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Related Concept Videos

Positive Regulator Molecules01:45

Positive Regulator Molecules

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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 biological clock is involved in many aspects of regulating complex physiology in all animals. It was in 1935 when German zoologists, Hans Kalmus and Erwin Bünning, discovered the existence of circadian rhythm in Drosophila melanogaster. However, the internal molecular mechanisms behind the circadian clock remained a mystery until 1984, when Jeffrey C. Hall, Michael Rosbash, and Michael W. Young discovered the expression of the Per gene oscillating over a 24-hour cycle. In subsequent...
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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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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.
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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.
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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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Related Experiment Video

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Studying Cell Cycle-regulated Gene Expression by Two Complementary Cell Synchronization Protocols
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Synchronization of MEL cell commitment with cordycepin.

R Levenson, J Kernen, D Housman

    Cell
    |December 1, 1979
    PubMed
    Summary

    Cordycepin, a nucleotide analogue, blocks erythroid differentiation in mouse erythroleukemia (MEL) cells. This finding reveals a new molecular mechanism controlling cell commitment to terminal differentiation.

    Area of Science:

    • * Molecular biology
    • * Cell differentiation
    • * Cancer research

    Background:

    • * Mouse erythroleukemia (MEL) cells are a model system for studying erythroid differentiation.
    • * Commitment to terminal differentiation involves complex molecular events.
    • * Nucleotide analogues can modulate cellular processes.

    Purpose of the Study:

    • * To investigate the effect of cordycepin on MEL cell differentiation.
    • * To identify the role of cordycepin in the molecular events of erythroid commitment.
    • * To explore cordycepin's potential to block differentiation at a specific stage.

    Main Methods:

    • * Treatment of differentiating MEL cells with varying doses of cordycepin.
    • * Assessment of cell commitment and cytotoxicity.

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  • * Reversal experiments with cordycepin in the presence of an inducer.

    • Main Results:

    • * Cordycepin rapidly inhibits MEL cell commitment to erythroid differentiation.
    • * Inhibition occurs at non-cytotoxic doses.
    • * Reversal of cordycepin treatment allows for rapid and synchronous cell commitment.

    Conclusions:

    • * Cordycepin uncovers a previously unrecognized aspect of erythroid differentiation commitment.
    • * MEL cells can be arrested just before commitment by cordycepin.
    • * Cordycepin offers a tool to study the precise molecular timing of cell fate decisions.