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Abnormal Proliferation

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...

DNA Damage can Stall the Cell Cycle

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 Molecules

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.

Overview of Cell Death

Overview of Cell Death

Cell death is an essential process where the body gets rid of old or damaged cells. Cell proliferation and death need to be balanced, as an imbalance between the two may lead to cancer or autoimmune diseases.
Cell death was observed in the early 19th century, but there was no experimental evidence to prove it. In 1842, Carl Vogt first discovered cell death in a metamorphic toad; however, it was not termed ‘cell death.’ Scientists discovered different cell death pathways only in the...

Molecular Factors Affecting Cell Division

Molecular Factors Affecting Cell Division

Several external and internal factors influence the initiation and inhibition of cell division. For instance, the death of nearby cells or the release of human growth hormone (hGH) promotes cell division. In contrast, lack of hGH or crowding of cells can inhibit cell division.
Several proteins function as internal regulators to ensure each cell cycle stage is completed faithfully before proceeding to the next. Regulator molecules may act directly or influence the activity or production of other...

The Intrinsic Apoptotic Pathway

The Intrinsic Apoptotic Pathway

Internal cellular stress, such as cellular injury or hypoxia, triggers intrinsic apoptosis. The B-cell lymphoma 2 (Bcl-2) family of proteins are the primary regulators of the intrinsic apoptotic pathway. For example, during DNA damage, checkpoint proteins, such as Ataxia Telangiectasia Mutated (ATM protein) and Checkpoints Factor-2 (Chk2) proteins, are activated. These proteins phosphorylate p53 which further activates pro-apoptotic proteins, such as Bax, Bak, PUMA, and Noxa, and inhibits...

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Related Experiment Video

Updated: Sep 29, 2025

Use of LysoTracker to Detect Programmed Cell Death in Embryos and Differentiating Embryonic Stem Cells

Use of LysoTracker to Detect Programmed Cell Death in Embryos and Differentiating Embryonic Stem Cells

Published on: October 11, 2012

Cell Death and the p53 Enigma During Mammalian Embryonic Development.

Sonam Raj¹, Sushil K Jaiswal², Melvin L DePamphilis²

¹National Cancer Institute, Bethesda, MD 20892, USA.

Stem Cells (Dayton, Ohio)

|March 19, 2022

Summary

Programmed cell death (PCD) in embryonic stem cells (ESCs) is largely p53-independent, though p53 can influence its initiation under certain conditions. This finding clarifies the role of the p53 tumor suppressor in early development.

Keywords:

apoptosis cell cycle differentiation embryo p53 pluripotent programmed cell death stem cells

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Last Updated: Sep 29, 2025

Use of LysoTracker to Detect Programmed Cell Death in Embryos and Differentiating Embryonic Stem Cells

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Published on: October 11, 2012

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

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Published on: August 4, 2019

Cell Death Associated with Abnormal Mitosis Observed by Confocal Imaging in Live Cancer Cells

Cell Death Associated with Abnormal Mitosis Observed by Confocal Imaging in Live Cancer Cells

Published on: August 21, 2013

Area of Science:

Developmental Biology
Cellular Biology
Cancer Biology

Background:

Twelve forms of programmed cell death (PCD) are known, but their roles in mammalian embryonic development and the involvement of the p53 tumor suppressor are unclear.
Studies on p53's role in PCD in mouse ESCs (mESCs) and human ESCs (hESCs) yield contradictory results.
Pluripotent stem cells are crucial models for embryonic development and regenerative medicine.

Purpose of the Study:

To reconcile conflicting data regarding p53's role in PCD during embryonic development.
To clarify the mechanisms of PCD in ESCs and their dependence on p53.
To understand the implications for regenerative medicine and developmental biology.

Main Methods:

Review and reconciliation of existing experimental data on PCD and p53 in ESCs and embryonic development.
Analysis of p53's lethality threshold in mice during gastrulation.
Consideration of how experimental conditions affect PCD outcomes in ESCs.

Main Results:

p53 is not required for mouse embryonic development.
G2-checkpoint activation in mouse ESCs is p53-independent and typically results in noncanonical apoptosis.
PCD rates and extents are generally equivalent regardless of p53 presence, but p53 can accelerate PCD initiation in ESCs and blastocysts under specific conditions.
DNA damage post-differentiation in vitro or in vivo induces p53-dependent cell cycle arrest and senescence.

Conclusions:

The role of p53 in PCD during early embryonic development is context-dependent and less critical than previously assumed for ESCs.
Experimental conditions significantly influence observed p53 dependence in ESCs.
p53-dependent pathways are more prominent in differentiated cells, mediating cell cycle arrest and senescence after DNA damage.