Tutor profile: Maya V.
What type of reaction is the reaction between acetic anhydride with aminophenol, what is the product of this reaction, and finally how could the purity of the product of this reaction be assessed?
Acetic anhydride may be reacted with with aminophenol in an amide forming reaction to synthesize acetaminophen. The crude product of this reaction may be purified through organic laboratory techniques including decolorization, recrystallization, and vacuum filtration. The purify of the final product may be analyzed using thin layer chromatography.
Write an example of a an amino acid sequence likely to form (a) an alpha helix, (b) a disulfide bond. For each sequence, explain why the amino acids in the polypeptide are likely to take on this structure.
a) MAKLSIDKVEASHMAELGP This polypeptide is likely to form an alpha helical structure because of the favorable hydrogen bonding interactions that can occur between n and n+4 side chains of amino acids. Methionine, alanine, leucine, glutamate, and lysine are all common in alpha helices. Proline and glycine are rare in alpha helices because glycine introduces flexibility in the chain, while proline is only common at one end of an alpha helix as its steric conformation introduces a kink in the rigid helical structure. b) MTPCMGELCPVDACGYLI This sequence is likely to contain disulfide bonds because these form between cystine residues greater than five resides apart.
Why does Sickle Cell disease persist in regions where malaria is endemic and what phenomenon is this an example of?
Sickle Cell disease is an inherited disorder caused by a mutation in a gene that encodes a subunit of the oxygen transporting protein hemoglobin. The characteristic mutation in Sickle Cell disease results in a misfolded hemoglobin subunit, known as HbS. These HbS subunits polymerize, or stick together, and the resulting structure forces red blood cells into an abnormal "sickle" shape. These sickled red blood cells do not efficiently carry oxygen or flow through the capillaries, causing anemia, vaso-occlusive crisis, and acute chest syndrome, among other severe complications. The Sickle Cell allele must be inherited from both parents (homozygosity) for the disease phenotype. Heterozygotes (those with one copy of the mutation) do not have Sickle Cell disease but express both HbS and healthy hemoglobin. Despite the severity of the disorder, its prevalence is relatively high, and the overlap between regions with high prevalence of Sickle Cell disease and malaria is striking. Malaria is a mosquito-borne, parasitic infection common in tropical climates. The microorganism that causes malaria, Plasmodium falciparum (P. falciparum), enters the body through a mosquito bite, infects red blood cells, and continues to reproduce, hijacking the cellular machinery within red blood cells. Malaria is a severe infection, however in 1954, a protective effect of Sickle Cell heterozygosity against malaria, as well as a higher rate of the HbS allele in regions with endemic malaria, was described. It has been found that as P. falciparum infects sickled red blood cells, dysfunctional molecular machinery in sickled red blood cells make them less hospitable to malaria. When the relationship between malaria and the HbS allele is viewed through the lens of natural selection, it is clear that this parasite exerts strong selective pressure in regions where malaria is endemic. As homozygotic individuals do not suffer from Sickle Cell disease but are protected from malaria, they are more likely to reproduce and pass on their genetic material. This has favored the HbS mutation in regions where malaria is endemic, and explains the high rate of the HbS allele and Sickle Cell disease in these communities. This is a prototypic example of the balanced polymorphism phenomenon. This equilibrium between heterozygotic advantage and homozygotic disease has resulted in the continued presence of Sickle Cell disorder in regions with endemic malaria. Key concepts: Genetic mutation, homozygote, heterozygote, allele, phenotype, natural selection, selective pressure, balanced polymorphism
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