1. Explain why RT has RDDP and DDDP activity. (1
Points)2a. Explain the process by which RT lengthens the
primer strand. (1 Points)2b. In the mutagenesis HIV-1 RT paper by Harris et althe researchers did not use the natural form of RT
for their studies. What did they use instead?(1 Points)3. M184V is an interesting mutation. Compare
the activity of this mutation and its affect on polymerization and fidelity. (1
Points)4. It seems that the RNase H activity in each
of the mutants was not affected by the amino substitutions. Why do you think
this is the case? (5 Points)5. In the Harris
et al. paper the researchers test the pyrophosphorolysis activity of WT HIV-1 RT and its
dNTP-binding pocket mutants. However the gel products are below the primer:template
while the other gel products in the rest of the figures are above the primer:template.
Explain why this is. (1 Points)6. Explain how reverse transcriptase creates
mutations specifically in the b3-b4 loop. (1 Points)7. In the Harris et al. paper the Y183A mutation was
pretty much dead but the Y183F mutation rescued a small amount of the
activity. Explain the reasoning behind this. (1 Points)8. By studying the structure of Reverse Transcriptase
by Huang et al. it can easily be
determined why the mutation K65R is a multi-drug resistance mutation. What is
the reasoning behind this statement? (1 Points)9. From the structure of the closed complex explain
the importance of the b3-b4 loop? (5-points)10. What is the importance (function) of the Y183
residue? (This question you may go out of the paper to search for. The best
place to find the answer is in the primary literature like Pubmed or Google
Scholar).(10 Points)11. The speed at which the RT can function is limited
to a specific step in the polymerization event. What step in the RT mechanism
controls the rate at which RT can proceed at incorporating the dNTPs? (1
Points)Extra Credit: (5 Points)A. Why was the H-helix used to create the cross
linkage?