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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, a...

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, a...

S-Cdk Initiates DNA Replication

S-Cdk Initiates DNA Replication

The cell cycle is a series of events leading to DNA duplication followed by the division of cell content to form two daughter cells. The cell cycle progresses in four stages—the cell increases in size (gap 1 or G1-phase), duplicates its DNA (synthesis or S-phase), prepares to divide (gap 2 or G2-phase), and divides (mitosis or M-phase).
Two states at the origin of replication
In eukaryotes, the initiation of replication occurs at many sites on the chromosomes, called the origins of replication.

S-Cdk Initiates DNA Replication

S-Cdk Initiates DNA Replication

The cell cycle is a series of events leading to DNA duplication followed by the division of cell content to form two daughter cells. The cell cycle progresses in four stages—the cell increases in size (gap 1 or G1-phase), duplicates its DNA (synthesis or S-phase), prepares to divide (gap 2 or G2-phase), and divides (mitosis or M-phase).
Two states at the origin of replication
In eukaryotes, the initiation of replication occurs at many sites on the chromosomes, called the origins of replication.

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...

Prokaryotic DNA Replication

Prokaryotic DNA Replication

DNA replication has three main steps: initiation, elongation, and termination. Replication in prokaryotes begins when initiator proteins bind to the single origin of replication (ori) on the cell's circular chromosome. Replication then proceeds around the entire circle of the chromosome in each direction from the two replication forks, resulting in two DNA molecules.
Many Proteins Work Together to Replicate the Chromosome
Replication is coordinated and carried out by a host of specialized...

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Related Experiment Video

Updated: May 15, 2026

Visualization of DNA Replication in the Vertebrate Model System DT40 using the DNA Fiber Technique

Visualization of DNA Replication in the Vertebrate Model System DT40 using the DNA Fiber Technique

Published on: October 27, 2011

KCTD10 resolves co-directional transcription-replication conflicts.

Bin Chen¹, Jake A Kloeber², Jinzhou Huang¹

¹Department of Oncology, Mayo Clinic, Rochester, MN 55905, USA.

Trends in Cell Biology

|May 13, 2026

Summary

This summary is machine-generated.

Co-directional transcription-replication conflicts (TRCs) are actively regulated events impacting genome stability. A Cullin 3-KCTD10 complex detects these conflicts, remodeling RNA polymerase II for replisome bypass.

Keywords:

CUL3–KCTD10 ubiquitin ligase TCEA2 ubiquitination co-directional transcription–replication conflicts genome stability

More Related Videos

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

Related Experiment Videos

Last Updated: May 15, 2026

Visualization of DNA Replication in the Vertebrate Model System DT40 using the DNA Fiber Technique

Visualization of DNA Replication in the Vertebrate Model System DT40 using the DNA Fiber Technique

Published on: October 27, 2011

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
Genetics
Biochemistry

Background:

Co-directional (CD) transcription-replication conflicts (TRCs) occur when DNA replication and transcription machinery move in the same direction.
While often viewed as less severe than head-on TRCs, CD TRCs are frequent, actively regulated events crucial for genome stability.

Purpose of the Study:

To investigate the regulatory mechanisms underlying CD TRCs.
To elucidate the role of the Cullin 3-KCTD10 ubiquitin ligase complex in managing these conflicts.

Main Methods:

The study focuses on the function of the Cullin 3-Potassium channel tetramerization domain containing 10 (KCTD10) ubiquitin ligase complex.
Investigated the nonproteolytic ubiquitination of the elongation factor TCEA2.
Examined the remodeling of RNA polymerase II to facilitate replisome bypass.

Main Results:

The Cullin 3-KCTD10 complex acts as a bivalent sensor for CD collisions.
This complex directs nonproteolytic ubiquitination of TCEA2, leading to transient remodeling of RNA polymerase II.
This remodeling allows the replication machinery (replisome) to bypass transcriptional machinery.

Conclusions:

CD TRCs are dynamic decision points involving negotiation between replication and transcription priorities.
Conflict geometry, ubiquitin signaling, and genome maintenance are functionally integrated.
The sensing-driven remodeling mechanism highlights a novel pathway for maintaining genome stability during co-directional conflicts.