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

AUTOR(ES)

Biddle, F. G.

RESUMO

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.

Documentos Relacionados

• Genetics of Cortisone-Induced Cleft Palate in the Mouse—embryonic and Maternal Effects
• Genes in mice that affect susceptibility to cortisone-induced cleft palate are closely linked to Ir genes on chromosomes 2 and 17.
• Leukokinetic studies: XIII. A non-steady-state kinetic evaluation of the mechanism of cortisone-induced granulocytosis
• Genetic control of renin activity in the submaxillary gland of the mouse.
• Genome scan for teratogen-induced clefting susceptibility loci in the mouse: Evidence of both allelic and locus heterogeneity distinguishing cleft lip and cleft palate