Answer:
1. The average heterozygosity at this locus should be decreasing over time
3. Diploidy is helping to preserve the sickle-cell allele at this locus
Step-by-step explanation:
Sickle cell anemia is caused by a mutation in the beta hemoglobin gene. The mutation substitutes amino acid valine for glutamic acid. The mutation makes the hemoglobin less soluble. The mutated hemoglobin forms crystal-like structures and affects the shape of RBCs. The RBCs carrying the mutated hemoglobin are sickle-shaped. The mutation is recessive in nature and the disease is expressed in homozygous recessive genotype. However, the heterozygous genotype exhibit resistance to malaria pathogen since the pathogen can not survive in altered RBCs. The presence of one normal allele prevents these heterozygous individuals to be affected by the disease.
Therefore, the heterozygous genotype for sickle cell anemia is preferred by natural selection in malaria-prone regions such as Africa. The individuals with African ancestry would have higher heterozygosity at the beta hemoglobin locus. In American populations, homozygous recessive genotypes have a higher frequency as the disease is not expressed in recessive conditions and malaria is not prevalent there. So, the U.S. populations of African-Americans would exhibit reduced heterozygosity at the locus over generations.