Related Experiment Video

Updated: Aug 21, 2026

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

The effect of methyl methanesulfonate (MMS)-induced excision repair on p53-dependent apoptosis in human lymphoid

J C Ryu1, Y R Seo, M L Smith

  • 1Toxicology Laboratory, Korea Institute of Science and Technology, Cheongryang, Seoul. ryujc@kist.re.kr

Research Communications in Molecular Pathology and Pharmacology
|July 19, 2001
PubMed

Insights

The tumor suppressor p53 influences apoptosis following genotoxic stress. Differences in apoptosis between cells with wild-type and mutant p53 were not due to DNA repair capacity.

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Cancer Research

Background:

  • The tumor suppressor p53 is crucial in preventing cancer through cell cycle arrest, DNA repair, and apoptosis.
  • Understanding the interplay between cellular responses and apoptosis after genotoxic stress is vital.

Purpose of the Study:

  • To investigate the role of DNA strand breaks from repair processes in cellular responses to DNA damage.
  • To examine the impact on p53-dependent apoptosis in human lymphoid cells after genotoxic stress.

Main Methods:

  • Utilized two isogenic human lymphoid cell lines: TK6 (wild-type p53) and WI-L2-NS (mutant p53).
  • Administered methyl methanesulfonate (MMS) to induce DNA damage.
  • Assessed cellular sensitivity, apoptosis induction, and DNA repair capacity using comet assays.

Main Results:

  • A significant difference in sensitivity to MMS (50 microg/ml) was observed between the wild-type and mutant p53 cell lines.
  • A clear p53-mediated contribution to MMS-induced cell death via apoptosis was evident.
  • No significant differences in the repair of MMS-induced DNA lesions were detected between the two cell lines.

Conclusions:

  • The observed differences in apoptosis induction are not attributable to variations in DNA strand break frequency or repair capacity.
  • p53 status significantly influences apoptosis following genotoxic stress, independent of DNA repair efficiency.

More Related Videos

Dual Immunofluorescence of γH2AX and 53BP1 in Human Peripheral Lymphocytes05:34

Dual Immunofluorescence of γH2AX and 53BP1 in Human Peripheral Lymphocytes

Published on: July 14, 2023

Knockdown of FAM83A to Verify Its Role in Cervical Cancer Cell Growth and Cisplatin Sensitivity04:20

Knockdown of FAM83A to Verify Its Role in Cervical Cancer Cell Growth and Cisplatin Sensitivity

Published on: February 9, 2024

Related Concept Videos

Mismatch Repair01:36

Mismatch Repair

Overview
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...
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...
The Intrinsic Apoptotic Pathway01:31

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...
Mismatch Repair01:20

Mismatch Repair

Organisms are capable of detecting and fixing nucleotide mismatches that occur during DNA replication. This sophisticated process requires identifying the new strand and replacing the erroneous bases with correct nucleotides. Mismatch repair is coordinated by many proteins in both prokaryotes and eukaryotes.
The Mutator Protein Family Plays a Key Role in DNA Mismatch Repair
The human genome has more than 3 billion base pairs of DNA per cell. Prior to cell division, that vast amount of genetic...
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...