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Related Concept Videos

Mitochondria01:37

Mitochondria

Mitochondria are eukaryotic cellular organelles that are known to produce energy through a process called oxidative phosphorylation. Besides their primary function, mitochondria are involved in various cellular processes, including cell growth, differentiation, signaling, metabolism, and senescence. Age-related changes cause a decline in mitochondrial quality and integrity due to increased mitochondrial mutations and oxidative damage. Thus, aging can severely impact mitochondrial functions,...
Replication in Eukaryotes01:29

Replication in Eukaryotes

In eukaryotic cells, DNA replication is highly conserved and tightly regulated. Multiple linear chromosomes must be duplicated with high fidelity before cell division, so there are many proteins that fulfill specialized roles in the replication process. Replication occurs in three phases: initiation, elongation, and termination, and ends with two complete sets of chromosomes in the nucleus.
Many Proteins Orchestrate Replication at the Origin
Eukaryotic replication follows many of the same...
Replication in Eukaryotes02:31

Replication in Eukaryotes

Overview
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...
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.

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Phosphorus-31 Magnetic Resonance Spectroscopy: A Tool for Measuring In Vivo Mitochondrial Oxidative Phosphorylation Capacity in Human Skeletal Muscle
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Telomere dysfunction induces metabolic and mitochondrial compromise.

Ergün Sahin1, Simona Colla, Marc Liesa

  • 1Belfer Institute for Applied Cancer Science, Dana-Farber Cancer Institute, Boston, Massachusetts 02115, USA.

Nature
|February 11, 2011
PubMed
Summary

Telomere dysfunction impairs mitochondrial function by activating p53, which represses key metabolic regulators. Restoring these factors or deleting p53 improves mitochondrial health and organ function, revealing a critical telomere-p53-PGC axis.

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Area of Science:

  • Molecular Biology
  • Genetics
  • Mitochondrial Biology

Background:

  • Telomere dysfunction causes tissue atrophy and functional decline.
  • Its impact extends to quiescent tissues, necessitating investigation into common mechanisms.

Purpose of the Study:

  • To identify common molecular mechanisms underlying telomere dysfunction's impact across diverse tissues.
  • To elucidate the link between telomere biology and mitochondrial function.

Main Methods:

  • Transcriptomic network analyses in mice lacking telomerase components (Tert or Terc).
  • Investigated the role of p53 (Trp53) and peroxisome proliferator-activated receptor gamma, coactivator 1 alpha and beta (PGC-1α/β).
  • Assessed mitochondrial biogenesis, function, gluconeogenesis, and cardiac function.

Main Results:

  • Telomere dysfunction led to profound repression of PGC-1α and PGC-1β.
  • Mice exhibited impaired mitochondrial function, decreased gluconeogenesis, and cardiomyopathy.
  • p53 directly represses PGC-1α/β promoters, linking telomere dysfunction to metabolic pathways.

Conclusions:

  • A direct telomere-p53-PGC axis links telomere maintenance to mitochondrial and metabolic homeostasis.
  • This axis contributes to organ failure and reduced organismal fitness under telomere stress.
  • Targeting this axis may offer therapeutic potential for telomere-related diseases.