Final answer:
The alpha globin gene, like other genes, is subject to ongoing evolution. Mutations in alpha globin can lead to hemoglobinopathies, and the sickle cell mutation in beta globin persists in populations due to the malaria resistance it provides in heterozygous individuals, despite its severe effects in homozygous individuals.
Step-by-step explanation:
The evolution of the alpha globin gene and its relevance to sickle cell anemia is an ongoing process. Changes in our genetic material are continuous, and this includes the genes responsible for hemoglobin, which comprises two alpha and two beta chains. In sickle cell anemia, a mutation in the beta globin gene causes a single amino acid substitution, where valine replaces glutamic acid, which significantly impacts the protein's structure and function. This mutation results in the characteristic sickle-shaped red blood cells that obstruct capillary flow and delivery of oxygen causing anemia symptoms. Despite the negative evolutionary effects associated with this genetic mutation, such as a decreased life expectancy, the sickle-cell gene remains relatively common due to the heterozygous advantage it provides against malaria, making it a subject of continuous evolutionary interest.
Mutations similar to those affecting hemoglobin can also arise in the alpha globin gene, contributing to other types of hemoglobinopathies. This ongoing evolutionary process highlights the dynamic nature of genes, which may confer survival benefits in certain environments, such as areas where malaria is prevalent, despite having deleterious effects when the mutation is homozygous. Therefore, even though heterozygous individuals with the sickle cell trait possess some normal hemoglobin, natural selection can maintain the mutation within populations.