| Popis: |
For years teratologists have had access to mice with spontaneously occurring mutations resulting in unique phenotypes. Animals with defects in many organ systems are available and provide valuable information about the origin of specific congenital malformations. However, most of these mutations involve recessive genes, and the genes themselves are unknown (Kalter 1980). Consequently, there are no markers available to identify mutant embryos before they overtly exhibit an altered phenotype. Thus it is difficult to investigate the earliest cellular events and mechanisms responsible for abnormal phenotypes, since only 25% of all embryos in a litter are affected and there is no way to identify which embryos they are before they exhibit grossly abnormal morphology. As a result, the amount of information provided by these models has been limited, and interpretations of the cellular mechanisms of teratogenesis somewhat speculative. |
