| First Author | Shiroishi T | Year | 1987 |
| Journal | Proc Natl Acad Sci U S A | Volume | 84 |
| Issue | 9 | Pages | 2819-23 |
| PubMed ID | 3495003 | Mgi Jnum | J:25926 |
| Mgi Id | MGI:73629 | Doi | 10.1073/pnas.84.9.2819 |
| Citation | Shiroishi T, et al. (1987) Lethal deletion of the complement component C4 and steroid 21-hydroxylase genes in the mouse H-2 class III region, caused by meiotic recombination. Proc Natl Acad Sci U S A 84(9):2819-23 |
| abstractText | A recombinant H-2 haplotype, designated aw18, was produced that underwent meiotic recombination in the E alpha (I-E alpha chain)--Slp (sex-limited protein) interval of the H-2 class III region between B10.A (H-2a) and wild-derived B10.MOL-SGR (H-2wm7) strains. It appeared that the H-2aw18 haplotype has a single, recessive, lethal mutation, since homozygotes for H-2aw18 were not detected in progeny generated from the intercross of mice that were heterozygous for this H-2 haplotype. Nine newly established recombinant H-2 haplotypes, which arose from the heterozygous mice that resulted from a cross between common inbred H-2 haplotypes and the aw18 haplotype, allowed us to map the lethal gene to the class III region of the H-2 complex. Southern blot analysis indicated that the aw18 haplotype has a deletion of the C4 gene and a deletion of one of the steroid 21-hydroxylase genes. This result was confirmed by an immunodiffusion test that demonstrated the absence of production of the C4 protein in mice of haplotype H-2aw18. All data that were obtained supported the hypothesis that the meiotic, presumably unequal, recombination between homologous chromosomes of the H-2a and H-2wm7 haplotypes caused the deletion of the C4 and the 21-hydroxylase genes. |
