Mead et al. (2003) analyzed whether a polymorphism in the human PRP gene influenced susceptibility to prion infection that is transmitted by ritual cannibalism of the brains of deceased relatives, which took place (prior to the 1950s) in the Fore people of New Guinea. Prion disease in this population is an incurable and fatal neurodegenerative disorder known as kuru. It is called a "spongiform encephalopathy" disease because the brain's cerebral cortex develops numerous tiny holes, so that it comes to resemble a sponge.
At codon 129 in the PRP protein, some gene copies have the amino acid methionine ("M allele"), while others have the amino acid valine ("V allele"). A census of 140 Fore individuals who were not exposed to kuru infection (non-cannibals) found 31 MM homozygotes, 72 MV heterozygotes, and 37 VV homozygotes. However, in a sample of 30 Fore adults that had engaged multiple times in ritual cannibalism (and who had survived without developing kuru), 4 had genotype MM, 23 had genotype MV, and 3 had genotype VV.
Do these data indicate that cannibalism has caused natural selection at the PRP locus? One way to analyze this is to consider the "non-cannibal" group to represent a sample that has not experienced any natural selection. If these individuals were exposed to selection from kuru infection, then it's possible that the sample genotype composition might be altered to look like the other group of 30 adults who had survived cannibalism without developing kuru. So we can consider these two groups to provide evidence on what population composition would look like before vs. after natural selection had acted.
Question 1: Why might it not be valid to assume that the n=140 and n=30 groups can be directly compared to reveal what a population would look like before vs. after selection has acted?
Question 2: Does the n=140 (unexposed) sample have a composition that differs significantly from Hardy-Weinberg genotype proportions?
Question 3: Use these data to estimate the relative fitness of each genotype.
Mead et al. (2003) analyzed whether a polymorphism in the human PRP gene influenced susceptibility to prion infection that is transmitted by ritual cannibalism of the brains of deceased relatives, which took place (prior to the 1950s) in the Fore people of New Guinea. Prion disease in this population is an incurable and fatal neurodegenerative disorder known as kuru. It is called a "spongiform encephalopathy" disease because the brain's cerebral cortex develops numerous tiny holes, so that it comes to resemble a sponge.
At codon 129 in the PRP protein, some gene copies have the amino acid methionine ("M allele"), while others have the amino acid valine ("V allele"). A census of 140 Fore individuals who were not exposed to kuru infection (non-cannibals) found 31 MM homozygotes, 72 MV heterozygotes, and 37 VV homozygotes. However, in a sample of 30 Fore adults that had engaged multiple times in ritual cannibalism (and who had survived without developing kuru), 4 had genotype MM, 23 had genotype MV, and 3 had genotype VV.
Do these data indicate that cannibalism has caused natural selection at the PRP locus? One way to analyze this is to consider the "non-cannibal" group to represent a sample that has not experienced any natural selection. If these individuals were exposed to selection from kuru infection, then it's possible that the sample genotype composition might be altered to look like the other group of 30 adults who had survived cannibalism without developing kuru. So we can consider these two groups to provide evidence on what population composition would look like before vs. after natural selection had acted.
Question 1: Why might it not be valid to assume that the n=140 and n=30 groups can be directly compared to reveal what a population would look like before vs. after selection has acted?
Question 2: Does the n=140 (unexposed) sample have a composition that differs significantly from Hardy-Weinberg genotype proportions?
Question 3: Use these data to estimate the relative fitness of each genotype.
