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Related Concept Videos

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...
Mismatch Repair01:36

Mismatch Repair

Overview
Mismatch Repair01:36

Mismatch Repair

Overview
Mutations01:39

Mutations

Overview
Mutations01:39

Mutations

Overview

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Related Experiment Video

Updated: Jul 4, 2026

Analysis of Somatic Hypermutation in the JH4 intron of Germinal Center B cells from Mouse Peyer's Patches
09:35

Analysis of Somatic Hypermutation in the JH4 intron of Germinal Center B cells from Mouse Peyer's Patches

Published on: April 20, 2021

II. Correlations between secondary structure stability and mutation frequency during somatic hypermutation.

Barbara E Wright1, Karen H Schmidt, Nick Davis

  • 1Division of Biological Sciences, The University of Montana, Missoula, MT 59812, USA. barbara.wright@mso.umt.edu

Molecular Immunology
|July 1, 2008
PubMed
Summary
This summary is machine-generated.

Secondary structures and base mutability in antibody genes are linked to transcription levels. This suggests a model where increasing transcription sequentially activates mutable sites during affinity maturation.

More Related Videos

Assessing Somatic Hypermutation in Ramos B Cells after Overexpression or Knockdown of Specific Genes
08:12

Assessing Somatic Hypermutation in Ramos B Cells after Overexpression or Knockdown of Specific Genes

Published on: November 1, 2011

Related Experiment Videos

Last Updated: Jul 4, 2026

Analysis of Somatic Hypermutation in the JH4 intron of Germinal Center B cells from Mouse Peyer's Patches
09:35

Analysis of Somatic Hypermutation in the JH4 intron of Germinal Center B cells from Mouse Peyer's Patches

Published on: April 20, 2021

Assessing Somatic Hypermutation in Ramos B Cells after Overexpression or Knockdown of Specific Genes
08:12

Assessing Somatic Hypermutation in Ramos B Cells after Overexpression or Knockdown of Specific Genes

Published on: November 1, 2011

Area of Science:

  • Immunology
  • Molecular Biology
  • Genetics

Background:

  • Antibody genes undergo somatic hypermutation to enhance antigen binding.
  • The mechanisms regulating the location and timing of these mutations are not fully understood.
  • Variable region genes (VH5, VH94, VH186.2) are critical for antibody diversity.

Purpose of the Study:

  • To analyze the role of secondary structures and base mutability in antibody genes at varying transcription and supercoiling levels.
  • To investigate the correlation between transcription, secondary structure stability, and the formation of mutable sites.
  • To understand how encoded differences in CDRs influence mutagenesis during affinity maturation.

Main Methods:

  • Analysis of secondary structures within variable region antibody genes (VH5, VH94, VH186.2).
  • Assessment of base mutability in relation to transcription and supercoiling.
  • Examination of encoded differences in stem length and GC pairs in CDRs.

Main Results:

  • Increasing transcription levels correlate with enhanced secondary structure stability.
  • Higher transcription and stability are associated with the successive formation of mutable sites.
  • Encoded differences in CDR stem length and GC content exist between low and high transcription conditions.

Conclusions:

  • The findings support a model of somatic hypermutation coordinated by transcription levels.
  • Mutability is sequentially activated at specific sites as transcription increases during affinity maturation.
  • Structural features within CDRs contribute to the stepwise regulation of antibody gene mutagenesis.