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. 2021 Dec 21;10(1):5. doi: 10.3390/microorganisms10010005

Figure 2.

Figure 2

Examples of stress regulators in E. coli. General stress response. (a) In response to oxidative stress, RpoS occurs in direct regulation by binding to RNA polymerase (RNAP) and recognizes the promoter thus allowing expression of katG and katE catalase and peroxidase expression. Likewise, in response to low pH, binding of RpoS to RNAP induces expression of the transcriptional regulator, gadX. (b) Under nutrient limitation, RpoS is indirectly regulated by the transcription factor DskA or by the alarmone ppGpp (orange circle) that leads to the augmentation of the anti-adaptor IraP and releases RpoS to activate stress gene expression. Nutrient stress. (c) Under nutrient deficient conditions, a mis-regulation of cAMP signaling for nutrient availability allows binding of cAMP to the cAMP Receptor Protein (CRP) which activates the protein and specific binding with target DNA sequences regulating the expression of genes involved in acid stress (gadX) or in oxidative stress (oxyR). (d) In nutrient deprivation, exogenous leucine (pink circle) influences the Lrp regulon and modulates Lrp directly. Presence of leucine concentrations represses the transcription of the ilvH promoter whereas in the absence of leucine, ilvH is directly activated by Lrp. Inversely, leucine releases Lrp to bind to the sdaA promoter and activates its expression. Oxidative stress. (e) In response to oxidative stress due to excess levels of prooxidants (H2O2, O2, OH), depending on whether the stress is mediated, bacteria respond by two regulatory systems, the peroxide regulon (OxyR) or the superoxide regulon (SoxR/S). OxyR activates genes involved in catalase and peroxidase expression (katE and katG). When oxidized, the sensor SoxR activates soxS transcription resulting in expression of superoxide dismutase (sodA and sodB). Envelope stress. (f) The two-component system consists of the inner membrane, the sensor histidine kinase (CpxA) and the cytoplasmic response regulator CpxR. Envelope stress conditions lead to phosphorylation of CpxA which transfers the phosphate group to CpxR. Phosphorylated CpxR-P functions as a transcriptional regulator which controls the expression of numerous genes including some virulence factors. Heat shock. (g) In a simple pathway, during temperature upshift (30 °C to 42 °C), the Heat Shock Response (HSR) is induced by the increase of RpoH levels, primarily due to an enhanced translation of rpoH mRNA and stabilization of the protein. The elevated temperature disturbs protein homeostasis and induces accumulation of misfolded proteins. Chaperones DnaK and GroEL/S which are proteins helping to activate or degrade RpoH and regulate heat shock gene transcription.

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