The lactose (lac) operon responsibl

The lactose (lac) operon responsible for the degradation of the sugar lactose is an inducible operon under positive and negative regulation (see Figure 3-6). Normally the bacteria use glucose and not lactose. In the absence of lactose the operon is repressed by the binding of the repressor protein to the operator sequence, thus impeding the RNA polymerase function. In the absence of glucose, however, the addition of lactose reverses this repression. Full expression of the lac operon also requires a protein-mediated, positive-control mechanism. In E. coli, when glucose decreases in the cell, cAMP increases to promote usage of other sugars for metabolism. Binding of cAMP to a protein called the catabolite gene-activator protein (CAP) allows it to bind to a specific DNA sequence present in the promoter. The CAP-cAMP complex enhances binding of the RNA polymerase to the promoter, thus allowing an increase in the frequency of transcription initiation.
The tryptophan operon (trp operon) contains the structural genes necessary for tryptophan biosynthesis and is under dual transcriptional control mechanisms (Figure 13-8). Although tryptophan is essential for protein synthesis, too much tryptophan in the cell can be toxic; therefore its synthesis must be regulated. At the DNA level the repressor protein is activated by an increased intracellular concentration of tryptophan to prevent transcription. At the protein synthesis level, rapid translation of a “test peptide” at the beginning of the mRNA in the presence of tryptophan allows the formation of a double-stranded loop in the RNA, which terminates transcription. The same loop is formed if no protein synthesis is occurring, a situation in which tryptophan synthesis would similarly not be required. This regulates tryptophan synthesis at the mRNA level in a process termed attenuation, in which mRNA synthesis is prematurely terminated.
The expression of the components of virulence mechanisms are also coordinately regulated from an operon. Simple triggers, such as temperature, osmolarity, pH, nutrient availability, or the concentration of specific small molecules, such as oxygen or iron, can turn on or turn off the transcription of a single gene or a group of genes. Salmonella invasion genes within a pathogenicity island are turned on by high osmolarity and low oxygen, conditions present in the gastrointestinal tract or an endosomal vesicle within a macrophage. E. coli senses its exit from the gut of a host by a drop in temperature and inactivates its adherence genes. Low iron levels can activate expression of hemolysin in E. coli or diphtheria toxin from Corynebacterium diphtheriae, potentially to kill cells and provide iron. Quorum sensing for virulence factors of S. aureus and biofilm production by Pseudomonas spp. were discussed above. An example of coordinated control of virulence genes for S. aureus based on the growth rate, availability of metabolites, and the presence of a quorum is presented in Figure 13-9.
Replication of DNA