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Translesion DNA Polymerases

Translesion DNA Polymerases

Translesion (TLS) polymerases rescue stalled DNA polymerases at sites of damaged bases by replacing the replicative polymerase and installing a nucleotide across the damaged site. Doing so, TLS allows additional time for the cell to repair the damage before resuming regular DNA replication.
TLS polymerases are found in all three domains of life - archaea, bacteria, and eukaryotes. Of the different classes of TLS polymerases, members of the Y family are fitted with specialized structures that...

Replication in Eukaryotes

Replication in Eukaryotes

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

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

Proofreading

Proofreading

Synthesis of new DNA molecules is carried out by the enzyme DNA polymerase, which adds nucleotides on the daughter strand complementary to the template DNA strand. DNA polymerase has a higher affinity to add the correct base and ensures fidelity during DNA replication. Furthermore, it exhibits proofreading activity during replication, using an exonuclease domain that cuts off incorrect nucleotides from the nascent DNA strand.
Errors During Replication are Corrected by the DNA Polymerase Enzyme

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Related Experiment Video

Updated: Jun 4, 2026

Single-Molecule Fluorescence Visualization of DNA Polymerase Dynamics at G-Quadruplexes

Single-Molecule Fluorescence Visualization of DNA Polymerase Dynamics at G-Quadruplexes

Published on: April 4, 2025

Polymerase epsilon is required to maintain replicative senescence.

Abhyuday M Deshpande¹, Iglika G Ivanova, Vasil Raykov

¹Institute for Ageing and Health, Institute of Human Genetics, Centre for Life, Newcastle upon Tyne NE1 3BZ, United Kingdom.

Molecular and Cellular Biology

|February 16, 2011

Summary

Replicative senescence involves a permanent cell cycle arrest. DNA polymerase epsilon and Exo1 maintain this arrest by creating a cycle of DNA damage and repair, ensuring senescence permanence in yeast.

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Last Updated: Jun 4, 2026

Single-Molecule Fluorescence Visualization of DNA Polymerase Dynamics at G-Quadruplexes

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Strand-Specific Analysis of Proteins at Replicating DNA Strands by Enrichment and Sequencing of Protein-Associated Nascent DNA Method

Strand-Specific Analysis of Proteins at Replicating DNA Strands by Enrichment and Sequencing of Protein-Associated Nascent DNA Method

Published on: May 2, 2025

Area of Science:

Cellular biology
Molecular genetics
DNA replication and repair

Background:

Replicative senescence is a permanent cell cycle arrest triggered by telomere shortening.
Understanding the molecular mechanisms maintaining permanent arrest is crucial.

Purpose of the Study:

To identify factors influencing replicative senescence in yeast with impaired telomere elongation.
To elucidate the paradoxical roles of DNA polymerase epsilon and Mrc1 in senescence.

Main Methods:

Screening for factors affecting senescence in budding yeast.
Analyzing DNA dynamics (double- and single-stranded DNA) at telomeres during senescence.
Investigating checkpoint activation pathways (Rad24-Rad17 and Rad9-53BP1).

Main Results:

DNA polymerase epsilon (Pol ε) and Exo1 nuclease synergistically maintain replicative senescence.
Mrc1 protein facilitates escape from senescence.
Evidence of cyclical DNA resection and resynthesis at telomeres was observed.
Alternating DNA damage types (ssDNA and double-strand break-like structures) activate distinct checkpoint pathways.

Conclusions:

A "vicious circle" of alternating DNA resection and resynthesis, each activating different checkpoints, ensures permanent senescence.
This cyclical process prevents checkpoint adaptation and maintains the permanent cell cycle arrest.