Abstract:
:The Pms2 gene is involved in DNA mismatch repair in mammalian cells, and has recently been shown to affect hypermutation of mammalian immunoglobulin genes. We have studied hypermutation of a lambda1 transgene in chronically stimulated Peyer's patch B cells of both young and old mice deficient in function of Pms2. In young (3-4 months) mice, somatic hypermutation is fourfold lower in PMS2-deficient mice than in control mice. This difference is statistically significant (P < 0.05). In contrast, in older mice (9 months of age), hypermutation levels are indistinguishable in the Pms2-/- and Pms2+/+ backgrounds. In the older mice, there was no clear difference in the fraction of clones carrying either any mutations or at least two mutations when PMS2-deficient mice were compared with their wild-type littermates. As genomic instability increases with age, this observation is difficult to reconcile with the hypothesis that highly mutated B cells cannot survive in Peyer's patches. Moreover, there were clear differences apparent in the mutation spectra of the Pms2-/- and Pms2+/+ mice. In the PMS2-deficient background, deletion and insertion mutations were found, and there was a significant decrease in the ratio of A mutations to T mutations in comparison with the Pms2+/+ controls. Our data support the hypothesis that PMS2 functions in somatic hypermutation, and are most consistent with the hypothesis that the role of PMS2 is direct rather than indirect.
journal_name
Mol Immunoljournal_title
Molecular immunologyauthors
Kong Q,Maizels Ndoi
10.1016/s0161-5890(99)00027-9subject
Has Abstractpub_date
1999-02-01 00:00:00pages
83-91issue
2eissn
0161-5890issn
1872-9142pii
S0161589099000279journal_volume
36pub_type
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