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

5.8K
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,...
5.8K
Homologous Recombination02:31

Homologous Recombination

50.6K
The basic reaction of homologous recombination (HR) involves two chromatids that contain DNA sequences sharing a significant stretch of identity. One of these sequences uses a strand from another as a template to synthesize DNA in an enzyme-catalyzed reaction. The final product is a novel amalgamation of the two substrates. To ensure an accurate recombination of sequences, HR is restricted to the S and G2 phases of the cell cycle. At these stages, the DNA has been replicated already and the...
50.6K
DNA Damage can Stall the Cell Cycle02:37

DNA Damage can Stall the Cell Cycle

9.2K
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...
9.2K
Nucleotide Excision Repair01:08

Nucleotide Excision Repair

37.1K
Overview
37.1K
Fixing Double-strand Breaks02:04

Fixing Double-strand Breaks

12.6K
The double-stranded structure of DNA has two major advantages. First, it serves as a safe repository of genetic information where one strand serves as the back-up in case the other strand is damaged. Second, the double-helical structure can be wrapped around proteins called histones to form nucleosomes, which can then be tightly wound to form chromosomes. This way, DNA chains up to 2 inches long can be contained within microscopic structures in a cell. A double-stranded break not only damages...
12.6K
Base Excision Repair01:54

Base Excision Repair

22.4K
One of the common DNA damages is the chemical alteration of single bases by alkylation, oxidation, or deamination. The altered bases cause mispairing and strand breakage during replication. This type of damage causes minimal change to the DNA double helix structure and can be repaired by the base excision repair (BER) pathways. BER corrects damaged DNA sequences by removing the damaged base and restoring the original base sequence using the complementary strand as a template.
The first step of...
22.4K

You might also read

Related Articles

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

Sort by
Same author

Targeting of Gpx8-CSF1 axis resets the immune milieu of lung tumor and overcomes resistance to anti-PD-1 therapy.

Cell death and differentiation·2026
Same author

[Forensic Identification of Unilateral Separated Hyoid Bone Misdiagnosed as Hyoid Bone Fracture： A Case Report].

Fa yi xue za zhi·2026
Same author

Psychological resilience mediates associations between stress related factors and short video addiction among university students.

Scientific reports·2026
Same author

Deciphering O‑GlcNAc-Dependent Signaling Via Integrated Proteomics and Phosphoproteomics.

ACS omega·2026
Same author

Case report: Whole-exome sequencing reveals a novel variant in a patient with epilepsy presenting with fever.

Frontiers in genetics·2026
Same author

Multifaceted roles of PDS5B in RAD51-dependent homology-directed DNA repair and replication fork protection.

Nature communications·2026

Related Experiment Video

Updated: Jul 6, 2025

Visualization of DNA Repair Proteins Interaction by Immunofluorescence
07:55

Visualization of DNA Repair Proteins Interaction by Immunofluorescence

Published on: June 26, 2020

10.2K

The FANCI/FANCD2 complex links DNA damage response to R-loop regulation through SRSF1-mediated mRNA export.

Anne Olazabal-Herrero1, Boxue He2, Youngho Kwon3

  • 1Department of Oncology and Pediatrics, Lombardi Comprehensive Cancer Center, Georgetown University, Washington, DC 20057, USA; Section of Hematology, Department of Internal Medicine, Yale School of Medicine and Yale Cancer Center, New Haven, CT 06511, USA.

Cell Reports
|January 2, 2024
PubMed
Summary

The splicing factor SRSF1 and FANCD2 protein work together to prevent harmful R-loop buildup by regulating mRNA export. This interaction is vital for maintaining genomic stability in Fanconi anemia (FA).

Keywords:
CP: Molecular biologyDNA damageFANCD2NXF1R-loopsRNASRSF1mRNA exportmonoubiquitination

More Related Videos

Assessment of Global DNA Double-Strand End Resection using BrdU-DNA Labeling coupled with Cell Cycle Discrimination Imaging
06:44

Assessment of Global DNA Double-Strand End Resection using BrdU-DNA Labeling coupled with Cell Cycle Discrimination Imaging

Published on: April 28, 2021

4.0K
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

10.3K

Related Experiment Videos

Last Updated: Jul 6, 2025

Visualization of DNA Repair Proteins Interaction by Immunofluorescence
07:55

Visualization of DNA Repair Proteins Interaction by Immunofluorescence

Published on: June 26, 2020

10.2K
Assessment of Global DNA Double-Strand End Resection using BrdU-DNA Labeling coupled with Cell Cycle Discrimination Imaging
06:44

Assessment of Global DNA Double-Strand End Resection using BrdU-DNA Labeling coupled with Cell Cycle Discrimination Imaging

Published on: April 28, 2021

4.0K
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

10.3K

Area of Science:

  • Molecular Biology
  • Genetics
  • Cancer Research

Background:

  • Fanconi anemia (FA) involves DNA repair defects, leading to genomic instability and cancer susceptibility.
  • The FANCI/FANCD2 (ID2) complex is central to DNA repair and replication fork protection.
  • R-loop accumulation is a consequence of FA pathway defects and contributes to genomic instability.

Purpose of the Study:

  • To investigate the interaction between splicing factor SRSF1 and FANCD2 in regulating R-loop formation.
  • To elucidate the role of SRSF1 and FANCD2 in mRNA export and its connection to genomic stability.

Main Methods:

  • Co-immunoprecipitation to assess physical interaction between SRSF1 and FANCD2.
  • Western blotting to detect FANCD2 monoubiquitination.
  • RNA immunoprecipitation and mRNA export assays.
  • Analysis of R-loop accumulation in cells with SRSF1 mutations.

Main Results:

  • SRSF1 and FANCD2 physically interact and cooperate to suppress R-loop formation.
  • SRSF1 enhances FANCD2 monoubiquitination in an RNA-dependent manner.
  • FANCD2 monoubiquitination is essential for SRSF1-NXF1 complex assembly and mRNA export.
  • Cancer-associated SRSF1 mutants show impaired interaction with FANCD2, leading to reduced mRNA export and increased R-loops.

Conclusions:

  • SRSF1 and FANCD2 interaction links DNA damage response to R-loop avoidance through mRNA export regulation.
  • This pathway is critical for maintaining genomic integrity, particularly in the context of Fanconi anemia and cancer.