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DNA Damage Can Stall the Cell Cycle

DNA Damage Can Stall the Cell Cycle

In response to DNA damage, cells can pause the cell cycle to assess and repair the breaks. However, the cell must check the DNA at certain critical stages during the cell cycle. If the cell cycle pauses before DNA replication, the cells will contain twice the amount of DNA. On the other hand, if cells arrest after DNA replication but before mitosis, they will contain four times the normal amount of DNA. With a host of specialized proteins at their disposal,cells must use the right protein at...

DNA Damage can Stall the Cell Cycle

DNA Damage can Stall the Cell Cycle

In response to DNA damage, cells can pause the cell cycle to assess and repair the breaks. However, the cell must check the DNA at certain critical stages during the cell cycle. If the cell cycle pauses before DNA replication, the cells will contain twice the amount of DNA. On the other hand, if cells arrest after DNA replication but before mitosis, they will contain four times the normal amount of DNA. With a host of specialized proteins at their disposal,cells must use the right protein at...

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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,...

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Related Experiment Video

Updated: Mar 30, 2026

Author Spotlight: Investigating the Motion Dynamics of the Eukaryotic Replisome Components at the Single-Molecule Level

Author Spotlight: Investigating the Motion Dynamics of the Eukaryotic Replisome Components at the Single-Molecule Level

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PTEN Controls the DNA Replication Process through MCM2 in Response to Replicative Stress.

Jiawen Feng¹, Jing Liang¹, Jiaju Li¹

¹Institute of Systems Biomedicine, Center for Molecular and Translational Medicine, Department of Pathology, School of Basic Medicine, Peking-Tsinghua Center for Life Sciences, Peking University Health Science Center, Beijing 100191, PRC.

|November 10, 2015

Summary

The tumor suppressor PTEN dephosphorylates MCM2, restricting DNA replication fork progression. Loss of PTEN function causes replication defects and genomic instability, highlighting PTEN

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Area of Science:

Molecular Biology
Cancer Biology
Genetics

Background:

PTEN is a critical tumor suppressor frequently altered in human cancers.
Nuclear PTEN plays a role in genome maintenance.
The phosphatidylinositol 3-kinase (PI3K)-AKT pathway is a key signaling cascade regulated by PTEN.

Purpose of the Study:

To investigate the role of PTEN in regulating DNA replication.
To identify novel PTEN interacting partners involved in DNA replication.
To elucidate the mechanism by which PTEN maintains genomic stability.

Main Methods:

Co-immunoprecipitation to identify PTEN-interacting proteins.
In vitro kinase assays to assess PTEN's dephosphorylation activity.
Analysis of DNA replication fork progression under replicative stress.
Assessment of chromosomal aberrations in PTEN-deficient cells.

Main Results:

PTEN physically associates with minichromosome maintenance complex component 2 (MCM2).
PTEN dephosphorylates MCM2 at serine 41 (S41), restricting replication fork progression.
PTEN deficiency leads to unrestrained replication fork progression and increased chromosomal aberrations.
Cells expressing a phosphomimic MCM2 mutant (S41D) phenocopy PTEN disruption.

Conclusions:

PTEN regulates DNA replication through direct interaction and dephosphorylation of MCM2.
PTEN is essential for preventing replication defects and maintaining genomic stability under stress.
This study reveals a novel mechanism for PTEN's tumor suppressor activity involving MCM2 and DNA replication.