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 Experiment Videos

A replication model for sister-chromatid exchange

R B Painter

    Mutation Research
    |May 1, 1980
    PubMed
    Summary
    This summary is machine-generated.

    This study presents a model for sister-chromatid exchanges, proposing double-strand breaks at replication junctions initiate the process. DNA replication blocks influence exchange persistence, impacting genetic stability.

    Related Concept Videos

    You might also read

    Related Articles

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

    Sort by
    Same author

    A Mode of Preventing Pitting in Small-Pox.

    Buffalo medical and surgical journal·2023
    Same author

    Genetic discrimination in health insurance: an overview and analysis of the issues.

    The Nursing clinics of North America·2000
    Same author

    Cloning of a candidate gene for ataxia-telangiectasia group D.

    American journal of human genetics·1992
    Same author

    Replication intermediates as substrates for DNA rearrangements.

    Mutation research·1991
    Same author

    Modification of deoxyribose-phosphate residues by extracts of ataxia telangiectasia cells.

    Mutation research·1990
    Same author

    On tritium, DNA, and serendipity.

    Radiation research·1990
    Same journal

    Monoallelic germline RAD51C, RAD51D, and BRIP1 variants in hereditary cancer testing: Variant spectrum and clinical counselling implications.

    Mutation research·2026
    Same journal

    Prediction of hepatocellular carcinoma associated biomarkers in TP53 gene; A comprehensive in silico analysis.

    Mutation research·2026
    Same journal

    IDH1 mutation promotes angiogenesis via upregulation of hypoxia inducible factor 1 alpha in glial tumors.

    Mutation research·2026
    Same journal

    Targeting overexpressed oncogenes in esophageal cancer through miRNA-mediated gene silencing: Insights from binding affinity and thermodynamic profiling.

    Mutation research·2026
    Same journal

    The active compound quercetin from Polygonum cuspidatum targets COL3A1 to enhance CD8⁺ T cell cytotoxicity in gastric cancer.

    Mutation research·2026
    Same journal

    E2F1 promotes LIHC malignant phenotype via NEK2-mediated Wnt/β-catenin and Notch activation and EMT.

    Mutation research·2026
    See all related articles

    Area of Science:

    • Molecular Biology
    • Genetics
    • Cell Biology

    Background:

    • Sister-chromatid exchanges (SCEs) are crucial for DNA repair and genetic diversity.
    • Understanding the precise molecular mechanisms underlying SCE formation is essential.

    Purpose of the Study:

    • To propose a novel model for the production of sister-chromatid exchanges.
    • To elucidate the role of DNA replication dynamics and double-strand breaks in SCEs.

    Main Methods:

    • Theoretical modeling of DNA replication.
    • Analysis of double-strand break generation at replication forks.
    • Investigating the impact of replication inhibitors on SCEs.

    Main Results:

    • A model where double-strand breaks at junctions between fully and partially duplicated replicon clusters initiate SCEs.

    Related Experiment Videos

  • Agents blocking DNA fork displacement prolong the condition for SCE initiation.
  • Agents inhibiting cluster initiation have minimal impact on SCE formation.

    • Conclusions:

    • The proposed model provides a mechanistic explanation for sister-chromatid exchange formation.
    • Replication fork dynamics and double-strand break repair are key determinants of SCEs.
    • This model aids in understanding the cellular response to DNA replication stress.