Cystic fibrosis (CF) is the most common genetic disease in Americans of Northern European origin. Like malaria, it is thought to provide some benefit to carriers. Using what you know of classical (Mendelian) genetics, molecular genetics and evolutionary genetics, answer the following questions: (1) CF typically pops up de novo in families, in other words, there is no family history. Why is this an unsurprising trend? ( 2 pt); (2) What do you expect in the genotype, protein phenotype, and organismic phenotype of a carrier? (3 pt); (3) Describe (briefly) what goes on in the tissue of an affected individual and why this could confer heterozygote advantage
Okay so I understand that being a carrier has helped fight off cholera, similarly to how sickle cell works for carriers and malaria. For part 1) is it not surprising no family history is needed to obtain the mutation because being a carrier it can help you survive, or is it being in that location that increases chances regardless of genetic history?
2) the genotype would remain heterozygous, lets say (CC) for the dominant alleles and infected (cc) recessive, protein phenotype would take the shape of the disease? and the organism phenotype would not change
3)as far as tissue goes in the infected, I understand that it builds mucus in the lungs, which is a good place for bacteria to grow and does things to the intestines. Heterozygotes are able to secrete half as much liquid so they do not dehydrate as quickly or lose as much liquids compared to those infected?
Any patching to what I have down would be great, thanks guys and girls!
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