I have started working on Bgl operon in E. coli at IISc, Bangalore. It is a type of cryptic genes, which means that there is no reason for a cell to maintain those genes in its genome. Bgl operon is normally in inactive state due to an indirect repeat ahead of promoter which prevents its recognition by RNA polymerase. It further has attenuation control mechanism.
The point is that the inverted repeats render the operon inactive hence it is unable to metabolise salicin (Bgl’s normal function). It is only due to mutation in inverted repeats which can activate the operon.
Now two questions come into the mind:
1. Since encountering of salicin is a very unlikely event, why is Bgl operon present in the genome in the first place.
2. Even if it is maintained, why is it in inactive state which renders it unable to utilize salicin. Only after the mutation (which is again unlikely) it is able to metabolize salicin if present in environment.
For explaining these questions, we have two hypothesises:
1. Bgl operon has some other function also (apart from normal metabolization of salicin)
2. Bgl is maintained because a cell can expect salicin in the environment in future. But it cannot afford to waste its cellular resources on an inducible operator because the probablity of encountering salicin is extremely low.
I intuitively believe in second hypothesis, but evidence suggests otherwise.