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Monday, February 11, 2019

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

Background to the endIn early 1995, an M.D-Ph.D student, Jennifer Brown, was breeding mice with an inactivated form of the element FosB. With the inactivation of the gene, legal pups from the mutated mice died quickly. Observing this occurrance, Brown run aground 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 effeminate 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 comp ard them to those of the normal mice. The Test ResultsFosB Mutant Development and AbnormalitiesFosB sport homozygous females were born and developed as any normal mouse, but were disco biscuit 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. H owever, twenty-four to fourty-eight hours after 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 sequestrate 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 pregnancy relied in the beginning upon the genotype of the mother, and was independent of father or pup genotype. This supports the idea that the endurance 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 feature ana... ...aper think that this is involved with the hypothalamus. The hypothalamus is located in the brain stem.The gene renewal did not effect any other functions of the mice. This indicates that FosB is exclusive t o nurturing behavior. 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 hot topic in current scientific society. What questions qualification be raised by such a discovery? If this gene does exist in humans, should people 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 abuse? 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 before making up their minds.

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