Follow-up Work
Following the 1949 paper, Itano left the Pauling laboratory to work with Neel; in the following years they used electrophoresis to identify a number of other human hemoglobin variants, including some associated with other diseases. At Caltech, a comparison of the amino acid content of normal and sickle cell hemoglobins showed that they had several differences in chemical makeup, but did not explain the difference in electric charge that made electrophoretic separation possible. The cause of this difference was pinpointed in 1956 and 1957, when Vernon Ingram used protein fingerprinting to show that the key difference between normal hemoglobins and sickle cell hemoglobins was a single difference in one chain of the protein: a glutamic acid residue on the normal hemoglobin in place of a valine residue on the sickle cell hemoglobin.
The molecular disease concept put forward in the 1949 paper also became the basis for Linus Pauling's view of evolution. In the 1960s, by which time it had been shown that sickle cell trait confers resistance to malaria and so the gene had both positive and negative effects and demonstrated heterozygote advantage, Pauling suggested that molecular diseases were actually the basis of evolutionary change. He also advocated eugenic policies, such as marking all who carry the sickle cell trait and other molecular disease genes, to reduce the number of children born with genetic diseases.
Read more about this topic: Sickle Cell Anemia, A Molecular Disease
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