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Related Concept Videos

M-Cdk Drives Transition Into Mitosis02:15

M-Cdk Drives Transition Into Mitosis

Checkpoints throughout the cell cycle serve as safeguards and gatekeepers, allowing the cell cycle to progress in favorable conditions and slow or halt it in problematic ones. This regulation is known as the cell cycle control system.
Cyclin-dependent kinases, or Cdks, work in concert with cyclins to control cell cycle transitions. M-Cdk, a complex of Cdk1 bound to M cyclin, is a well-known example of this coordinated control that drives the transition from the G2 to the M phase.
M cyclin...
M-Cdk Drives Transition Into Mitosis02:15

M-Cdk Drives Transition Into Mitosis

Checkpoints throughout the cell cycle serve as safeguards and gatekeepers, allowing the cell cycle to progress in favorable conditions and slow or halt it in problematic ones. This regulation is known as the cell cycle control system.
Cyclin-dependent kinases, or Cdks, work in concert with cyclins to control cell cycle transitions. M-Cdk, a complex of Cdk1 bound to M cyclin, is a well-known example of this coordinated control that drives the transition from the G2 to the M phase.
M cyclin...
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...
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.
Positive Regulator Molecules01:45

Positive Regulator Molecules

To consistently produce healthy cells, the cell cycle—the process that generates daughter cells—must be precisely regulated.

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Related Experiment Video

Updated: May 20, 2026

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

Cdk1-dependent control of membrane-trafficking dynamics.

Derek McCusker1, Anne Royou, Christophe Velours

  • 1European Institute of Chemistry and Biology, 33607 Pessac, France.

Molecular Biology of the Cell
|July 7, 2012
PubMed
Summary

This study explores how Cdk1, a key cell cycle regulator, influences membrane trafficking in yeast. While Cdk1 is known to activate proteins that guide cell growth, the researchers found that Cdk1 inhibition leads to growth defects similar to those seen when actin is disrupted. However, unlike actin disruption, Cdk1 inhibition does not cause a buildup of vesicles inside the cell. Instead, exocytic vesicles are redirected away from the growing bud, possibly to the vacuolar system. Additionally, Cdk1 inhibition disrupts the organization of endocytic and exocytic zones at the growth site. These findings suggest that Cdk1 modulates membrane trafficking dynamics, likely to coordinate cell surface growth with the cell cycle.

Keywords:
Cdk1 function in yeastMembrane trafficking regulationCell cycle coordinationBudding yeast growth mechanisms

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Identification of Cyclin-dependent Kinase 1 Specific Phosphorylation Sites by an In Vitro Kinase Assay
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Experimental Approaches to Study Mitochondrial Localization and Function of a Nuclear Cell Cycle Kinase, Cdk1
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Last Updated: May 20, 2026

Combining Mitotic Cell Synchronization and High Resolution Confocal Microscopy to Study the Role of Multifunctional Cell Cycle Proteins During Mitosis
08:33

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

Identification of Cyclin-dependent Kinase 1 Specific Phosphorylation Sites by an In Vitro Kinase Assay
12:26

Identification of Cyclin-dependent Kinase 1 Specific Phosphorylation Sites by an In Vitro Kinase Assay

Published on: May 3, 2018

Experimental Approaches to Study Mitochondrial Localization and Function of a Nuclear Cell Cycle Kinase, Cdk1
13:15

Experimental Approaches to Study Mitochondrial Localization and Function of a Nuclear Cell Cycle Kinase, Cdk1

Published on: February 25, 2016

Area of Science:

  • Cell cycle regulation in yeast biology
  • Membrane trafficking in cell biology
  • Cytoskeletal dynamics in developmental biology

Background:

Polarized cell growth in budding yeast relies on precise coordination of membrane trafficking and cytoskeletal organization. Prior research has shown that Cdk1 activates Rho-family GTPases, which in turn regulate actin cytoskeleton polarization to guide membrane delivery to growth sites. However, the extent of Cdk1's role in membrane trafficking remains unclear. This gap motivated a closer examination of Cdk1's influence beyond its known functions. Established knowledge includes the role of Rho GTPases in actin organization and vesicle targeting. Yet, no prior work had resolved whether Cdk1 directly modulates vesicle dynamics. The secretory pathway's reliance on actin is well-documented, but its interplay with Cdk1 is less understood. This study addresses whether Cdk1 contributes to membrane trafficking beyond GTPase activation. The findings may clarify how cell cycle regulators coordinate growth with trafficking events.

Purpose Of The Study:

The aim of this work is to determine whether Cdk1 has roles in membrane trafficking beyond its activation of Rho-family GTPases. The specific problem involves understanding how Cdk1 inhibition affects polarized growth and vesicle dynamics. The motivation stems from the observation that Cdk1 is essential for growth initiation but its broader trafficking functions remain unexplored. The study tests whether Cdk1 inhibition leads to trafficking defects similar to those caused by actin disruption. The research focuses on whether Cdk1's effects are limited to GTPase activation or extend to vesicle targeting. The goal is to assess the direct role of Cdk1 in membrane trafficking dynamics. The study also examines how Cdk1 inhibition impacts endocytic and exocytic zones. The findings may reveal how Cdk1 coordinates trafficking with growth and cell cycle progression.

Main Methods:

The study uses budding yeast as a model system to investigate Cdk1's role in membrane trafficking. Cdk1 inhibition is achieved through pharmacological agents or genetic manipulation. Membrane trafficking is monitored using fluorescent markers for vesicles and growth sites. Actin depolymerization is used as a control to compare trafficking defects. Post-Golgi vesicle dynamics are tracked to assess targeting accuracy. Endocytic and exocytic zones are analyzed for structural organization. The researchers employ live-cell imaging to observe vesicle behavior in real time. Quantitative analysis includes measuring vesicle accumulation and mistargeting events.

Main Results:

Cdk1 inhibition leads to severe cell surface growth defects, comparable to actin depolymerization. However, unlike actin disruption, Cdk1 inhibition does not cause intracellular vesicle accumulation. Instead, exocytic vesicles are rapidly mistargeted away from the growing bud. The misdirected vesicles appear to be redirected toward the endomembrane or vacuolar system. Endocytic and exocytic zones at the growth site show disorganization after Cdk1 inhibition. These findings suggest that Cdk1 modulates trafficking dynamics beyond GTPase activation. The mistargeting effect is distinct from actin-related trafficking defects. The results indicate that Cdk1 coordinates membrane trafficking with growth progression.

Conclusions:

The authors propose that Cdk1 modulates membrane trafficking dynamics, which is likely important for coordinating growth with the cell cycle. Their findings suggest that Cdk1's role extends beyond activating Rho-family GTPases. The study shows that Cdk1 inhibition causes trafficking defects distinct from actin disruption. The mistargeting of vesicles to endomembrane or vacuolar regions is a novel observation. The disorganization of endocytic and exocytic zones supports this conclusion. The researchers suggest that Cdk1's trafficking effects are essential for growth coordination. These findings may inform future studies on cell cycle-trafficking interactions. The authors do not propose broader implications beyond their stated claims.

Cdk1 inhibition causes vesicle mistargeting and growth defects, distinct from actin disruption effects.

Exocytic vesicles are rapidly redirected away from the growing bud toward endomembrane/vacuolar regions.

To compare trafficking defects caused by Cdk1 inhibition with those from actin disruption.

Cdk1 inhibition disrupts organization of endocytic and exocytic zones at growth sites.

Mistargeting suggests Cdk1 modulates trafficking dynamics to coordinate growth with the cell cycle.

They suggest Cdk1 modulates membrane trafficking dynamics to coordinate growth with cell cycle progression.