| First Author | Shin HS | Year | 1983 |
| Journal | Nature | Volume | 306 |
| Issue | 5941 | Pages | 380-3 |
| PubMed ID | 6316154 | Mgi Jnum | J:7253 |
| Mgi Id | MGI:55724 | Doi | 10.1038/306380a0 |
| Citation | Shin HS, et al. (1983) Inversion in the H-2 complex of t-haplotypes in mice. Nature 306(5941):380-3 |
| abstractText | Mouse t-haplotypes demonstrate strong linkage disequilibrium between t-lethal genes and specific H-2 types, presumably a result of recombination suppression between t and normal chromosomes. The observation of free recombination occurring between two complementary t-haplotypes suggested a chromosomal mismatch between t and normal chromosomes. Recent data showing the H-2 complex to be misplaced relative to two other markers, T and tf, in t-haplotypes suggested that chromosomal rearrangement in t-haplotypes might be the basis for their 'mismatch' with the normal chromosome. Here, to analyse the molecular nature of the rearrangement, we have cloned a polymorphic H-2 class I restriction fragment, which had previously been shown to map centromeric to the serologically defined H-2 complex in t-haplotypes. Genetic mapping studies show that this cloned t-DNA is homologous to the H-2 D region of wild-type chromosomes, and that the E alpha Ia gene maps telomeric to this DNA fragment in t-haplotypes, in contrast to its orientation in wild-type chromosomes. These results give molecular evidence for an inversion of H-2 in t-haplotypes, which may be at least partially responsible for recombination suppression and thus for linkage disequilibrium. |
