Problem:

Rous sarcma virus (RSV) carries an oncogene called Src, which encodes an active tyrosine kinase that phosphorylates something else and causes unchecked cell proliferation. Normally Src carreis an attached fatty acid called myristoylate, which in turn binds to the cytoplasmic side of the phospholipid membrane. A mutant version of the same Src seems to be spread evenly around the cell. The mutant form does not bind to the phospholipid membrane. When you infect cells with BOTH the normal (wildtype) and the mutant, both RSV proteins are produced.

Required:

Question 1: What is the relative concentration of normal Src to mutant Scr just inside the membrane? Near the nucleus?

Question 2: The target for Src phosphorylation is stuck in the membrane. Briefly explain why the mutant Src does not cause cell proliferation?

Could someone explain this to me?