Sometimes the term catabolite repression has been used to describe the glucose effect that is independent of the operon-specific regulator, such as the Lac repressor. Here, we shall use it as a general name for the glucose effect as originally defined. According to this view, which is apparently generally accepted, catabolite repression includes all forms of the glucose effect, regardless of their mechanisms. We also concentrate on catabolite repression in E. coli. Although several mechanisms of glucose catabolite repression are now understood in E. coli, a common feature is that glucose causes catabolite repression ultimately by modulating the activity of transcription factors involved in the regulation of target operons.
Figure 1. Mechanism of catabolite repression in the glucose-lactose system (4). When both lactose and glucose are present, glucose is transported and phosphorylated by the glucose PTS (IIAG/c + IICBG/c), increasing the concentration of the nonphosphorylated form of IIAGlc, which prevents the uptake of lactose by inhibiting the Lac permease activity. Thus, the concentration of lac inducer is very low in the presence of glucose, so the Lac repressor is active and represses transcription of the lac operon. It should be noted that glucose does not affect the binding of cAMP-CRP to the promoter, because the levels of cAMP and CRP are not reduced by the presence of glucose.
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The second mechanism of catabolite repression is inducer exclusion, by which glucose lowers the intracellular concentration of inducers necessary for the induction of catabolic operons (7). The target of glucose signaling in inducer exclusion is operon-specific regulators, such as the Lac repressor. The dephosphorylated enzyme IIAGlc, which accumulates in the presence of glucose, binds to and inactivates (for example) the Lac permease, resulting in an increase of the active unliganded Lac repressor (see Lac Operon). Inducer exclusion is a mechanism by which glucose inhibits more strictly the expression of target operons.