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Related Concept Videos

DNA Damage can Stall the Cell Cycle02:36

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 Cycle02:36

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...
Restarting Stalled Replication Forks02:37

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...
The DNA Replication Fork01:02

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 forks, one in...
The DNA Replication Fork01:02

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 forks, one in...
S-Cdk Initiates DNA Replication02:38

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.

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Related Experiment Video

Updated: Jun 5, 2026

Quantifying Replication Stress in Ovarian Cancer Cells Using Single-Stranded DNA Immunofluorescence
06:25

Quantifying Replication Stress in Ovarian Cancer Cells Using Single-Stranded DNA Immunofluorescence

Published on: February 10, 2023

A RHNO1-ATR/Chk1 positive feedback loop sustains the DNA replication stress response.

Niphat Jirapongwattana, Catalina Trujillo Jaramillo, Carley M Conover

    Biorxiv : the Preprint Server for Biology
    |June 4, 2026
    PubMed
    Summary

    RAD9-HUS1-RAD1 interacting nuclear orphan 1 (RHNO1) stabilizes ATR/Chk1 signaling, crucial for cancer cell survival during replication stress. RHNO1 upregulation prevents checkpoint collapse and genomic instability, offering a potential therapeutic target.

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    Quantifying Replication Stress in Ovarian Cancer Cells Using Single-Stranded DNA Immunofluorescence
    06:25

    Quantifying Replication Stress in Ovarian Cancer Cells Using Single-Stranded DNA Immunofluorescence

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    Laser Microirradiation to Study In Vivo Cellular Responses to Simple and Complex DNA Damage
    10:44

    Laser Microirradiation to Study In Vivo Cellular Responses to Simple and Complex DNA Damage

    Published on: January 31, 2018

    Area of Science:

    • Molecular Biology
    • Cancer Biology
    • Cellular Signaling

    Background:

    • Cancer cells exhibit elevated DNA replication stress, making them reliant on ATR/Chk1 signaling for survival.
    • The maintenance of ATR/Chk1 signaling during prolonged replication stress is not fully understood.

    Purpose of the Study:

    • To investigate the role of RHNO1 in cancer progression.
    • To elucidate RHNO1's involvement in maintaining ATR/Chk1 signaling during the DNA replication stress response.

    Main Methods:

    • Depletion of RHNO1 using in vitro and in vivo models.
    • Analysis of RHNO1 stabilization and degradation pathways.
    • Investigation of RHNO1's interaction with ATR/Chk1 signaling and replication forks.

    Main Results:

    • RHNO1 depletion inhibits cancer cell proliferation and tumor growth.
    • RHNO1 is upregulated and stabilized post-replication stress, independent of initial ATR/Chk1 activation.
    • RHNO1 is required for sustained ATR/Chk1 signaling, preventing checkpoint collapse and genomic instability.
    • ATR/Chk1 signaling stabilizes RHNO1 via phosphorylation, promoting its localization to stressed replication forks.

    Conclusions:

    • RHNO1 is essential for sustaining the ATR/Chk1-mediated replication stress response.
    • A positive feedback loop exists where ATR/Chk1 signaling stabilizes RHNO1, which in turn maintains the signaling.
    • RHNO1 is a critical component of the replication stress response and a potential therapeutic target in ATR/Chk1-dependent cancers.