nutrient sensing pathways to telomere integrity and cell fate decisions.