Sickle-cell mutation

The sickle-cell mutation is a genetic alteration in the beta-globin gene of the hemoglobin, characterized by a single nucleotide substitution (A to T) in the DNA sequence. This mutation leads to the replacement of glutamic acid with valine at the sixth position of the beta-globin chain, resulting in hemoglobin S (HbS) instead of normal hemoglobin A (HbA). When deoxygenated, HbS polymers form, causing red blood cells to assume a rigid, sickle-like shape. This sickling process can lead to various complications, including pain crises, increased risk of infection, anemia, and organ damage, due to impaired blood flow and oxygen delivery. The sickle-cell trait, where individuals carry one copy of the mutated gene (heterozygous), provides some resistance to malaria, which explains the higher prevalence of this mutation in regions where malaria is endemic. Problem: In sickle-cell disease, a glutamate to valine substitution results in formation of HbS molecules, which: A) Aggregate abnormally and cannot adequately carry O2 B) Have abnormally high-affinity binding for O2 C) Stabilize the wall of the red blood cell against oxidative damage D) Cause experience high levels of repulsion between neighboring HbS molecules