Abstract
Two related strains of mice, A/J and CL/Fr, differ in the frequency of spontaneous cleft lip produced in term fetuses: 10% versus 25%. In order to examine the nature of the genetic basis for this difference, various crosses between the strains were made. The results indicated that genes acting in the mothers, rather than in the embryos, caused the strain difference, and that their effect may be on CL(P) embryo survival rather than occurrence. The A/J strain alleles were dominant to those of CL/Fr, and a one-locus difference can explain the data. The importance of genetic maternal effects on CL(P) frequency in mice, with dominance, should be borne in mind when the polygenic, additive threshold model is applied to human data. Neither effect is allowed within the model, yet if the traits are homologous between species, these effects may well be present in man as in the mouse.
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