(original) (raw)

TY - JOUR AU - Rogers, John H. AU - Willison, Keith R. PY - 1983 DA - 1983/08/01 TI - A major rearrangement in the H–2 complex of mouse t haplotypes JO - Nature SP - 549 EP - 552 VL - 304 IS - 5926 AB - 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. SN - 1476-4687 UR - https://doi.org/10.1038/304549a0 DO - 10.1038/304549a0 ID - Rogers1983 ER -