An additional control system is superimposed on the repressor– operator system. This system exists because cells have specific enzymes that favor glucose uptake and metabolism. If both lactose and glucose are present, synthesis of β-galactosidase is not induced until all the glucose has been utilized. Thus, the cell conserves its metabolic machinery (that, for example, induces the lac enzymes) by utilizing any existing glucose before going through the steps of creating new machinery to metabolize the lactose. The operon model outlined earlier in this chapter will not account for the suppression of induction by glucose, so we must modify it.Continue Reading W.B.C.S. Main 2018 Question Answer – Zoology – Catabolite Repression.

Studies indicate that in fact some catabolic breakdown product of glucose (no exact identity is yet known) prevents activation of the lac operon by lactose, so this effect was originally called catabolite repression. The effect of the glucose catabolite is exerted on an important cellular constituent called cyclic adenosine monophosphate (cAMP).

When glucose is present in high concentrations, the cAMP concentration is low; as the glucose concentration decreases, the concentration of cAMP increases correspondingly. The high concentration of cAMP is necessary for activation of the lac operon. Mutants that cannot convert ATP into cAMP cannot be induced to produce β-galactosidase, because the concentration of cAMP is not great enough to activate the lac operon. In addition, there are other mutants that do make cAMP but cannot activate the lac enzymes, because these mutants lack yet another protein, called catabolite activator protein (CAP), made by the crp gene. CAP forms a complex with cAMP, and it is this complex that is able to bind to the CAP site of the operon. The DNA-bound CAP is then able to interact physically with RNA polymerase and essentially increase the affinity of RNA polymerase for the lac promoter. In this way, the catabolite repression system contributes to the selective activation of the lac operon.

Glucose control is accomplished because a glucose breakdown product inhibits formation of the CAP-cAMP complex required for RNA polymerase to attach at the lac promoter site. Even when there is a shortage of glucose catabolites and CAP-cAMP forms, the enzymes taking part in lactose transport and metabolism are produced only if lactose is present. This level of control is accomplished because lac operon inducers must bind to the repressor protein to remove it from the operator site and permit transcription of the lac operon. Thus, the cell conserves its energy and resources by producing the lactose-metabolizing enzymes only when they are both needed and useful. These concepts are summarized in  which also depicts the bending of the DNA resulting from CAP-cAMP binding to the CAP site, presumably increasing the affinity of RNA polymerase to the promoter.