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. 1977 Feb;85(2):289–302. doi: 10.1093/genetics/85.2.289

Cortisone-Induced Cleft Palate in the Mouse. a Search for the Genetic Control of the Embryonic Response Trait

F G Biddle 1, F C Fraser 1
PMCID: PMC1213632  PMID: 863228

Abstract

The cause of the difference in the mean tolerance (ED50 ) to cortisone-induced cleft palate between the embryos of the A/J and C57BL/6J strains appears to be due to a small number of genes. A single major gene effect and a polygenic model, in the sense of many equal and additive genes, have been ruled out. The embryonic tolerance of C57BL/6J is greater than and dominant to that of A/J; two or three loci, possibly with independent effects, appear to explain the variability. A component of the variation in embryonic response may be associated with or linked to the major histocompatibility locus (H-2). No evidence was found to support the hypothesis of X-chromosome linked susceptibility to cortisone-induced cleft palate.

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Selected References

These references are in PubMed. This may not be the complete list of references from this article.

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