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Altered Ig hypermutation pattern and frequency in complementary mouse models of DNA polymerase ζ activity.

To test the hypothesis that DNA polymerase ζ participates in Ig hypermutation, we generated two mouse models of Pol ζ function: a B cell-specific conditional knockout and a knock-in strain with a Pol ζ mutagenesis-enhancing mutation. Pol ζ-deficient B cells had a reduction in mutation frequency at Ig loci in the spleen and in Peyer's patches, whereas knock-in mice with a mutagenic Pol ζ displayed a marked increase in mutation frequency in Peyer's patches, revealing a pattern that was similar to mutations in yeast strains with a homologous mutation in the gene encoding the catalytic subunit of Pol ζ. Combined, these data are best explained by a direct role for DNA polymerase ζ in Ig hypermutation.

Pubmed ID: 22547703

Authors

  • Daly J
  • Bebenek K
  • Watt DL
  • Richter K
  • Jiang C
  • Zhao ML
  • Ray M
  • McGregor WG
  • Kunkel TA
  • Diaz M

Journal

Journal of immunology (Baltimore, Md. : 1950)

Publication Data

June 1, 2012

Associated Grants

  • Agency: NIEHS NIH HHS, Id: Z01 ES065070
  • Agency: NIEHS NIH HHS, Id: Z01 ES101603
  • Agency: Intramural NIH HHS, Id: ZIA ES101603-09

Mesh Terms

  • Animals
  • B-Lymphocytes
  • DNA-Directed DNA Polymerase
  • Enzyme Activation
  • Gene Knock-In Techniques
  • Gene Rearrangement, B-Lymphocyte, Heavy Chain
  • Mice
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Mice, Transgenic
  • Models, Animal
  • Somatic Hypermutation, Immunoglobulin