Complementation studies with mouse translocations

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Abstract
When heterozygotes for reciprocal translocations are intercrossed, the fusion of complementary unbalanced gametes normally gives fully viable, balanced zygotes. If one parent is homozygous for a genetic marker not carried by the other, the frequency of homozygous progeny resulting from such complementation can indicate whether the marker is distal or proximal to the translocation break point and thus fix the centromeric (proximal) end of the linkage group concerned. By the use of mouse translocations T(8;16)17H, T(10;18)18H, T(7;18)50H, and T(5;13)264Ca in this way, the centromeres were located at the rl, nv, nr, and dy ends of chromosomes 5, 7, 8, and 10, in line with findings by cytologic methods. Estimated frequencies of adjacent-2 disjunction (associated with complementation for interstitial segments) for T(2;9)11H, T50H, and T264Ca were 14 %, 29 %, and 12% respectively. In certain translocation intercrosses, the expected genetically marked complementation types failed to appear or else failed to survive the neonatal period. This phenomenon is associated with a maternal duplication and complementary paternal deficiency of the distal ends of chromosomes 2, 8, and possibly 7 (from other evidence). Data from other chromosomes show normal complementation, but a number remain to be tested. The possibility that haploid expression of particular maternal or paternal genes is important for normal mouse development is discussed.