In the absence of AraC, RNA polymerase initiates transcription of the araC gene in the direction awway form its upstream neighbor, araBAD. The ara BAD ooperon is expressed at a low basal level.
When AraC is present, but neither L-arabinose nor CAP-cAMP (high glucose), AraC binds to araO1, araO2 and araI1. araO1 is the operator for the araC gene; its association with AraC blocks araC transcription so that this process is autoregulatory, although this requires high levels of AraC. The binding of AraC to AraI1 represses the expression of araBAD (negative control). A series of deletion mutations indicate that the presence of araO2 is also required for the repression of araBAD. The large 211 bp separation between araO2 and araI1 suggests that the DNA between them is looped such that a dimeric molecule of AraC protein simultaneously binds to both araO2 and araI1. This is corroborated by the observation that the level of repression is greatly diminished by the insertion of 5 bp (one half turn) of DNA between these two sites, thereby transfering araO2 to the opposite face of the DNA relative to araI1 in the putative loop. An insertion of 11 bp of DNA (one full turn) has no such effect.
When L-arabinose is present it allosterically induces the AraC subunits bound to araO2 to instead bind araI2. This activates RNA polymerase to transcribe the araBAD genes (positive control). CAP-cAMP binds to a site between araO1 and araI1 (although in most other CAP binding operons, CAP-cAMP binds adjacent to RNA polymerase), where it functions both to help break the loop between araO2 and araI1 and to increase the affinity of AraC for araI2. araC gene remains repressed by AraC-L-arabinose at araO1.