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Related Concept Videos

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.
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...
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...
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...

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Related Experiment Video

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Studying Proteolysis of Cyclin B at the Single Cell Level in Whole Cell Populations
10:54

Studying Proteolysis of Cyclin B at the Single Cell Level in Whole Cell Populations

Published on: September 17, 2012

Protein aggregation behavior regulates cyclin transcript localization and cell-cycle control.

Changhwan Lee1, Huaiying Zhang, Amy E Baker

  • 1Department of Biological Sciences, Dartmouth College, Hanover, NH 03755, USA.

Developmental Cell
|June 18, 2013
PubMed
Summary
This summary is machine-generated.

Specific G1 cyclin transcripts cluster in multinucleate cells, controlled by an RNA-binding protein. This localization synchronizes cell-cycle timing by reducing mRNA differences between nuclei.

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Related Experiment Videos

Last Updated: May 10, 2026

Studying Proteolysis of Cyclin B at the Single Cell Level in Whole Cell Populations
10:54

Studying Proteolysis of Cyclin B at the Single Cell Level in Whole Cell Populations

Published on: September 17, 2012

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

4D Imaging of Protein Aggregation in Live Cells
08:59

4D Imaging of Protein Aggregation in Live Cells

Published on: April 5, 2013

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Genetics

Background:

  • Active transcript localization is poorly understood outside of early development and specialized cells.
  • Multinucleate cells exhibit asynchronous nuclear cycling within a shared cytoplasm, presenting a unique model for cell cycle regulation.

Purpose of the Study:

  • To investigate the mechanism and function of cytoplasmic transcript localization in multinucleate cells.
  • To determine the role of RNA-binding proteins and specific protein domains in transcript positioning.
  • To understand how transcript localization influences cell cycle synchrony.

Main Methods:

  • Utilized live-cell imaging to observe G1 cyclin transcript localization in multinucleate cells.
  • Employed genetic manipulation to delete a polyglutamine (polyQ) stretch in a key RNA-binding protein.
  • Quantified mRNA levels and cell cycle progression across asynchronous nuclei.

Main Results:

  • Identified heterogeneous, clustered localization of a specific G1 cyclin transcript in the cytoplasm.
  • Demonstrated that aggregation of an RNA-binding protein drives this transcript clustering.
  • Showed that deletion of the polyQ stretch in the RNA-binding protein leads to random transcript distribution.
  • Observed that randomizing transcript localization synchronizes cell cycle timing and reduces nuclear mRNA variability.

Conclusions:

  • Nonrandom G1 cyclin transcript localization is crucial for regulating asynchronous cell cycle timing in multinucleate cells.
  • The polyQ-dependent behavior of RNA-binding proteins is a key mechanism for achieving spatially variable transcripts.
  • This mechanism may be broadly utilized, given the association between polyQ expansions and RNA-binding motifs, to generate cellular heterogeneity.