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DNA Replication

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DNA replication involves the separation of the two strands of the double helix, with each strand serving as a template from which the new complementary strand is copied. After replication, each double-stranded DNA includes one parental or “old” strand and one “new” strand. This is known as semiconservative replication. The resulting DNA molecules have the same sequence and are divided equally into the two daughter cells.
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Related Experiment Video

Updated: May 24, 2026

Iterative Optimization of DNA Duplexes for Crystallization of SeqA-DNA Complexes

Iterative Optimization of DNA Duplexes for Crystallization of SeqA-DNA Complexes

Published on: November 1, 2012

Cohesin acetylation speeds the replication fork.

Marie-Emilie Terret¹, Rebecca Sherwood, Sadia Rahman

¹Molecular Biology Program, Memorial Sloan-Kettering Cancer Center, 1275 York Avenue, New York, New York 10065, USA.

|November 13, 2009

Summary

The replication factor C (RFC)-CTF18 clamp loader regulates replication fork speed and cohesin acetylation, which is crucial for genome duplication and preventing DNA damage. This study reveals a novel mechanism involving cohesin modification for fork progression.

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Area of Science:

Molecular Biology
Cell Biology
Genetics

Background:

Cohesin links sister chromatids and regulates chromatin accessibility.
Replication forks must overcome cohesin-associated obstacles during DNA replication.
The mechanism by which replication forks navigate cohesin is largely unknown.

Purpose of the Study:

To investigate the role of the RFC-CTF18 clamp loader in replication fork progression.
To elucidate the function of cohesin acetylation in DNA replication.
To understand the link between cohesin regulation and genome stability.

Main Methods:

Single-molecule analysis in human cells.
Investigation of cohesin acetylation and its impact on replication forks.
Analysis of cells with mutations in cohesin acetyltransferases (ESCO1, ESCO2) and Roberts' syndrome patient cells.

Main Results:

RFC-CTF18 controls replication fork velocity, spacing, and restart, and is essential for SMC3 acetylation and sister chromatid cohesion.
Cohesin acetylation is critical for replication fork processivity; its absence leads to slow forks.
SMC3 acetylation status dictates fork speed by modulating cohesin's interaction with WAPL and PDS5A.

Conclusions:

A novel mechanism for clamp-loader-dependent fork progression mediated by cohesin post-translational modification and structural remodeling is described.
Dysregulation of this cohesin acetylation-dependent process leads to DNA damage accumulation.
Defects in this pathway may contribute to cohesinopathies like Roberts' syndrome.