RpoS

The gene rpoS (RNA polymerase, sigma S) encodes the sigma factor sigma-38 (σ38, or RpoS), a 37.8 kD protein in Escherichia coli. Sigma factors are proteins that regulate transcription in bacteria. Sigma factors can be activated in response to different environmental conditions. rpoS is transcribed in late exponential phase, and RpoS is the primary regulator of stationary phase genes. RpoS is a central regulator of the general stress response and operates in both a retroactive and a proactive manner: it not only allows the cell to survive environmental challenges, but it also prepares the cell for subsequent stresses (cross-protection). The transcriptional regulator CsgD is central to biofilm formation, controlling the expression of the curli structural and export proteins, and the diguanylate cyclase, adrA, which indirectly activates cellulose production. The rpoS gene most likely originated in the γ branch of the proteobacteria.

Regulatory mechanisms that control RpoS exist at various levels of gene and protein organization: transcription, translation, degradation, and protein activity. These processes occur in response to stresses such as near-UV radiation, acid, temperature or osmotic shock, oxidative stress, and nutrient deprivation. While many key regulatory entities have been identified in these areas, the precise mechanisms by which they signal rpoS transcription, translation, proteolysis or activity remain largely uncharacterized.

Transcription of rpoS in E. coli is mainly regulated by the chromosomal rpoSp promoter. rpoSp promotes transcription of rpoS mRNA, and is induced upon entry into stationary phase in cells growing on rich media via an unknown mechanism. Flanking rpoSp are two putative cAMP-CRP (cyclic AMP-cAMP receptor protein) binding sites that seem to control rpoS transcription in an antagonistic manner. The position of the first site upstream of the major rpoS promoter corresponds to a “classical activator” similarly found in the lac promoter thereby suggesting that its effects on transcription are activating (Lange and Hengge-Aronis, 1994); in contrast, the location of the second cAMP-CRP site is indicative of inhibitory action. In exponential phase, crp mutants exhibit high levels of rpoS expression, suggesting that cAMP-CRP inhibits rpoS transcription. Upon entry into stationary phase, on the other hand, cAMP-CRP may upregulate rpoS transcription (Hengge-Aronis, 2002). While these observations may explain the seemingly dual nature of the cAMP-CRP binding sites, they require an explanation of phase-dependent selection of cAMP-CRP site activation to fully account for the contradictory data. Additional regulatory controls for rpoS transcription include: BarA, a Histidine sensor kinase which can activate OmpR and thereby promote porin synthesis; levels of small molecules such as ppGppp which may hinder transcriptional elongation or stability in response to amino acid limitation, or carbon, nitrogen or phosphorus starvation (Gentry et al., 1993). Despite the numerous controls on rpoS transcription, cellular rpoS mRNA levels remain high during exponential phase and the majority of extracellular stimuli do not significantly affect rpoS transcription.

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