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Related Concept Videos

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Related Experiment Video

Updated: May 17, 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

Identification of core DNA elements that target somatic hypermutation.

Kristin M Kohler1, Jessica J McDonald, Jamie L Duke

  • 1Department of Immunobiology, Yale University School of Medicine, New Haven, CT 06520, USA.

Journal of Immunology (Baltimore, Md. : 1950)
|October 23, 2012
PubMed
Summary

Somatic hypermutation (SHM) preferentially targets Ig genes. A novel 1.9-kb element, DIVAC, from chicken IgL enhances activation-induced deaminase (AID)-dependent mutation activity, revealing dispersed elements crucial for SHM targeting.

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Last Updated: May 17, 2026

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Published on: March 31, 2022

Area of Science:

  • Immunology
  • Molecular Biology
  • Genetics

Background:

  • Somatic hypermutation (SHM) diversifies immunoglobulin (Ig) genes, crucial for antibody affinity maturation.
  • Activation-induced deaminase (AID) mediates SHM by deaminating deoxycytosine residues in activated B cells.
  • SHM and AID preferentially target Ig loci, but the underlying mechanisms remain unclear.

Purpose of the Study:

  • To identify and characterize elements responsible for the preferential targeting of SHM and AID activity to Ig loci.
  • To understand the molecular mechanisms governing SHM targeting within Ig genes.

Main Methods:

  • Utilized an SHM reporter cassette assay in chicken DT40 B cells, inserted into the Ig L chain locus (IgL).
  • Performed systematic deletion analysis of a 1.9-kb chicken IgL-derived element (DIVAC).
  • Employed chromatin immunoprecipitation (ChIP) to assess epigenetic marks and RNA polymerase II phosphorylation.

Main Results:

  • Identified a 1.9-kb DIVAC element from chicken IgL that significantly enhances AID-dependent mutation activity.
  • Deletion analysis revealed that targeting activity is dispersed, with two critical regions: an IgL enhancer region and a 3' element.
  • DIVAC increased serine-5 phosphorylated RNA polymerase II, suggesting an impact on transcriptional elongation/pausing, without altering other epigenetic marks.

Conclusions:

  • Multiple, dispersed DNA elements, exemplified by DIVAC, collaborate to recruit and activate the SHM machinery.
  • These elements play a critical role in ensuring the preferential targeting of SHM to Ig gene variable regions.
  • Understanding these targeting mechanisms is key to comprehending antibody diversification and B cell maturation.