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Inhibition of Cdk Activity

Inhibition of Cdk Activity

The orderly progression of the cell cycle depends on the activation of Cdk protein by binding to its cyclin partner. However, the cell cycle must be restricted when undergoing abnormal changes. Most cancers correlate to the deregulated cell cycle, and since Cdks are a central component of the cell cycle, Cdk inhibitors are extensively studied to develop anticancer agents. For instance, cyclin D associates with several Cdks, such as Cdk 4/6, to form an active complex. The cyclin D-Cdk4/6 complex...

Separation of Sister Chromatids

Separation of Sister Chromatids

At the transition from prophase to metaphase, there is a reduction in cohesion along the chromosomal arms, resulting in the resolution of sister chromatids. However, residual cohesin connections remain to hold the sister chromatids together until the transition from metaphase to anaphase. The residual connection prevents any premature separation of sister chromatids, blocking the risks of aneuploidy within the daughter cells.
At the onset of anaphase, separase, a proteolytic enzyme, is...

Positive Regulator Molecules

Positive Regulator Molecules

Mitotic cell division results in daughter cells that exactly resemble the parent cell. However, errors in the DNA replication or distribution of genetic material may lead to genetic mutations that may be passed down to every new cell formed from the resulting abnormal cell. Propagation of such mutant cells is restricted through checkpoint mechanisms present at different stages of the cell cycle. These checkpoints involve regulator molecules that either promote or demote cell cycle events.

Anaphase Promoting Complex

Anaphase Promoting Complex

The stepwise destruction of specific proteins is necessary for the progression and completion of the cell cycle. Such proteins are ubiquitinated by ubiquitin ligases and then subsequently destroyed by the proteasome. The SCF (Skp1/Cullin/F-box) and the anaphase-promoting complex (APC) are two important ubiquitin ligases involved in cell cycle progression. While SCF is active throughout the cell cycle, APC gets activated during metaphase to anaphase transition. Cdc20 or Cdh1 binds to APC and...

Negative Regulator Molecules

Negative Regulator Molecules

Positive regulators allow a cell to advance through cell cycle checkpoints. Negative regulators have an equally important role as they terminate a cell’s progression through the cell cycle—or pause it—until the cell meets specific criteria.

The Spindle Assembly Checkpoint

The Spindle Assembly Checkpoint

The spindle assembly checkpoint is a molecular surveillance mechanism ensuring the fidelity of chromosome segregation during anaphase. The checkpoint monitors the completion of all the prerequisite steps before chromosome segregation to determine whether the segregation process should proceed or be delayed.
Many proteins function together to control the spindle assembly checkpoint. Mutations affecting these proteins may allow cells to proceed into anaphase prematurely, resulting in the...

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Related Experiment Video

Updated: Aug 1, 2025

Combining Mitotic Cell Synchronization and High Resolution Confocal Microscopy to Study the Role of Multifunctional Cell Cycle Proteins During Mitosis

Combining Mitotic Cell Synchronization and High Resolution Confocal Microscopy to Study the Role of Multifunctional Cell Cycle Proteins During Mitosis

Published on: December 5, 2017

Alternative CDC20 translational isoforms tune mitotic arrest duration.

Mary-Jane Tsang^1,2, Iain M Cheeseman^3,4

¹Whitehead Institute for Biomedical Research, Cambridge, MA, USA.

|April 26, 2023

Summary

Cells balance mitotic arrest and slippage using CDC20 protein isoforms. A truncated CDC20 isoform bypasses checkpoint control, promoting cell cycle exit and impacting cancer treatment sensitivity.

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Published on: May 14, 2016

Area of Science:

Cell Biology
Molecular Biology
Cancer Research

Background:

Mitotic errors trigger the spindle-assembly checkpoint (SAC), inhibiting CDC20 and causing cell cycle arrest.
Persistent errors can lead to mitotic slippage, where cells exit mitosis into a tetraploid state, avoiding cell death.

Purpose of the Study:

To elucidate the molecular mechanisms balancing mitotic arrest and slippage.
To investigate the role of CDC20 translational isoforms in regulating mitotic duration.

Main Methods:

Analysis of conserved, alternative CDC20 translational isoforms in human cells.
Investigating the impact of these isoforms on SAC-mediated inhibition and mitotic exit.
Modeling the role of isoform ratios and turnover in controlling mitotic arrest duration.

Main Results:

Identified alternative CDC20 translational isoforms that modulate mitotic arrest duration.
A truncated CDC20 isoform is resistant to SAC inhibition, promoting mitotic exit.
Relative levels of CDC20 isoforms act as a timer for mitotic exit, with the truncated Met43 isoform being key.

Conclusions:

The balance between mitotic arrest and slippage is controlled by CDC20 translational isoform ratios.
Alterations in CDC20 isoform levels or their translational control impact anti-mitotic drug sensitivity.
Findings have implications for cancer diagnosis and therapeutic strategies.