Further studies on the asymmetry of chromosome 15 duplication in trisomic leukemias of heterozygous origin: preferential status of the AKR chromosome.
Four combinations of translocation heterozygotes with cytogenetically distinct chromosomes 15 were used to investigate whether the T-cell leukemia-associated preferential duplication of the AKR-derived chromosome 15 (AKR-15) is determined by factors within this chromosome, or is due to genes within the AKR genotype, but outside chromosome 15. Two of the four combinations were also used to determine whether the AKR-15 duplication preference could be cancelled by MCF-viremia in permissive F1 hybrids. Chemically and virally induced 15-trisomic leukemias showed the same AKR-15 duplication preference, which was due to some autonomous property of AKR-15 itself. It was maintained in (C57BL 6;15 X C57BL) F1 leukemias, where 6;15 is the only AKR-derived chromosome propagated on the C57BL/background. In the (C57BL 6;15 X AKR) F1 hybrid cross where both chromosomes 15 are of AKR origin, duplication occurred at random. To approach the second question, MCF viremia was induced by neonatal virus inoculation into permissive (AKR 6;15 X B6Fv-In) F1 hosts. The preferential duplication status of the AKR-derived 6;15 remained unchanged.
D000818:Animals; D002871:Chromosome Banding; D004171:Diploidy; D005819:Genetic Markers; D006579:Heterozygote; D007621:Karyotyping; D009052:Leukemia Virus, Murine; D007942:Leukemia, Experimental / Q000139:chemically induced / Q000235:genetics* / Q000382:microbiology; D051379:Mice; D008806:Mice, Inbred AKR / Q000235:genetics*; D008810:Mice, Inbred C57BL / Q000235:genetics; D014178:Translocation, Genetic; D014314:Trisomy
D005819:Genetic Markers