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Related Concept Videos

Overview of DNA Repair02:25

Overview of DNA Repair

In order to be passed through generations, genomic DNA must be undamaged and error-free. However, every day, DNA in a cell undergoes several thousand to a million damaging events by natural causes and external factors. Ionizing radiation such as UV rays, free radicals produced during cellular respiration, and hydrolytic damage from metabolic reactions can alter the structure of DNA. Damages caused include single-base alteration, base dimerization, chain breaks, and cross-linkage.
Chemically...
Base Excision Repair01:54

Base Excision Repair

One of the common DNA damages is the chemical alteration of single bases by alkylation, oxidation, or deamination. The altered bases cause mispairing and strand breakage during replication. This type of damage causes minimal change to the DNA double helix structure and can be repaired by the base excision repair (BER) pathways. BER corrects damaged DNA sequences by removing the damaged base and restoring the original base sequence using the complementary strand as a template.
The first step of...
Overview of Cell Death01:30

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 20th century...
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...
Fixing Double-strand Breaks02:04

Fixing Double-strand Breaks

The double-stranded structure of DNA has two major advantages. First, it serves as a safe repository of genetic information where one strand serves as the back-up in case the other strand is damaged. Second, the double-helical structure can be wrapped around proteins called histones to form nucleosomes, which can then be tightly wound to form chromosomes. This way, DNA chains up to 2 inches long can be contained within microscopic structures in a cell. A double-stranded break not only damages...

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A Standard Methodology to Examine On-site Mutagenicity As a Function of Point Mutation Repair Catalyzed by CRISPR/Cas9 and SsODN in Human Cells
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Cell death caused by single-stranded oligodeoxynucleotide-mediated targeted genomic sequence modification.

Chenli Liu1, Zai Wang, Michael S Y Huen

  • 1Department of Biochemistry, The University of Hong Kong, Hong Kong SAR, People's Republic of China.

Oligonucleotides
|August 6, 2009
PubMed
Summary

Single-stranded oligodeoxynucleotides (ssODNs) for gene repair improve correction efficiency when mismatch repair (MMR) proteins are defective, but this leads to non-viable cells. MMR is not involved in ssODN-induced cell death.

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Area of Science:

  • Molecular Biology
  • Gene Therapy
  • Cellular Biology

Background:

  • Targeted gene repair using single-stranded oligodeoxynucleotides (ssODNs) is a key tool in biotechnology and gene therapy.
  • Current limitations include low repair frequency, variability, and poor viability of corrected cells.

Purpose of the Study:

  • To investigate the low viability and cell death observed in ssODN-mediated gene repair.
  • To explore the role of ATM/ATR kinase and mismatch repair (MMR) proteins in ssODN-induced cellular responses.

Main Methods:

  • Analysis of cell division and apoptosis markers (caspases, PARP-1) in ssODN-treated cells.
  • Assessment of cell death independence from ATM/ATR kinase signaling.
  • Evaluation of gene correction efficiency and cell viability in cells with defective MMR systems.

Main Results:

  • A significant population of ssODN-corrected cells exhibited failed division and increased apoptosis.
  • ssODN-induced cell death was largely independent of ATM/ATR kinase.
  • Defective MMR enhanced gene correction efficiency but prevented the generation of viable corrected clones.

Conclusions:

  • ssODN-mediated gene repair triggers significant cellular genotoxic responses, leading to apoptosis and poor cell viability.
  • While MMR proteins are critical for ssODN repair outcomes, they are not implicated in the observed cell death.
  • Further research is needed to overcome these viability issues for effective gene therapy applications.