The male-sterile reciprocal autosomal translocation T(16;17)43H displays a high frequency of adjacent-2 disjunction in meiosis of translocation heterozygotes. One haploid product of this abnormal chromosome segregation leads to viable partial trisomy of chromosome 17 after fertilization. The frequency of trisomics increases in the progeny of T43H/+ females when the wild-type allelic form of T-t complex is substituted for t12, tw32 or t6 recessive lethal haplotypes. Indirect evidence supports the idea that the suppression of crossing-over by t haplotypes is linked with the increase in adjacent-2 disjunction and subsequent Ts43H trisomy. The possible use of Ts43H trisomy for genetic dissection of the T-t complex is briefly discussed.

Segmental trisomy of mouse chromosome 17: introducing an alternative model of Down's syndrome