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

Geminin prevents rereplication during xenopus development.

Sarah L Kerns1, Susanna J Torke, Jacqueline M Benjamin

  • 1Division of Cardiology, Department of Cell and Molecular Biology, and Feinberg Cardiovascular Research Institute, Feinberg School of Medicine, Northwestern University, Chicago, Illinois 60611, USA.

The Journal of Biological Chemistry
|December 21, 2006
PubMed
Summary
This summary is machine-generated.

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

LANTERN: Leveraging Local Ancestry Tracts to Enhance Rare-Variant Aggregate Association Testing.

medRxiv : the preprint server for health sciences·2026
Same author

Genetic determinants of fatigue up to 2 years after radiotherapy in prostate cancer patients.

Nature communications·2026
Same author

Renal Impairment and Late Toxicities Comparing Contemporary Chemotherapy Regimens for Testicular Cancer in a Real-World Setting.

Journal of the National Comprehensive Cancer Network : JNCCN·2026
Same author

Cardiovascular disease risk among long-term testicular cancer survivors following contemporary cisplatin-based chemotherapy.

Journal of the National Cancer Institute·2026
Same author

Association of Genetic Predisposition to Inflammation With Cancer-Related Cognitive Impairment and Fatigue in Women Who Received Chemotherapy for Nonmetastatic Breast Cancer.

JCO precision oncology·2025
Same author

Extracellular vesicle proteomics identify neutrophils as potential mediators of bladder radiotoxicity in prostate cancer.

Cancer letters·2025
Same journal

Wanted and unwanted modifications of mRNA, and their effect on gene expression and signaling.

The Journal of biological chemistry·2026
Same journal

TGF-β2 drives lipid droplet accumulation in chondrocytes through the TβRI/p-Smad3/Fabp5 axis.

The Journal of biological chemistry·2026
Same journal

Macrophage-specific targeting of histone demethylases with small-molecule inhibitors suppresses inflammatory response in vivo.

The Journal of biological chemistry·2026
Same journal

Substrate and target selectivity of 4'-fluoroadenosine against viral and host polymerases.

The Journal of biological chemistry·2026
Same journal

Correction: Characterization of Mast2 kinase defines structural features, regulation, and substrates.

The Journal of biological chemistry·2026
Same journal

Isotope-Edited ESEEM: A New Method for Probing Copper Binding Sites in Neurodegenerative Proteins.

The Journal of biological chemistry·2026
See all related articles

Geminin protein prevents DNA replication origins from firing more than once per cell cycle. Geminin depletion causes embryonic lethality by disrupting Cdt1 regulation, leading to abnormal DNA replication.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Developmental Biology

Background:

  • Maintaining genomic stability requires cell cycle regulation, specifically ensuring DNA replication origins fire only once.
  • Geminin is a protein that inhibits Cdt1, an essential replication factor, to prevent re-replication.
  • The precise role of Geminin in preventing embryonic defects, whether through controlling replication or affecting cell differentiation, remains unclear.

Purpose of the Study:

  • To investigate the role of Geminin in preventing a second round of DNA replication during the cell cycle.
  • To determine if Geminin depletion phenotypes in Xenopus embryos are caused by DNA overreplication or effects on cell differentiation.

Main Methods:

  • Utilized Xenopus embryos and replication extracts to study Geminin and Cdt1 interactions.

Related Experiment Videos

  • Expressed non-Geminin-binding and non-degradable Cdt1 mutants in embryos and cell extracts.
  • Analyzed cell cycle progression and DNA replication patterns.

    • Main Results:

    • Expressing a Cdt1 mutant that cannot bind Geminin in Xenopus embryos replicated the phenotype of geminin depletion.
    • This Cdt1 mutant induced a partial second round of DNA replication in vitro.
    • A non-degradable Cdt1 mutant also reproduced the geminin-deficient phenotype and augmented rereplication when Geminin was depleted.

    Conclusions:

    • Geminin is essential for suppressing a second round of DNA replication in vivo.
    • The embryonic phenotype of Geminin depletion is due to aberrant Cdt1 regulation.
    • Cdt1 activity is regulated through both Geminin binding and protein degradation pathways.