Related Experiment Videos
Cortisone-induced cleft palate in the mouse. A search for the genetic control of the embryonic response trait
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.
Insights
Genetic factors influence cortisone-induced cleft palate susceptibility. Embryonic tolerance differences between A/J and C57BL/6J mouse strains are likely controlled by a few genes, not a single major gene or polygenic model.
Area of Science:
- Developmental biology
- Genetics
- Teratology
Background:
- Cortisone administration during pregnancy can induce cleft palate in mouse embryos.
- Significant differences exist in the susceptibility of various mouse strains to teratogen-induced birth defects.
- Understanding the genetic basis of this susceptibility is crucial for developmental toxicology research.
Purpose of the Study:
- To investigate the genetic underpinnings of differential embryonic response to cortisone-induced cleft palate between A/J and C57BL/6J mouse strains.
- To determine the mode of inheritance and the number of genes involved in cortisone teratogenesis.
Main Methods:
- Quantitative genetic analysis of embryonic response to cortisone in different mouse crosses.
- Statistical modeling to assess single gene, polygenic, and multifactorial inheritance patterns.
- Examination of potential linkage to the major histocompatibility locus (H-2) and X-chromosome.
Main Results:
- The difference in mean tolerance (ED50) to cortisone-induced cleft palate is attributed to a small number of genes.
- A single major gene effect and a purely polygenic model were excluded.
- C57BL/6J embryonic tolerance is dominant over A/J, with two or three loci potentially explaining the variability.
- A portion of the variation may be associated with or linked to the H-2 locus.
- No evidence supported X-chromosome linkage.
Conclusions:
- Cortisone-induced cleft palate susceptibility in these mouse strains is controlled by a limited number of genes with additive and possibly dominant effects.
- The genetic architecture is complex, involving a few loci rather than a single major gene or numerous small additive genes.
- The major histocompatibility complex (H-2) may play a role in modulating the embryonic response.