| First Author | Shimizu T | Year | 2005 |
| Journal | Immunol Lett | Volume | 98 |
| Issue | 2 | Pages | 259-64 |
| PubMed ID | 15860226 | Mgi Jnum | J:105111 |
| Mgi Id | MGI:3613436 | Doi | 10.1016/j.imlet.2004.11.022 |
| Citation | Shimizu T, et al. (2005) Normal immunoglobulin gene somatic hypermutation in Pol kappa-Pol iota double-deficient mice. Immunol Lett 98(2):259-64 |
| abstractText | Somatic hypermutation (SHM) occurs in the variable region of immunoglobulin genes in germinal center B cells where it plays an important role in affinity maturation of the T cell-dependent immune response. Although the precise mechanism of SHM is still unknown, it has been suggested that error-prone DNA polymerases (Pol) are involved in SHM. Poliota is a member of the error-prone Y-family of DNA polymerases which exhibit translesion synthesis activity in vitro and are highly mutagenic when replicating on non-damaged DNA templates. In BL2 cell line stimulated to induce SHM, the induction is Poliota-dependent. However, in 129-derived strains of mice deficient in Poliota, SHM is normal. One possible explanation for this discrepancy is that a Poliota deficiency in mice might be compensated for by another error-prone DNA polymerase, such as Polkappa, which also belongs to the Y-family of DNA polymerases. Although SHM in Polkappa-deficient mice is normal, their deficiency might be compensated for by Poliota. In this study, we generated Polkappa-Poliota double-deficient mice and examined them for SHM. We found that the double-deficient mice had the normal SHM frequency and profile, rendering them indistinguishable from Polkappa-deficient mice and thus conclude that Poliota and Polkappa are dispensable for SHM in mice. |
