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Related Concept Videos

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.
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...
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
Mismatch Repair01:20

Mismatch Repair

Organisms are capable of detecting and fixing nucleotide mismatches that occur during DNA replication. This sophisticated process requires identifying the new strand and replacing the erroneous bases with correct nucleotides. Mismatch repair is coordinated by many proteins in both prokaryotes and eukaryotes.
The Mutator Protein Family Plays a Key Role in DNA Mismatch Repair
The human genome has more than 3 billion base pairs of DNA per cell. Prior to cell division, that vast amount of genetic...

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Updated: Jun 19, 2026

Utilizing Murine Inducible Telomerase Alleles in the Studies of Tissue Degeneration/Regeneration and Cancer
08:34

Utilizing Murine Inducible Telomerase Alleles in the Studies of Tissue Degeneration/Regeneration and Cancer

Published on: April 13, 2015

Telomerase reverse transcriptase-dependent telomere equilibration mitigates tissue dysfunction in mTert

Marie Meznikova1, Natalie Erdmann, Rich Allsopp

  • 1Ontario Cancer Institute/Campbell Family Institute for Cancer Research, Toronto, ON, Canada.

Disease Models & Mechanisms
|October 21, 2009
PubMed
Summary
This summary is machine-generated.

Telomere erosion in mice with telomerase gene mutations can lead to telomere lengthening over generations, suggesting a potential adaptation mechanism. This finding may inform strategies for mitigating telomere-related diseases and cancer therapies.

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Related Experiment Videos

Last Updated: Jun 19, 2026

Utilizing Murine Inducible Telomerase Alleles in the Studies of Tissue Degeneration/Regeneration and Cancer
08:34

Utilizing Murine Inducible Telomerase Alleles in the Studies of Tissue Degeneration/Regeneration and Cancer

Published on: April 13, 2015

Telomere Length and Telomerase Activity; A Yin and Yang of Cell Senescence
12:08

Telomere Length and Telomerase Activity; A Yin and Yang of Cell Senescence

Published on: May 22, 2013

In vitro Reconstitution of the Active T. castaneum Telomerase
09:25

In vitro Reconstitution of the Active T. castaneum Telomerase

Published on: July 14, 2011

Area of Science:

  • Genetics
  • Molecular Biology
  • Cell Biology

Background:

  • Dyskeratosis congenita (DKC) is linked to autosomal dominant mutations in telomere-associated factors, causing proliferative abnormalities and telomere erosion.
  • Telomerase gene heterozygous mice (mTert, mTerc) model telomerase haploinsufficiency but do not fully replicate DKC.
  • Phenotypes in heterozygous mice vary with telomere length and generational exposure to heterozygosity.

Purpose of the Study:

  • To investigate the long-term effects of telomerase gene heterozygosity on telomere length and disease development in mice.
  • To explore potential telomere adaptation mechanisms in response to gradual erosion.
  • To assess the implications for human diseases and cancer therapy.

Main Methods:

  • Generation and analysis of mouse strains with varying telomere lengths and heterozygous or nullizygous telomerase genes (mTert, mTerc) over multiple generations.
  • Monitoring of telomere length dynamics, survival rates, and phenotypic manifestations.
  • Evaluation of radioprotection capacity in bone marrow.

Main Results:

  • Prolonged mTert heterozygosity (over ten generations) did not induce disease and resulted in telomere length resetting to wild-type levels.
  • Telomere lengthening was observed in heterozygous progeny inheriting short telomeres from nullizygous parents, but not in nullizygotes.
  • Nullizygotes maintained radioprotection competence for three generations, indicating sustained function despite telomere erosion.

Conclusions:

  • Gradual telomere erosion in the presence of telomerase may trigger a subsequent telomere extension or adaptation mechanism, analogous to yeast.
  • This adaptive response could have implications for understanding telomere maintenance in normal human cells and DKC.
  • The findings may guide strategies to mitigate stem cell toxicity from telomerase inhibition in cancer therapy.