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Related Concept Videos

Inhibition of Cdk Activity02:34

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...
Inhibition of CDK Activity02:34

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...
Anaphase Promoting Complex00:50

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...
Separation of Sister Chromatids02:17

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...
The Spindle Assembly Checkpoint02:19

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...
Positive Regulator Molecules02:39

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.

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Related Experiment Video

Updated: Jun 6, 2026

Protein Purification Technique that Allows Detection of Sumoylation and Ubiquitination of Budding Yeast Kinetochore Proteins Ndc10 and Ndc80
12:28

Protein Purification Technique that Allows Detection of Sumoylation and Ubiquitination of Budding Yeast Kinetochore Proteins Ndc10 and Ndc80

Published on: May 3, 2015

Cdk1 and SUMO regulate Swe1 stability.

Kobi J Simpson-Lavy1, Michael Brandeis

  • 1The Department of Genetics, The Silberman Institute of Life Sciences, The Hebrew University of Jerusalem, Jerusalem, Israel.

Plos One
|December 15, 2010
PubMed
Summary
This summary is machine-generated.

Budding yeast Swe1 protein levels are regulated by SUMOylation at K594, a modification critical for its timely degradation and proper cell cycle control. Impaired SUMOylation delays degradation, impacting cell cycle progression.

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Related Experiment Videos

Last Updated: Jun 6, 2026

Protein Purification Technique that Allows Detection of Sumoylation and Ubiquitination of Budding Yeast Kinetochore Proteins Ndc10 and Ndc80
12:28

Protein Purification Technique that Allows Detection of Sumoylation and Ubiquitination of Budding Yeast Kinetochore Proteins Ndc10 and Ndc80

Published on: May 3, 2015

In Vitro SUMOylation Assay to Study SUMO E3 Ligase Activity
09:45

In Vitro SUMOylation Assay to Study SUMO E3 Ligase Activity

Published on: January 29, 2018

In Vivo Detection and Analysis of Rb Protein SUMOylation in Human Cells
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In Vivo Detection and Analysis of Rb Protein SUMOylation in Human Cells

Published on: November 2, 2017

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Biochemistry

Background:

  • Swe1/Wee1 kinase is a key regulator of the cell cycle, inhibiting Cdk1-Clb2 and acting as a mitotic switch.
  • Swe1 protein levels are primarily controlled by ubiquitin-mediated degradation, influenced by interactions with mitotic kinases.
  • Previous work demonstrated Swe1's ability to sense cell cycle progression via Cdk1-Clb2, Cdc5, and Hsl1 levels.

Purpose of the Study:

  • To investigate a novel mechanism regulating Swe1 protein levels.
  • To elucidate the role of post-translational modifications in Swe1 stability and function.
  • To understand how Swe1 degradation is controlled during the cell cycle.

Main Methods:

  • Site-directed mutagenesis to create the swe1(K594R) mutant.
  • Analysis of Swe1 protein levels and activity in wild-type and mutant yeast strains.
  • SUMOylation assays using Siz1 SUMO ligase.
  • Cellular localization studies using microscopy.
  • Sensitivity assays to osmotic stress.

Main Results:

  • Saccharomyces cerevisiae Swe1 is modified by Smt3/SUMOylation at residue K594 in a Cdk1-dependent manner.
  • The swe1(K594R) mutant, unable to be SUMOylated, exhibits significantly delayed degradation compared to wild-type Swe1.
  • Cells expressing the swe1(K594R) mutant show elevated Swe1 protein levels and activity, indicated by increased Cdk1-Y19 phosphorylation.
  • The K594R mutant is mislocalized and not targeted to the bud neck, the site of wild-type Swe1 degradation.
  • Deletion of the Siz1 SUMO ligase gene (siz1Δ) results in elevated Swe1 protein levels and activity.
  • The swe1(K594R) mutant displays sensitivity to osmotic stress, correlating with its impaired Swe1 degradation regulation.

Conclusions:

  • SUMOylation of Swe1 at K594 by Siz1 is a novel regulatory mechanism controlling its stability and degradation.
  • This SUMOylation event is crucial for targeting Swe1 to the bud neck for degradation, ensuring proper cell cycle progression.
  • Disruption of Swe1 SUMOylation leads to increased Swe1 activity and sensitivity to cellular stress, highlighting the importance of regulated degradation.