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. |