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Telomeres and Telomerase

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 Telomerase

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.

Replication in Eukaryotes

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 Eukaryotes

Replication in Eukaryotes

Replicative Cell Senescence

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 Senescence

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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Related Experiment Video

Updated: Jun 26, 2026

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

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

Published on: May 22, 2013

Telomere length maintenance--an ALTernative mechanism.

N J Royle¹, J Foxon, J N Jeyapalan

¹Department of Genetics, University of Leicester, Leicester, UK. njr@le.ac.uk

Cytogenetic and Genome Research

|February 4, 2009

Summary

The Alternative Lengthening of Telomeres (ALT) mechanism, used in 10% of human tumors, involves complex telomere mutations. The break-induced replication (BIR) model may explain these mutations and telomere instability in ALT+ cancers.

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

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Modified Terminal Restriction Fragment Analysis for Quantifying Telomere Length Using In-gel Hybridization

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Published on: July 10, 2017

Area of Science:

Genetics
Cancer Biology
Molecular Biology

Background:

The Alternative Lengthening of Telomeres (ALT) mechanism is active in approximately 10% of human tumors, particularly sarcomas.
ALT+ cancers exhibit heterogeneous telomere lengths, extrachromosomal telomeric DNA, ALT-associated promyelocytic bodies (APBs), and telomere-sister chromatid exchanges (T-SCE).
A link exists between minisatellite instability (MS32) and the ALT mechanism, though the precise nature of this relationship remains unclear.

Purpose of the Study:

To investigate the complex telomere mutations observed in ALT+ cell lines and tumors.
To explore the potential role of the break-induced replication (BIR) model in explaining ALT-associated phenomena.
To review the relationship between minisatellite instability and the ALT mechanism.

Main Methods:

Single molecule analysis of telomeric DNA from ALT+ cell lines and tumors.
Review of the break-induced replication (BIR) model in the context of ALT.
Analysis of telomere-sister chromatid exchanges (T-SCE) and minisatellite instability (MS32).

Main Results:

Single molecule analysis revealed complex telomere mutations in ALT+ samples, distinct from those in telomerase-expressing cells.
These complex mutations cannot be fully explained by T-SCE alone, suggesting an alternative intermolecular process.
The break-induced replication (BIR) model is proposed as a potential explanation for high T-SCE frequency and complex telomere mutations.

Conclusions:

The Alternative Lengthening of Telomeres (ALT) mechanism is associated with unique and complex telomere mutations.
The break-induced replication (BIR) model offers a plausible framework for understanding key features of the ALT pathway.
Further research is needed to elucidate the exact relationship between minisatellite instability and the ALT mechanism.