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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

Restarting Stalled Replication Forks

Restarting Stalled Replication Forks

DNA replication is initiated at sites containing predefined DNA sequences known as origins of replication. DNA is unwound at these sites by the minichromosome maintenance (MCM) helicase and other factors such as Cdc45 and the associated GINS complex.The unwound single strands are protected by replication protein A (RPA) until DNA polymerase starts synthesizing DNA at the 5’ end of the strand in the same direction as the replication fork. To prevent the replication fork from falling apart,...

Restarting Stalled Replication Forks

Restarting Stalled Replication Forks

The DNA Replication Fork

The DNA Replication Fork

An organism’s genome needs to be duplicated in an efficient and error-free manner for its growth and survival. The replication fork is a Y-shaped active region where two strands of DNA are separated and replicated continuously. The coupling of DNA unzipping and complementary strand synthesis is a characteristic feature of a replication fork. Organisms with small circular DNA, such as E. coli, often have a single origin of replication; therefore, they have only two replication...

The DNA Replication Fork

The DNA Replication Fork

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Related Experiment Video

Updated: Nov 2, 2025

G2-seq: A High Throughput Sequencing-based Technique for Identifying Late Replicating Regions of the Genome

G2-seq: A High Throughput Sequencing-based Technique for Identifying Late Replicating Regions of the Genome

Published on: March 22, 2018

Dynamics of replication origin over-activation.

Haiqing Fu¹, Christophe E Redon¹, Bhushan L Thakur¹

¹Developmental Therapeutics Branch, Center for Cancer Research, National Cancer Institute, Bethesda, MD, USA.

Nature Communications

|June 9, 2021

Summary

This summary is machine-generated.

Cancer cells can be driven to over-replicate DNA, a promising therapy. Our study reveals re-replicating cancer cells preferentially reactivate early DNA replication origins, unlike stress-induced cells activating dormant origins.

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Related Experiment Videos

Last Updated: Nov 2, 2025

G2-seq: A High Throughput Sequencing-based Technique for Identifying Late Replicating Regions of the Genome

G2-seq: A High Throughput Sequencing-based Technique for Identifying Late Replicating Regions of the Genome

Published on: March 22, 2018

Inducing a Site Specific Replication Blockage in E. coli Using a Fluorescent Repressor Operator System

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Published on: August 21, 2016

Direct Restart of a Replication Fork Stalled by a Head-On RNA Polymerase

Direct Restart of a Replication Fork Stalled by a Head-On RNA Polymerase

Published on: April 29, 2010

Area of Science:

Molecular Biology
Cancer Research
Cell Biology

Background:

Dysregulation of DNA replication safeguards is common in cancer.
Inducing excess DNA replication in cancer cells is a potential therapeutic strategy.

Purpose of the Study:

To investigate DNA synthesis patterns in cancer cells undergoing partial genome re-replication.
To understand the mechanisms and origin selection during cancer cell over-replication.

Main Methods:

Analysis of DNA synthesis patterns in re-replicating cancer cells.
Characterization of replication initiation events and origin usage.
Comparison with replication stress-induced cells.

Main Results:

Re-replicating cells exhibit slow replication and increased initiation events.
A skewed initiation pattern preferentially reactivated early-replicating origins.
Unlike replication stress, re-replication did not activate dormant origins but reused existing ones.

Conclusions:

Cancer cell over-replication can occur via distinct pathways activating different sets of replication origins.
The mechanism involves disproportionate pre-replication complex distribution on chromatin.
Understanding these pathways offers insights into cancer therapeutics targeting DNA replication.