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Related Concept Videos

DNA Damage can Stall the Cell Cycle02:36

DNA Damage can Stall the Cell Cycle

In response to DNA damage, cells can pause the cell cycle to assess and repair the breaks. However, the cell must check the DNA at certain critical stages during the cell cycle. If the cell cycle pauses before DNA replication, the cells will contain twice the amount of DNA. On the other hand, if cells arrest after DNA replication but before mitosis, they will contain four times the normal amount of DNA. With a host of specialized proteins at their disposal,cells must use the right protein at...
DNA Damage Can Stall the Cell Cycle02:36

DNA Damage Can Stall the Cell Cycle

In response to DNA damage, cells can pause the cell cycle to assess and repair the breaks. However, the cell must check the DNA at certain critical stages during the cell cycle. If the cell cycle pauses before DNA replication, the cells will contain twice the amount of DNA. On the other hand, if cells arrest after DNA replication but before mitosis, they will contain four times the normal amount of DNA. With a host of specialized proteins at their disposal,cells must use the right protein at...
Negative Regulator Molecules01:23

Negative Regulator Molecules

Positive regulators allow a cell to advance through cell cycle checkpoints. Negative regulators have an equally important role as they terminate a cell’s progression through the cell cycle—or pause it—until the cell meets specific criteria.
Abnormal Proliferation02:23

Abnormal Proliferation

Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the daughter...
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...
Replicative Cell Senescence02:15

Replicative Cell Senescence

Replicative cell senescence is a property of cells that allows them to divide a finite number of times throughout the organism's lifespan while preventing excessive proliferation. Replicative senescence is associated with the gradual loss of the telomere — short, repetitive DNA sequences found at the end of the chromosomes. Telomeres are bound by a group of proteins to form a protective cap on the ends of chromosomes. Embryonic stem cells express telomerase — an enzyme that adds the telomeric...

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Related Experiment Video

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Yeast As a Chassis for Developing Functional Assays to Study Human P53
14:57

Yeast As a Chassis for Developing Functional Assays to Study Human P53

Published on: August 4, 2019

Weak p53 permits senescence during cell cycle arrest.

Olga V Leontieva1, Andrei V Gudkov, Mikhail V Blagosklonny

  • 1Roswell Park Cancer Institute, Buffalo, NY, USA.

Cell Cycle (Georgetown, Tex.)
|November 6, 2010
PubMed
Summary

Cell cycle arrest can lead to senescence or quiescence. High p53 levels inhibit mTOR, promoting quiescence, while low p53 levels promote senescence during cell cycle arrest.

Area of Science:

  • Cellular senescence
  • Cell cycle regulation
  • Molecular biology

Background:

  • Cellular senescence is a state of irreversible cell cycle arrest.
  • The mechanistic target of rapamycin (mTOR) pathway plays a critical role in regulating cellular fate.
  • p53 is a tumor suppressor protein involved in cell cycle control and senescence.

Purpose of the Study:

  • To investigate the role of p53 and mTOR in determining cell fate (senescence vs. quiescence) during cell cycle arrest.
  • To elucidate the differential effects of various stimuli on cell cycle arrest outcomes.
  • To understand the concentration-dependent effects of drugs on cellular fate.

Main Methods:

  • Induction of cell cycle arrest using Nutlin-3a and doxorubicin (DOX) at varying concentrations.

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  • Monitoring of p53 levels and mTOR activity.
  • Assessment of cellular morphology and cell cycle status.

    • Main Results:

    • Nutlin-3a-induced p53 inhibited mTOR, leading to quiescence in WI-38 cells.
    • Doxorubicin (DOX) at low concentrations caused senescence by arresting the cell cycle without inhibiting mTOR.
    • High concentrations of DOX or Nutlin-3a induced high p53 levels, inhibiting mTOR and causing quiescence or preventing senescence.

    Conclusions:

    • Low p53 levels during prolonged cell cycle arrest favor senescence.
    • High p53 levels during cell cycle arrest tend to induce quiescence or cell death by inhibiting mTOR.
    • The concentration of stimuli and resulting p53 levels are critical determinants of cell cycle arrest outcomes.