A major rearrangement in the H–2 complex of mouse t haplotypes

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 development^1–3. The various t haplotypes also carry H–2 specificities which are different from those of other mice^3–8. This, together with the fact^9,10 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 idea^8–10, 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.