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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.
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Spontaneous mutations arise infrequently during DNA replication due to errors in the process. A key factor behind these errors is tautomeric shifts in nitrogenous bases, where bases transition from keto to enol forms or amino to imino forms. This shift can alter base-pairing rules, leading to mutations. Additionally, reactive oxygen species (ROS) arising from aerobic metabolism can damage DNA, resulting in depurination (loss of a purine base) or depyrimidination (loss of a pyrimidine base).
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Mouse Genome Engineering Using Designer Nucleases
12:04

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Published on: April 2, 2014

Creative deaminases, self-inflicted damage, and genome evolution.

Silvestro G Conticello1

  • 1Core Research Laboratory, Istituto Toscano Tumori, Florence, Italy. silvo.conticello@ittumori.it

Annals of the New York Academy of Sciences
|September 8, 2012
PubMed
Summary

The Activation-Induced Cytidine Deaminase (AID) and its homologs (APOBECs) are crucial for DNA/RNA editing in vertebrates. While essential for immunity, their mutagenic activity also contributes to diseases like cancer.

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Area of Science:

  • Molecular Biology
  • Genetics
  • Immunology

Background:

  • Organisms possess DNA repair mechanisms to prevent genetic damage.
  • The AID/APOBEC gene family in vertebrates uniquely induces targeted DNA/RNA damage via cytosine deamination.
  • These enzymes likely evolved from tRNA-editing deaminases.

Purpose of the Study:

  • To explore the evolutionary origins and diverse functions of the AID/APOBEC gene family.
  • To understand the dual role of AID/APOBECs in both genomic evolution and disease pathogenesis.

Main Methods:

  • Comparative genomics analysis to trace evolutionary history.
  • Functional assays to investigate DNA/RNA editing activities.
  • Analysis of gene duplication events and functional divergence.

Main Results:

  • AID is essential for antibody gene diversification.
  • APOBEC3s restrict viral and mobile element replication.
  • APOBEC1 targets both RNA and DNA.
  • AID/APOBECs have significantly shaped vertebrate genome evolution.
  • Dysregulation of AID/APOBECs is implicated in lymphoproliferative diseases and cancer.

Conclusions:

  • The AID/APOBEC family exhibits remarkable functional plasticity, originating from ancient editing enzymes.
  • These enzymes play a critical role in vertebrate immunity and genome evolution.
  • Their potent mutagenic capabilities present a double-edged sword, contributing to both beneficial adaptations and disease development.