Schriever-Schwemmer G, Adler I D
GSF-Forschungszentrum für Umwelt and Gesundheit, Institut für Säugertiergenetik, Neuherberg (FRG).
Cytogenet Cell Genet. 1993;64(2):122-7. doi: 10.1159/000133567.
A reciprocal translocation, T(7;15)33Ad, with presumed breakpoints in bands 7A1 and 15F3 was induced in late spermatids by injecting male (102/E1 x C3H/E1)F1 mice five times with acrylamide (50 mg/kg body weight). Outcrosses of the original semisterile T(7;15) female generated three males monosomic for the short marker 7(15) [Ms(7(15))] among a total of 15 males. The Ms(7(15)) males sired small litters and had reduced testes weights. From inter se matings of Ms(7(15)) animals, nullisomic progeny for chromosome 7(15) were obtained and mated to produce a breeding stock of mice with 38 chromosomes. For comparison, mice carrying the reciprocal translocation T(4;8), with similarly located breakpoints, were also analyzed. Fluorescent in situ hybridization (FISH) with major and minor satellite DNA probes and a telomeric DNA probe was utilized. The observed FISH signals suggest that in chromosomes 7 and 8 the breaks occurred within the pericentric heterochromatic block immediately below the centromere and in chromosomes 15 and 4 at a point near the distal telomeres. The long markers 15(7)and 4(8) are tandem fusion chromosomes. The short markers 7(15) and 8(4) also showed all appropriate FISH signals for intact chromosomes. The loss of the small chromosome 7(15) was compatible with survival, suggesting that no essential genes are located on the small reciprocal translocation product. The development of this tandem fusion stock is described as a laboratory example of one possible step in karyotypic evolution.
