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Related Concept Videos

Base Excision Repair01:54

Base Excision Repair

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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.
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Since the discovery of the two BER pathways, there has been a debate about how a cell chooses one pathway over the other and the factors determining this selection. Numerous in vitro experiments have pointed out multiple determinants for the sub-pathway selection. These are:
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DNA Distortion and Damage
Cells are regularly exposed to mutagens—factors in the environment that can damage DNA and generate mutations. UV radiation is one of the most common mutagens and is estimated to introduce a significant number of changes in DNA. These include bends or kinks in the structure, which can block DNA replication or transcription. If these errors are not fixed, the damage can cause mutations, which in turn can result in cancer or disease depending on which sequences are...
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Author Spotlight: High-Throughput Image-Based Quantification of Mitochondrial DNA Synthesis and Distribution
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Base Excision Repair in the Mitochondria.

Aishwarya Prakash1, Sylvie Doublié1

  • 1Department of Microbiology and Molecular Genetics, The Markey Center for Molecular Genetics, University of Vermont, Stafford Hall, 95 Carrigan Drive, Burlington, Vermont.

Journal of Cellular Biochemistry
|March 11, 2015
PubMed
Summary
This summary is machine-generated.

Human mitochondrial DNA (mtDNA) is vulnerable to damage from reactive oxygen species (ROS). This review examines DNA glycosylases involved in base excision repair (BER) to maintain mtDNA integrity and prevent mitochondrial dysfunction.

Keywords:
BASE EXCISION REPAIRDNA GLYCOSYLASESMITOCHONDRIAL DNA DAMAGE AND RESPONSEMITOCHONDRIAL DYSFUNCTIONOXIDATIVE PHOSPHORYLATIONREACTIVE OXYGEN SPECIES

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Area of Science:

  • Molecular Biology
  • Genetics
  • Biochemistry

Background:

  • The human mitochondrial genome (16.5 kb) encodes essential proteins for oxidative phosphorylation.
  • Mitochondrial DNA (mtDNA) is susceptible to reactive oxygen species (ROS) damage due to its lack of nucleosomal packaging.
  • Accumulated mtDNA damage can lead to mitochondrial dysfunction and disease.

Purpose of the Study:

  • To review human base excision repair (BER) DNA glycosylases.
  • To detail their subcellular localization (mitochondria and/or nucleus).
  • To summarize their structural, biochemical, and functional roles in DNA repair.

Main Methods:

  • Literature review of BER DNA glycosylase superfamilies.
  • Analysis of subcellular localization data.
  • Compilation of structural and biochemical properties.

Main Results:

  • Identified four human BER DNA glycosylase superfamilies.
  • Detailed their presence in mitochondria and/or nucleus.
  • Summarized their roles in excising damaged DNA bases.

Conclusions:

  • DNA glycosylases are crucial for repairing ROS-induced mtDNA damage.
  • Understanding their localization and function is key to addressing mitochondrial diseases.
  • Targeting BER pathways may offer therapeutic strategies for mitochondrial dysfunction.