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

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.
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https://www.hal.inserm.fr/inserm-00310380
Contributor : Frédéric Delbos <>
Submitted on : Friday, August 8, 2008 - 2:37:55 PM
Last modification on : Wednesday, November 25, 2020 - 2:52:07 PM
Long-term archiving on: : Thursday, June 3, 2010 - 6:08:53 PM

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Frédéric Delbos, Annie de Smet, Ahmad Faili, Said Aoufouchi, Jean-Claude Weill, et al.. Contribution of DNA polymerase eta to immunoglobulin gene hypermutation in the mouse.. Journal of Experimental Medicine, Rockefeller University Press, 2005, 201 (8), pp.1191-6. ⟨10.1084/jem.20050292⟩. ⟨inserm-00310380⟩

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