6 Human polyomavirus (PoV) can cause cancer, but it is not known exactly how. Po

Question

6 Human polyomavirus (PoV) can cause cancer, but it is not known exactly how. PoV integrates into the human DNA in the middle of a gene called MyBPC, which is a myosin binding protein. MyBPs are neither oncogenes nor tumor suppressor genes, though. So we have to form a hypothesis and test it. The figure shows virus insertion into the MyBPC gene. The part of the virus that inserts has a promoter (blue area). It also encodes a gene, VP1, and a short stretch called Agno that might or might not encode a gene. Integration occurs in the VP1 sequence, splitting it as shown. When the provirus is transcribed, it produces an mRNA that is a fusion between VP1 and MyBPC. Because this fusion does not maintain the MyBPC's normal reading frame, when the fusion mRNA is translated, a premature stop codon occurs at the location marked by *. 19 VP1-MYBPC1 Fusion Protein MYBPC1 Agno VP-1 MYBPC1 MYBPC1 PoV PoV provirus A. Suggest THREE specific ways in which this viral insertion might cause tumor formatiorn For each hypothesis, suggest which protein is involved, and what it might be doing to cause tumor formation 19 B. Now think of a technique that could be used to test each of your three hypotheses. What experiment could you do, and what would you look for to prove or disprove each hypothesis? 17

Explanation / Answer

Ans-

The PoV virus can lead to the conversion of normal cells into cancerous cells by stoping the synthesis of tumor supressor gene.

cell cycle i.e Cell growth and replication are tightly regulated processes.

PoV Viral proteins disrupt this growth cycle by interacting and binding with host proteins.

In addition PoV  malignancies severely affects the immunosuppressed population, particularly HIV-positive patients and organ-transplant recipients.

To proove the hypothesis-

One woud need to mutate the gene in such way that stop codon will be removed so that tumor supressor genes can be synthesised and they are capable of supressing the cancer.

The second hypothesis is disregulation of cell cycle regulatory proteins.

If we inhibits the cell cylce regulatory proteins and their upregulated actions , then cancerous cells will not be formed by PoV.

Third hypothesis is mutation in DNA replication mechnery. If abonrmal DNA synthesis goes on by mutation in gene, then cancer cells results.

So inhibiors of DNA replication enzymes would be used to proove that cancer cell formation occurs due to abnormal DNA synthesis/ replication

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