Gab operon
The "gab" operon is responsible for the conversion of γ-aminobutyrate (GABA) to succinate. The "gab" operon comprises three structural genes – "gabD", "gabT" and "gabP" – that encode for a succinate semialdehyde dehydrogenase, GABA transaminase and a GABA permease respectively. There is a regulatory gene "csiR", downstream of the operon, that codes for a putative transcriptional repressor and is activated when nitrogen is limiting. The "gab" operon has been characterized in "Escherichia coli" and significant homologies for the enzymes have been found in organisms such as "Saccharomyces cerevisiae", rats and humans. Limited nitrogen conditions activate the "gab" genes. The  enzymes produced by these genes convert GABA to succinate, which then enters the TCA cycle, to be used as a source of energy. The "gab" operon is also known to contribute to polyamine homeostasis during nitrogen-limited growth and to maintain high internal glutamate concentrations under stress conditions. Structure. The "gab" operon consists of three structural genes: Physiological significance of the operon. The "gabT" gene encodes for GABA transaminase, an enzyme that catalyzes the conversion of GABA and 2-oxoglutarate into succinate semialdehyde and glutamate. Succinate semialdehyde is then oxidized into succinate by succinate semialdehyde dehydrogenase which is encoded by  the "gabP" gene, thereby entering the TCA cycle as a usable source of energy. The "gab" operon contributes to homeostasis of polyamines such as putrescine, during nitrogen-limited growth. It is also known to maintain high internal glutamate concentrations under stress conditions. Regulation. Differential Regulation of Promoters. The expression of genes in the operon is controlled by three differentially regulated promoters, two of which are controlled by "RpoS" encoded sigma factor σ. Mechanism of Regulation. Activation. The "csiD" promoter ("csiD") is essential for the expression of "csiD"(carbon starvation induced gene), "ygaF" and the "gab" genes. The "csiD" is activated exclusively  under carbon starvation conditions and stationary phase during which cAMP accumulates in high concentrations in the cell. The binding of cAMP to the cAMP receptor protein(CRP) causes CRP to bind tightly to a specific DNA site in the "csiD" promoter, thus activating the transcription of genes downstream of the promoter. The "gabD" exerts an additional control over the "gabDTP" region. The "gabD" is activated by σ inducing conditions such as hyperosmotic and acidic shifts besides starvation and stationary phase. The "gabD" promoter on the other hand, is σ dependent and is activated under nitrogen limitation. In nitrogen limiting conditions, the  nitrogen regulator Nac binds to a site located just upstream of the promoter expressing the "gab" genes. The "gab" genes upon activation produce enzymes that degrade GABA to succinate. Repression. The presence of nitrogen activates the "csiR" gene located downstream of the "gabP" gene. The "csiR" gene encodes a protein that acts as a transcriptional repressor for "csiD-ygaF-gab" operon hence shutting off the GABA degradation pathway. Eukaryotic Analogue. GABA degradation pathways exists in almost all eukaryotic organisms and takes place by the action of similar enzymes. Although, GABA in "E.coli" is predominantly used as an alternative source of  energy through GABA degradation pathways, GABA in higher eukaryotic organisms acts as an inhibitory neurotransmitter and also as regulator of muscle tone. GABA degradation pathways in eukaryotes are responsible for the inactivation of GABA.