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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...
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
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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Related Experiment Video

Updated: Jun 26, 2026

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

Telomeres and reproductive aging.

David L Keefe1, Lin Liu

  • 1Department of Ob/Gyn, University of South Florida, Tampa, FL 33606, USA. dkeefe@hsc.usf.edu

Reproduction, Fertility, and Development
|January 21, 2009
PubMed
Summary
This summary is machine-generated.

Telomere shortening disrupts meiosis and causes reproductive aging in women. Experimentally shortening telomeres in mice recapitulated this human aging phenotype, suggesting a telomere theory of reproductive aging.

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Telomere Length and Telomerase Activity; A Yin and Yang of Cell Senescence
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Monochrome Multiplex Quantitative PCR Telomere Length Measurement
11:44

Monochrome Multiplex Quantitative PCR Telomere Length Measurement

Published on: March 22, 2024

Area of Science:

  • Reproductive biology
  • Genetics
  • Cell biology

Background:

  • Female reproductive aging is linked to increased infertility, miscarriage, and aneuploid offspring, with meiotic dysfunction as a key factor.
  • Telomeres, protective caps on chromosomes, are known to mediate aging in dividing cells and may play a role in meiotic aging.
  • The precise mechanisms by which aging disrupts female meiosis remain largely unknown, despite the growing trend of delayed childbearing.

Purpose of the Study:

  • To investigate the hypothesis that telomere shortening is a primary cause of age-related meiotic dysfunction in female mammals.
  • To explore the potential of telomere length as a biomarker for reproductive aging and its associated risks.

Main Methods:

  • Experimental shortening of telomeres in mice, which do not naturally exhibit age-related meiotic dysfunction.
  • Comparative analysis of telomere length and meiotic function in genetically modified mice and naturally aging human oocytes.
  • Investigation of oxidative stress and DNA damage response pathways in relation to telomere length and meiotic integrity.

Main Results:

  • Experimentally shortened telomeres in mice replicated the human reproductive aging phenotype, including meiotic errors.
  • Mouse telomeres, when shortened to lengths comparable to those in older women, induced age-related reproductive issues.
  • Oxidative stress was observed to increase with reproductive aging, leading to DNA damage at telomeric repeat sequences.

Conclusions:

  • Telomere shortening is proposed as a significant contributor to reproductive aging and associated meiotic defects, miscarriage, and infertility.
  • Telomere dysfunction, potentially driven by oxidative stress and aberrant recombination, underlies age-related declines in female fertility.
  • Understanding telomere dynamics offers a novel perspective on reproductive aging and potential therapeutic targets.