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Related Experiment Videos

APC/C--the master controller of origin licensing?

Umasundari Sivaprasad1, Yuichi J Machida, Anindya Dutta

  • 1Department of Biochemistry and Molecular Genetics, University of Virginia School of Medicine, Charlottesville, VA 22908, USA. us6n@virginia.edu

Cell Division
|February 27, 2007
PubMed
Summary

The anaphase-promoting complex/cyclosome (APC/C) inhibitor Emi1 prevents DNA replication errors. Depleting Emi1 caused cells to replicate DNA more than once, highlighting Emi1

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Area of Science:

  • Molecular Biology
  • Cell Cycle Regulation
  • Genetics

Background:

  • DNA replication requires strict cell cycle control to prevent re-replication before mitosis completion.
  • Pre-replicative complex (Cdt1, Cdc6, geminin) components were thought to be the primary regulators.
  • The anaphase-promoting complex/cyclosome (APC/C) activity oscillates during the cell cycle, influencing pre-replicative complex formation.

Purpose of the Study:

  • To investigate the role of Emi1 in preventing DNA re-replication.
  • To understand how Emi1 regulates APC/C activity in the context of replication control.
  • To explore the broader implications of APC/C regulation in endoreduplication and genomic instability.

Main Methods:

  • Depletion of Emi1 in cellular models.

Related Experiment Videos

  • Analysis of DNA replication frequency per cell cycle.
  • Assessment of APC/C inhibition by Emi1.
  • Literature review on APC/C and endoreduplication/genomic instability.

    • Main Results:

    • Depletion of Emi1 led to multiple rounds of DNA replication within a single cell cycle.
    • This re-replication phenotype was dependent on Emi1's ability to inhibit the APC/C.
    • Emi1 co-regulates multiple pathways preventing re-replication by controlling APC/C activity.

    Conclusions:

    • Emi1 plays a crucial role in preventing DNA re-replication by inhibiting the APC/C.
    • APC/C activity oscillation is critical for preventing re-replication, with Emi1 as a key regulator.
    • Dysregulation of APC/C by premature activation may contribute to genomic instability in tumors.