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J Exp Med. 2005 Apr 18;201(8):1191-6. Epub 2005 Apr 11.

Contribution of DNA polymerase eta to immunoglobulin gene hypermutation in the mouse.

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1
Institut National de la Santé et de la Recherche Medicale U373, Faculté de Médecine Necker-Enfants Malades-Université Paris V, 75730 Paris Cedex 15, France.

Abstract

The mutation pattern of immunoglobulin genes was studied in mice deficient for DNA polymerase eta, a translesional polymerase whose inactivation is responsible for the xeroderma pigmentosum variant (XP-V) syndrome in humans. Mutations show an 85% G/C biased pattern, similar to that reported for XP-V patients. Breeding these mice with animals harboring the stop codon mutation of the 129/Olain background in their DNA polymerase iota gene did not alter this pattern further. Although this G/C biased mutation profile resembles that of mice deficient in the MSH2 or MSH6 components of the mismatch repair complex, the residual A/T mutagenesis of pol eta-deficient mice differs markedly. This suggests that, in the absence of pol eta, the MSH2-MSH6 complex is able to recruit another DNA polymerase that is more accurate at copying A/T bases, possibly pol kappa, to assume its function in hypermutation.

PMID:
15824086
PMCID:
PMC2213152
DOI:
10.1084/jem.20050292
[Indexed for MEDLINE]
Free PMC Article
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