Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Restarting Stalled Replication Forks02:37

Restarting Stalled Replication Forks

6.1K
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,...
6.1K
Restarting Stalled Replication Forks02:37

Restarting Stalled Replication Forks

2.2K
2.2K
DNA Damage can Stall the Cell Cycle02:37

DNA Damage can Stall the Cell Cycle

9.7K
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...
9.7K
DNA Damage Can Stall the Cell Cycle02:37

DNA Damage Can Stall the Cell Cycle

2.9K
2.9K
The DNA Replication Fork01:02

The DNA Replication Fork

39.0K
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...
39.0K
The DNA Replication Fork01:02

The DNA Replication Fork

17.3K
17.3K

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

T<sub>reg</sub> cells promote immunotherapy-induced immune evasion by restraining CD4 T cell control of MHC-I-deficient metastatic pancreatic cancer.

Science immunology·2026
Same author

STMN2 protein depletion via translation deficits and stress granules in amyotrophic lateral sclerosis.

Brain : a journal of neurology·2026
Same author

Heads Up: Transcriptomics Reveal Functional Roles of Cannabis Glandular Trichome Stalks.

Plants (Basel, Switzerland)·2026
Same author

Weeding out variability: a proof-of-concept for producing uniform F<sub>1</sub> hybrid <i>Cannabis sativa</i> L. using single-seed descent.

Horticulture research·2026
Same author

Statins and genetic inhibition of the mevalonate pathway activate an ATF3-STMN2 regenerative program.

bioRxiv : the preprint server for biology·2026
Same author

Somatic mosaicism in ALS and FTD identifies focal mutations associated with widespread degeneration.

Nature genetics·2026

Related Experiment Video

Updated: Nov 22, 2025

Direct Restart of a Replication Fork Stalled by a Head-On RNA Polymerase
07:27

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

Published on: April 29, 2010

13.8K

Fanconi anemia and mTOR pathways functionally interact during stalled replication fork recovery.

Matthew Nolan1, Kenneth Knudson1, Marina K Holz2

  • 1University of Minnesota, Morris, MN, USA.

FEBS Letters
|January 10, 2021
PubMed
Summary

The mechanistic target of rapamycin (mTOR) pathway cooperates with Fanconi anemia (FA) proteins, including FANCD2, to restart stalled DNA replication forks and maintain genomic stability during replication stress.

Keywords:
DNA repairFanconi anemiamTORreplication restart

More Related Videos

Detection of Post-Replicative Gaps Accumulation and Repair in Human Cells Using the DNA Fiber Assay
10:32

Detection of Post-Replicative Gaps Accumulation and Repair in Human Cells Using the DNA Fiber Assay

Published on: February 3, 2022

7.1K
Intracellular Phosphoflow Cytometry of Acute Myeloid Leukemia Patient-Derived Xenotransplants
07:38

Intracellular Phosphoflow Cytometry of Acute Myeloid Leukemia Patient-Derived Xenotransplants

Published on: June 6, 2025

452

Related Experiment Videos

Last Updated: Nov 22, 2025

Direct Restart of a Replication Fork Stalled by a Head-On RNA Polymerase
07:27

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

Published on: April 29, 2010

13.8K
Detection of Post-Replicative Gaps Accumulation and Repair in Human Cells Using the DNA Fiber Assay
10:32

Detection of Post-Replicative Gaps Accumulation and Repair in Human Cells Using the DNA Fiber Assay

Published on: February 3, 2022

7.1K
Intracellular Phosphoflow Cytometry of Acute Myeloid Leukemia Patient-Derived Xenotransplants
07:38

Intracellular Phosphoflow Cytometry of Acute Myeloid Leukemia Patient-Derived Xenotransplants

Published on: June 6, 2025

452

Area of Science:

  • Molecular Biology
  • Genetics
  • Cellular Biology

Background:

  • Fanconi anemia (FA) proteins are crucial for DNA repair and replication fork restart.
  • Previous research indicates a link between the FA protein FANCD2 and the mechanistic target of rapamycin (mTOR) pathway.
  • The mTOR pathway is implicated in actin-dependent DNA replication fork restart.

Purpose of the Study:

  • To investigate the interaction and cooperation between mTOR and FANCD2 during replication stress.
  • To elucidate the role of this interaction in maintaining cellular stability and DNA repair.

Main Methods:

  • The study likely involved experiments to induce replication stress in cells.
  • Techniques to observe the interaction between mTOR and FANCD2 were employed.
  • Assays to measure DNA replication fork restart and nascent DNA strand degradation were performed.

Main Results:

  • mTOR interacts with and cooperates with FANCD2 during replication stress.
  • This interaction is essential for cellular stability and stalled replication fork restart.
  • The mTOR-FANCD2 cooperation prevents nucleolytic degradation of nascent DNA strands.

Conclusions:

  • A novel functional crosstalk exists between the mTOR and FA DNA repair pathways.
  • This crosstalk is vital for ensuring genomic stability.
  • The findings reveal a new mechanism for DNA replication fork maintenance.