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A potential donor gene for the bm1 gene conversion event in the C57BL mouse

Abstract

The mammalian major histocompatibility complex (MHC; H–2 complex in mouse) is a large multigene complex which encodes cell-surface antigens involved in the cellular immune response to foreign antigens1. Class I polypeptides expressed at the H–2K and H–2D (Fig. 1) loci of numerous mouse strains exhibit an unusually high degree of genetic polymorphism, which is assumed to be related to their function as primary recognition elements in the immune response. We suggested that this H–2 polymorphism may arise by gene conversion-like events between non-allelic class I genes. This is supported by our recent comparison of the DNA sequences of the normal H–2Kb gene sequence, from the C57BL/10 mouse, and a mutant2,3 form of this gene called H–2Kbm1 (ref. 4): the mutant allele differs from the H–2Kb gene in seven bases out of a region of 13 bases in exon 3 of the class I gene (which encodes α2 (C1) the second highly polymorphic protein domain), suggesting that this region of new sequence had been introduced into the H–2Kb sequence following unequal pairing of two class I genes in the genome of the C57BL mouse. Schulze et al. have obtained similar results5. Here we report work identifying a potential donor gene in our library of 26 class I genes cloned from the C57BL/10 mouse.

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References

  1. Klein, J. in Biology of the Mouse Histocompatibility-2 Complex, 192–230 (Springer, New York, 1975).

    Google Scholar 

  2. Bailey, D. W. & Kohn, H. J. Genet. Res. Camb. 6, 330–340 (1965).

    Article  CAS  Google Scholar 

  3. Nairn, R., Yamaga, K. & Nathenson, S. G. A. Rev. Genet. 14, 241–277 (1980).

    Article  CAS  Google Scholar 

  4. Weiss, E. H. et al. Nature 301, 671–764 (1983).

    Article  ADS  CAS  Google Scholar 

  5. Schulze, D. H. et al. Proc. natn. Acad. Sci. U.S.A. 80, 2007–2011 (1983).

    Article  ADS  CAS  Google Scholar 

  6. Reyes, A. A., Schold, M. & Wallace, R. B. Immunogenetics 16, 1–9 (1983).

    Article  Google Scholar 

  7. Maxam, A. & Gilbert, W. in Meth. Enzym. 65, 499–560 (1980).

    Google Scholar 

  8. Weiss, E. H. et al. EMBO J. 2, 453–462 (1983).

    Article  CAS  Google Scholar 

  9. Moore, K. W., Taylor-Sher, B., Sun, H.-Y., Eakle, K. A. & Hood, L. Science 215, 679–682 (1981).

    Article  ADS  Google Scholar 

  10. Kvist, S., Roberts, L. & Dobberstein, B. EMBO J. 2, 245–254 (1983).

    Article  CAS  Google Scholar 

  11. Grosveld, F. G., Dahl, H. H. M. deBoer, E. & Flavell, R. A. Gene 13, 227–237 (1981).

    Article  CAS  Google Scholar 

  12. Matteucci, M. D. & Caruthers, M. H. J. Am. Chem. Soc. 103, 3185 (1981).

    Article  CAS  Google Scholar 

  13. Southern, E. M. J. molec. Biol. 98, 503–517 (1975).

    Article  CAS  Google Scholar 

  14. Reyes, A. A., Schold, M., Itakura, K. & Wallace, R. B. Proc. natn. Acad. Sci. U.S.A. 79, 3270–3274 (1982).

    Article  ADS  CAS  Google Scholar 

  15. Chen-Pei, D. Tu & Cohen, S. N. Gene 10, 177–183 (1980).

    Article  Google Scholar 

  16. Mellor, A. L., Weiss, E. H., Kress, M., Jay, G. & Flavell, R. A. Cell (in the press).

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Mellor, A., Weiss, E., Ramachandran, K. et al. A potential donor gene for the bm1 gene conversion event in the C57BL mouse. Nature 306, 792–795 (1983). https://doi.org/10.1038/306792a0

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