A Defect in Nurturing in Mice Lacking the Immediate Early Gene FosB Ess

Background to the ProjectIn early 1995, an M.D-Ph.D student, Jennifer brownness, was breeding mice with an inactivated form of the gene FosB. With the inactivation of the gene, healthy pups from the mutated mice died quickly. law-abiding this occurrance, Brown found that the mother mice ignored her offspring. From this discovery, Brown proposed that the inactivation of the immediate early gene FosB causes a defect in the nurturing behaviors of female mice. To prove this, Brown bred a series of knockout mice with the inactivated FosB gene. She then observed the nurturing behaviors of the knockout mice and compared them to those of the normal mice. The Test ResultsFosB Mutant Development and AbnormalitiesFosB fluctuation homozygous females were born and developed as any normal mouse, but were ten percent smaller than wild type mice. When the fosB homozygous females were mated with fosB homozygous mutant males, the resulting pregnancies were normal and carried to term. However, twent y-four to fourty-eight hours afterward delivery, the mortality rate of the pups was in excess of fifty percent. The high occurrance of lethality could be attributed to either the mutant mothers, the mutant pups, or both. To single out the cause of the high mutant pup mortality rate, heterozygous males were mated with homozygous females and vice versa. As a result, it was found that the number of surviving pups in any given motherliness relied primarily upon the genotype of the mother, and was independent of father or pup genotype. This supports the idea that the survival relies heavily on the nurturing ability of the fosB mothers.Physical Trait AnalysisTo isolate the defect in the mother that contributed to the death of her pups, a physical trait ana... ...aper think that this is involved with the hypothalamus. The hypothalamus is located in the brain stem.The gene mutation did not effect any other functions of the mice. This indicates that FosB is exclusive to nurturing behavio r. The discovery of the functions of the FosB gene in mice could lead to similar discoveries for the human genome. Ethical ramifications of such discoveries are a acid topic in current scientific society. What questions might be raised by such a discovery? If this gene does exist in humans, should masses with mutated alleles not be allowed to raise their children? Should it be corrected in some way by science? Is having a mutated gene an excuse for child subvert? Is it a defense in court? The answers to these questions are not clearly defined, but there are several sources of information for the public to access forward making up their minds.