Answer:
1. The difference between the normal hemoglobin protein DNA sequence and the sickle cell hemoglobin DNA sequence is a base to base shift, in this case adenine (GAG) to thymine (GTG).
2. The difference affects the amino acid sequence of the protein by replacing glutamic acid (Glu) with valine (Val).
Explanation:
In sickle cell anemia, a change in the DNA nucleotide sequence is observed, where adenine is substituted by thymine, whose expression is the change in the amino acid sequence of globine β, incorporating valine instead of glutamic acid. This represents a molecular mutation - point mutation - by subtitution, which corresponds to missense mutation.
<u>Normal hemoglobin protein in a RBC</u>
DNA CTG ACT CCT GAG GAG AAG TCT
Amino acids Leu Thr Pro Glu Glu Lys Ser
<u>Sickle cell hemoglobin protein in a RBC</u>
DNA CTG ACT CCT <em>GTG</em> GAG AAG TCT
Amino acids Leu Thr Pro <em>Val</em> Glu Lys Ser
When GAG is transcribed to mRNA, the CUC codon is obtained, which codes for glutamic acid. Thymine substitution causes the DNA sequence to change to GTG, which is transcribed as CAC, the codon that encodes the amino acid valine. The <u>change from glutamic acid to valine in β-globin causes an altered hemoglobin, giving the abnormal erythrocytes observed in sickle cell disease</u>.
Answer:
Explanation:
I think it b c d sorry if wrong
Lipid bilayer model was proposed for its structure but it was modified and new structure is according to fluid mosaic model. Plasma membrane is selectively permible as it selects small molecules like lipid etc (composition is also of lipid and as solubility principle like dissolve like) so large and charged molecules like plasma and ion can't pass through it. Lipid are in form of layer so at the chain when ever other phosphate group attach the place conjugate molecule (phospholipid ) formed
