Question

Hagrid has purified a protein from unicom sweat and called UNI-1. He has then doned the Unit gone and inserted in rat zygotes (by microinjection) a recombinant construct containing the Uni-1 coding sequence its entire 5 UTR region, covering both the minimal promoter and a series of cutative regulatory als elements. The mutantrats develop glorious, luminous hair. Hagrid has also discovered that the UNI-1 protein binds very tightly to DNA and hypothesizes it is a transcription factor that regulates proliferation in the hair follide stem cells and therefore promotes hair growth. Since the stem cells of the hair follicle uniquely express the gene Lars, the best way in which Hagrid can find out whether his UNI-1 protein is indeed selectively expressed in hair follicle stem cells is to A. Introduce in rat zygotes a construct containing the SUTR of Unit ed to CFP and see the resulting m antras have green fluorescent har follicles but short hair one linked to the coding sequence of UNI-1 and see if the rats grow long glorious hair Bintroduce in rotzygohes cont i ng the W UTR of the L C. Both experiments will be helpful to understand the function of UNI-1 D. None of these experiments makes any sense whatsoever, sorry Hagrid

Answer 1

Question 1. The best way will be to introduce a construct containing the 5' UTR of Uni-1, minimal promoter of Uni-1 linked to GFP and a series of putative cis-elements in rat zygote. This will help to express GFP protein in the hair follicles and will also help to confirm the hypothesis.

So, my answer will be option D

Question 2. Answer is option A.

If a hydrophobic drug can be synthesized, which will mimic cortisol by binding to cortisol-binding proteins then the problems related to stress can be solved. And there will be no need for taking cortisol steroids from outside. This will help to reduce the side effects due to excessive steroid intake.

Question 3. Answer is option A.

SNARE proteins are the integral membrane proteins in the budding vesicles which are crucial for an eventual fusion of the vesicle with the correct target membrane.

Question 4. Answer is Option A.

Phosphatases remove phosphate from GTP but do not transfer the phosphate to GTP binding protein rather the phosphate is removed as inorganic phosphate.

Question 5. Answer is option D.

Sar1 acts as a GTPase. After pinching off of the vesicles the bound GTP is hydrolyzed into GDP which releases the coat proteins Sec13/31 from the vesicles. Now due to mutation Sar1 loses its activity and thus there will be no conversion of GTP to GDP. So more and more Sec13/31 will bind to the vesicles.