A major rearrangement in the H–2 complex of mouse t haplotypes (original) (raw)

Nature volume 304, pages 549–552 (1983)Cite this article

Abstract

A proportion of wild mice carry a chromosome 17 of which a large part is very different from the standard mouse chromosome 17. The affected region is called the t complex, and the anomalous chromosomal types are the t haplotypes. In combination with various other chromosomes 17, t haplotypes can produce crossover suppression, taillessness, transmission distortion, male sterility and lethality early in development1–3. The various t haplotypes also carry H–2 specificities which are different from those of other mice3–8. This, together with the fact9,10 that the lethality genes map to both sides of H–2, suggests that the major histocompatibility complex is contained within the t complex. The lack of recombination between t haplotypes and standard chromosomes 17 may be due to large-scale rearrangements. Genetic data support this idea8–10, in that the tufted gene, the H–2 complex and a group of _H–2_-related genes appear to be in inverted order in t haplotypes relative to the standard chromosome 17. The mapping of several _t_-lethal factors close to the _H–2_-related genes in t haplotypes9 suggests that breakpoint(s) may be found here. We have now investigated the major histocompatibility complex of t haplotypes by Southern blots using a variety of cloned DNA probes, and find a major rearrangement, specific to the t haplotypes, in the Qa-2,3 region of the complex. This involves the loss of several large homology units, probably including several class I _H–2_-related genes, and the creation of two possible breakpoints.

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References

  1. Bennett, D. Cell 6, 441–454 (1975).
    Article Google Scholar
  2. Silver, L. M. Cell 27, 239–240 (1981).
    Article CAS Google Scholar
  3. Klein, J. & Hammerberg, C. Immun. Rev. 33, 70–104 (1977).
    Article CAS Google Scholar
  4. Hammerberg, C. & Klein, J. Nature 258, 296–299 (1975).
    Article ADS CAS Google Scholar
  5. Levinson, J. R. & McDevitt, H. O. J. exp. Med. 144, 834–839 (1976).
    Article CAS Google Scholar
  6. Sturm, S., Figueroa, F. & Klein, J. Genet. Res. 40, 73–88 (1982).
    Article CAS Google Scholar
  7. Silver, L. M. Cell 29, 961–968 (1982).
    Article CAS Google Scholar
  8. Shin, H-S., Stavnezer, J., Artzt, K. & Bennett, D. Cell 29, 969–976 (1982).
    Article CAS Google Scholar
  9. Artzt, K., McCormick, P. & Bennett, D. Cell 28, 463–470 (1982).
    Article CAS Google Scholar
  10. Artzt, K., Shin, H.-S. & Bennett, D. Cell 28, 471–476 (1982).
    Article CAS Google Scholar
  11. Steinmetz, M., Winoto, A., Minard, K. & Hood, L. Cell 28, 489–498 (1982).
    Article CAS Google Scholar
  12. Margulies, D. H., Evans, G. A., Flaherty, L. & Seidman, J. G. Nature 295, 168–170 (1982).
    Article ADS CAS Google Scholar
  13. Steinmetz, M. et al. Cell 25, 683–692 (1981).
    Article CAS Google Scholar
  14. Goodenow, R. S. et al. Nature 300, 231–237 (1982).
    Article ADS CAS Google Scholar
  15. Cosman, D., Khoury, G. & Jay, G. Nature 295, 73–76 (1982).
    Article ADS CAS Google Scholar
  16. Winoto, A., Steinmetz, M. & Hood, L. Proc. natn. Acad. Sci. U.S.A. 80, 3425–3429 (1983).
    Article ADS CAS Google Scholar
  17. Steinmetz, M. et al. Cell 24, 125–134 (1981).
    Article CAS Google Scholar
  18. Gladstone, P., Fueresz, L. & Pious, D. Proc. natn. Acad. Sci. U.S.A. 79, 1235–1239 (1982).
    Article ADS CAS Google Scholar
  19. Flaherty, L., Zimmermann, D. & Hansen, T. H. Immunogenetics 6, 245–251 (1978).
    Article Google Scholar
  20. Axelrod, H. R., Artzt, K. & Bennett, D. Devl Biol. 86, 419–425 (1981).
    Article CAS Google Scholar
  21. Southern, E. M. J. molec. Biol. 98, 503–517 (1975).
    Article CAS Google Scholar

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Authors and Affiliations

  1. MRC Laboratory of Molecular Biology, Hills Road, Cambridge, CB2 2QH, UK
    John H. Rogers
  2. Institute of Cancer Research, Chester Beatty Laboratories, Fulham Road, London, SW3 6JB, UK
    Keith R. Willison

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  1. John H. Rogers
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  2. Keith R. Willison
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Rogers, J., Willison, K. A major rearrangement in the H–2 complex of mouse t haplotypes.Nature 304, 549–552 (1983). https://doi.org/10.1038/304549a0

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