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

First Author  Delbos F Year  2005
Journal  J Exp Med Volume  201
Issue  8 Pages  1191-6
PubMed ID  15824086 Mgi Jnum  J:98037
Mgi Id  MGI:3576981 Doi  10.1084/jem.20050292
Citation  Delbos F, et al. (2005) Contribution of DNA polymerase {eta} to immunoglobulin gene hypermutation in the mouse. J Exp Med 201(8):1191-6
abstractText  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 poleta-deficient mice differs markedly. This suggests that, in the absence of poleta, the MSH2-MSH6 complex is able to recruit another DNA polymerase that is more accurate at copying A/T bases, possibly polkappa, to assume its function in hypermutation.
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