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#CAP-cAMP

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Gene regulation in Prokaryotes

CAP-cAMP complex binds when

Catabolite repression couples glucose availability to cyclic AMP synthesis via adenylate cyclase. When glucose transport is low, EIIA phosphorylated activates cyclase, raising cAMP levels. Cyclic AMP binds catabolite activator protein CAP, inducing conformational shift allowing dimerization and DNA recognition. The CAP-cAMP complex binds conserved sites near catabolite-sensitive promoters including lac, ara, gal, facilitating RNA polymerase recruitment through alpha-CTD contact. When glucose abundant, cAMP falls, CAP remains inactive, transcription of alternative sugar operons reduced. Thus CAP-cAMP binding specifically signals carbon starvation and glucose limitation, coordinating hierarchical sugar utilization for energy efficiency.

Ref: Lodish et al., Molecular Cell Biology, 9th ed., Chapter 8: Bacterial Transcription Control and CAP-cAMP

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Gene regulation in Prokaryotes

Full activation of ara operon requires

The araBAD operon exemplifies dual positive control integrating substrate availability and catabolite status. In absence of arabinose, AraC represses by looping DNA between araO2 and araI1, occluding RNA polymerase. Arabinose binding converts AraC into an activator that occupies araI1 and araI2, contacting polymerase and inducing bending. Maximal transcription additionally needs glucose starvation signaling. Elevated cAMP binds CAP, which recognizes site upstream of araI, enhancing polymerase alpha-CTD interaction. Both arabinose and CAP-cAMP together relieve looping and stimulate initiation, enabling catabolism only when preferred sugars are depleted.

Ref: Alberts et al., Molecular Biology of the Cell, 7th ed., Chapter 7: Prokaryotic Transcription Regulation, ara Operon

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