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Related Concept Videos

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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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To consistently produce healthy cells, the cell cycle—the process that generates daughter cells—must be precisely regulated.
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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...
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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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The cell cycle regulation directs how a cell proceeds from one phase to the next and begins mitosis. The cell cycle control system includes intracellular regulatory molecules and external triggers. They provide "stop" or "advance" signals and operate at specific cell cycle stages termed checkpoints to ensure that a particular process is completed before the cell advances to the next phase.
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Related Experiment Video

Updated: Dec 13, 2025

Identification of Cyclin-dependent Kinase 1 Specific Phosphorylation Sites by an In Vitro Kinase Assay
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Evolutionarily Conserved Roles for Apontic in Induction and Subsequent Decline of Cyclin E Expression.

Xian-Feng Wang1, Jin-Xiao Liu2, Zhi-Yuan Ma2

  • 1Department of Gene Function and Phenomics, National Institute of Genetics, 1111 Yata, Mishima City, Shizuoka 411-8540, Japan; State Key Laboratory of Crop Biology, College of Life Sciences, Shandong Agricultural University, Tai'an, Shandong 271018, China.

Iscience
|August 1, 2020
PubMed
Summary

Transcription factors Apontic (Apt) and E2f1 control cyclin E expression crucial for cell cycle progression. Apt also regulates Rbf1, impacting chromatin and cyclin E repression, a conserved mechanism.

Keywords:
Biological SciencesCell BiologyMolecular Biology

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Area of Science:

  • Cell Biology
  • Developmental Biology
  • Genetics

Background:

  • Cyclin E is essential for initiating S phase, a critical step in the cell cycle.
  • Dysregulation of Cyclin E is linked to developmental abnormalities and cancer formation.
  • Precise control of Cyclin E levels is vital for normal organismal growth and development.

Purpose of the Study:

  • To elucidate the regulatory mechanisms governing Cyclin E expression in Drosophila.
  • To identify the specific transcription factors involved in Cyclin E induction.
  • To investigate the role of Apontic (Apt) in regulating Cyclin E and associated factors.

Main Methods:

  • Identification of transcription factor binding sites within the Drosophila cyclin E gene.
  • Gene knockout experiments to assess the function of Apontic (Apt) and E2f1.
  • Analysis of Cyclin E and Retinoblastoma family protein 1 (Rbf1) expression levels.
  • Comparative studies in mammalian cells to assess evolutionary conservation.

Main Results:

  • Apontic (Apt) and E2f1 transcription factors bind to motifs in the first intron of Drosophila cyclin E, directly driving its transcription.
  • Simultaneous knockout of apt and e2f1 genes completely abrogated Cyclin E expression.
  • Apt up-regulates Retinoblastoma family protein 1 (Rbf1), which contributes to chromatin compaction and repression of cyclin E.
  • The regulatory roles of Apt in controlling Cyclin E and Rbf1 are conserved in mammalian cells.

Conclusions:

  • Apt and E2f1 act in concert to induce cyclin E transcription in Drosophila.
  • Apt employs a dual mechanism involving direct cyclin E induction and indirect repression via Rbf1.
  • This intricate regulatory network ensures proper Cyclin E dynamics, essential for cell cycle control and development.
  • The evolutionary conservation highlights the fundamental importance of this pathway across species.