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Gm(a) (x) (g) (f) (b1) were examined in 84 random Norwegian families with 444 children allowing direct estimates of the f,b, a,g, ax,g, and a,b (including a,b0b1, a,b0st, and f,b0b1) gene complex frequencies and an upper estimate of the f,g frequency. Phcnotype and mating type patterns were random (non–assortative). Disturbed segregation ratios were found in ax,g/f,b×f,b/f,b families irrespective of sex of segregating parents, and in families with a,g/f,b in backcross if segregating parents were separated by sex. In the latter case excess a,g from females was balanced by excess f,b from males, this trend being present also in two other Norwegian family materials (tested for Gm(a) (x) (b1)). Gm(n) was examined in part of the material, allowing approximate frequency estimates of the polymorphic f,b,n, f,b,n–, a,g,n–, and ax,g,n– and the idiomorphic ax,g,n, a,g,n, a,b0st,n– and a,b b1,n– (fa, b0b1 unassigned). The information on the IgGl–IgG3 and the IgGl, IgG3–IgG2 linkage relations were estimated. A family with familial low Gm(g) activity was observed and interpretations included a genetically linked cis–IgC3–suppressor gene in analogy with thalassemia genes as well as a structural allele mutation.
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Gedde‐Dahl et al. (1971) studied this question.
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