Genetics of palate development

We are beginning to see a tantalizing picture by looking into the "genetic window" on the teratogenesis of cortisone-induced cleft palate and on normal palate development. We must continue to open this window. So far, all strains of mice that have been treated with cortisone do react with induced cleft palate and, from their dose-response behaviors, they appear to react in the same way. It is tempting to conclude that dosage tolerance is the only genetic variation in the reaction. We do not attach any significance to this because we must emphasize the fact that these different strains represent an insignificant sample of the hundreds of genetically different, recognized strains of the mouse. We have emphasized previously that systematic strain surveys must become an active part of teratological genetics in order to obtain an approximation of how much genetic variation exists in a trait in the species (e.g., Biddle, 1981). Now, we need to go beyond strain surveys. Crosses between strains must become part of this activity. Dominance appears to be a property of the homeostatic model of palate development as far as the cortisone probe is concerned, but it may not be a universal property. The significance of dominance and the architecture of gene action can only be interpreted by exploring more strain pairs in the mouse. A study of two or three or four strains is simply inadequate. From the crosses between a limited number of strains, major genetic factors in cortisone reactivity have been identified. These major genetic factors may regulate the homeostatic model of palate development, but we do not know this for a fact. The identification of major genetic factors has moved us to a new horizon; we can move now from a purely descriptive biology to a study of the functional biology of the process of palate development. This move will require not only the molecular probes with which to walk along the specific chromosomes to the major genetic factors but also a library of fully characterized strains of the mouse in which to use these probes. The library of strains that have been genetically characterized for the cleft palate reaction is missing.