Carbon catabolite repression in bacteria: choice of the carbon source and autoregulatory limitation of sugar utilization

Abstract

Carbon catabolite repression (CCR) in bacteria is generally regarded as a regulatory mechanism to ensure sequential utilization of carbohydrates. Selection of the carbon sources is mainly made at the level of carbohydrate-specific induction. Since virtually all carbohydrate catabolic genes or operons are regulated by specific control proteins and require inducers for high level expression, direct control of the activity of regulators or control of inducer formation is an efficient measure to keep them silent. By these mechanisms, bacteria are able to establish a hierarchy of sugar utilization. In addition to the control of induction processes by CCR, bacteria have developed global transcriptional regulation circuits, in which pleiotropic regulators are activated. These global control proteins, the catabolite gene activator protein (CAP), also known as cAMP receptor protein, in Escherichia coli or the catabolite control protein (CcpA) in Gram-positive bacteria with low GC content, act upon a large number of catabolic genes/operons. Since practically any carbon source is able to trigger global transcriptional control, expression of sugar utilization genes is restricted even in the sole presence of their cognate substrates. Consequently, CAP- or CcpA-dependent catabolite repression serves as an autoregulatory device to keep sugar utilization at a certain level rather than to establish preferential utilization of certain carbon sources. Together with other autoregulatory mechanisms that are not acting at the gene expression level, CCR helps bacteria to adjust sugar utilization to their metabolic capacities. Therefore, catabolic/metabolic balance would perhaps better describe the physiological role of this regulatory network than the term catabolite repression.