Y-chromosomal DNA is present in the genomes of most human XX males. In these cases, maleness is probably due to the presence of the Y-encoded testis-determining factor (TDF). By means of in situ hybridization of a probe (pDP105) detecting Y-specific DNA to metaphases from three XX males, it was demonstrated that the Y DNA is located on the tip of the short arm of an X chromosome. This finding supports the hypothesis that XX maleness is frequently the result of transfer of Y DNA, including TDF, to a paternally derived X chromosome.

Hybridization of probe pDP151 (locus D15S2) to genomic human DNAs digested with EcoRI revealed allelic restriction fragments 9 and 11 kilobase-pairs (kb) in length. Hybridization of pDP151 to EcoRI-digested DNAs from 21 Chinese hamster X human hybrid cell clones containing different subsets of human chromosomes demonstrated cosegregation of the 9 and 11 kb EcoRI fragments with human chromosome 15. D15S2 and two other polymorphic loci previously mapped to chromosome 15--D15S1 and D15S6--were localized to specific regions on human chromosome 15. Eight Chinese hamster X human somatic cell hybrid clones derived from a human donor heterozygous for a balanced translocation between chromosomes 15 and 22 [t(15;22)(q14;q13.3); Oliver et al, Cytogenet Cell Genet 22:503-510, 1978] were studied. After digestion of human and hybrid DNAs with HindIII and Southern blotting, pDP151 (D15S2) and pMS1-14 (D15S1) hybridized to fragments of 4 and 4.5 kb, respectively. Further, pMS1-14 (D15S1) and p9-1a (D15S6) hybridized to EcoRI fragments of 3.5 and 3.2 kb. All fragments cosegregated with the der(22) derivative chromosome containing region 15q14----15qter. In situ hybridization of these probes to normal human chromosomes mapped the corresponding loci with greater precision: D15S1 to 15q15----15q21, D15S2 to 15q15----15q22, and D15S6 to 15q22----15q24.

Random amplified polymorphic DNA (RAPD) was used with the objective of identifying DNA markers hnked to the sclerotinia crown and stem rot (SCSR) resistance of red clover. Bulked segregant analysis was used to detect polymorphism that should be hnked to SCSR resistance. Two bulks were made by pooling previously extracted DNA. Each bulk (one resistant, and the other susceptible) consisted of eight genotypes from an F2 population obtained from a cross between a susceptible and a resistant parent. A binomial model was used to select RAPD fragments with a low probabihty of no linkage with SCSR resistance. Four RAPD fragments were retained as candidate markers of SCSR resistance. Three are associated with resistance and one with susceptibility.