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Related Concept Videos

Mutations in Microorganisms01:18

Mutations in Microorganisms

Mutations are heritable changes in an organism’s genome involving alterations in the base sequence of DNA or RNA. These changes can influence cellular processes and phenotypic traits, potentially transforming the unaltered wild type into a mutant form. Such changes, termed forward mutations, are pivotal in shaping the genetic diversity of organisms.RNA viruses exhibit the highest mutation rates due to the absence of robust proofreading mechanisms during genome replication. In contrast,...
Mutations01:39

Mutations

Overview
Mutations01:35

Mutations

Mutations are changes in the sequence of DNA. These changes can occur spontaneously or they can be induced by exposure to environmental factors. Mutations can be characterized in a number of different ways: whether and how they alter the amino acid sequence of the protein, whether they occur over a small or large area of DNA, and whether they occur in somatic cells or germline cells.
Chromosomal Alterations Are Large-Scale Mutations
While point mutations are changes in a single nucleotide in...
Mutations01:39

Mutations

Overview
Spontaneous and Induced Mutations01:30

Spontaneous and Induced Mutations

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).
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...

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Related Experiment Video

Updated: Jun 27, 2026

Following the Dynamics of Structural Variants in Experimentally Evolved Populations
04:52

Following the Dynamics of Structural Variants in Experimentally Evolved Populations

Published on: February 3, 2023

Powerful mutators lurking in the genome.

Vincent Petit1, Jean-Pierre Vartanian, Simon Wain-Hobson

  • 1Molecular Retrovirology Unit, CNRS URA 3015, Institut Pasteur, 28 rue du Docteur Roux, 75724 Paris cedex 15, France.

Philosophical Transactions of the Royal Society of London. Series B, Biological Sciences
|December 2, 2008
PubMed
Summary

Human genome enzymes can cause hypermutation, acting as an antiviral defense. Research questions whether these enzymes, APOBEC3 cytidine deaminases, also hyperedit chromosomal DNA, potentially impacting cancer.

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Published on: March 7, 2019

Area of Science:

  • Molecular Biology
  • Genetics
  • Biochemistry

Background:

  • The human genome contains enzymes that deaminate polynucleotides, sometimes causing significant hypermutation.
  • These enzymes, including the APOBEC3 family of cytidine deaminases, are crucial in antiviral defense by rapidly mutating viral DNA.

Purpose of the Study:

  • To investigate the potential for APOBEC3 cytidine deaminases to hyperedit chromosomal DNA in humans.
  • To explore the unknown physiological functions and cancer-related roles of APOBEC3 genes.

Main Methods:

  • Analysis of polynucleotide deamination mechanisms.
  • Examination of APOBEC3 cytidine deaminase activity on viral and chromosomal DNA.
  • Investigation of mismatch repair efficiency in countering hypermutation.

Main Results:

  • APOBEC3 cytidine deaminases exhibit high specificity but can cause up to 90% residue editing, forming an antiviral barrier.
  • Evidence suggests APOBEC3 enzymes may also hyperedit chromosomal DNA, though such hypermutants have not been definitively described.
  • Efficient mismatch repair likely counteracts the formation of observable chromosomal hypermutants.

Conclusions:

  • APOBEC3 enzymes play a critical role in innate immunity against viral infections through hypermutation.
  • The potential for APOBEC3-mediated hypermutation of chromosomal DNA warrants further investigation.
  • Understanding the physiological roles and oncogenic potential of APOBEC3 genes is a key area for future research.