Regulation of Carbon Metabolism in Pseudomonas Species

Members of the genus Pseudomonas exhibit exceptional metabolic flexibility, deploying both transcriptional and post-transcriptional networks to manage the uptake and catabolism of diverse carbon sources. Unlike many bacteria that channel glucose primarily through glycolysis, Pseudomonas spp. employ the Entner–Doudoroff pathway alongside a phosphorylative branch, generating NADPH for biosynthesis and defence against oxidative stress. Central to this flexibility is carbon catabolite repression (CCR), a hierarchical mechanism that suppresses utilisation of secondary substrates when preferred carbon sources abound. Post-transcriptional actors include the RNA chaperone Hfq and the catabolite repression control protein Crc, which co-repress catabolic mRNAs via A-rich sequence motifs, while the regulatory RNA CrcZ antagonises this repression upon depletion of favoured nutrients. At the transcriptional tier, sensor regulators such as HexR, PtxS and RccR monitor intracellular metabolites—particularly 6-phosphogluconate and gluconate—to modulate expression of operons encoding key enzymes (Zwf, Edd, Eda, Glk). The integration of these layers endows Pseudomonas with rapid metabolic adjustment to changing environments, underpinning their roles in soil and rhizosphere ecology, industrial biocatalysis and opportunistic infections.

Research from Nature Portfolio

Recent work has highlighted how fluctuations in host-derived glucose impact Pseudomonas aeruginosa colonisation. Mutants deficient in glucose transporters and kinases (oprB, gltK, gtrS, glk) show marked attenuation on glucose as sole carbon source, revealing their pivotal roles in uptake and initial catabolism. In vivo models of hyperglycaemia demonstrate that elevated airway glucose correlates with increased bacterial burden, an effect reversible by pharmacological reduction of glucose levels. These studies underscore the direct link between environmental carbon availability and pathogenic potential, and illustrate how modulation of host metabolism can influence bacterial growth dynamics.

Regulation of Carbon Metabolism in Pseudomonas Species publication trend

The graph below shows the total number of articles in regulation of carbon metabolism in pseudomonas species across all publications each year (not limited to Nature Index journals).

Technical terms

Carbon catabolite repression (CCR): Hierarchical regulatory system that prioritises utilisation of preferred carbon sources by repressing genes involved in catabolism of less favoured substrates.

Entner–Doudoroff pathway: Distinct glycolytic alternative in Pseudomonas, converting glucose to pyruvate and glyceraldehyde-3-phosphate while generating NADPH.

RNA chaperone Hfq: Conserved RNA-binding protein that facilitates interactions between small RNAs and their mRNA targets, modulating translation and mRNA stability.

Crc protein: Accessory factor in Pseudomonas that enhances Hfq-mediated translational repression of catabolic genes under nutrient-rich conditions.

CrcZ RNA: Small non-coding RNA induced upon relief of CCR that binds Hfq, thereby relieving repression of alternative catabolic pathways.

HexR regulator: Transcriptional repressor of the RpiR family that senses 6-phosphogluconate to control expression of Entner–Doudoroff and phosphorylative branch operons.

References

1. Interplay between the catabolite repression control protein Crc, Hfq and RNA in Hfq-dependent translational regulation in Pseudomonas aeruginosa. Nucleic Acids Research (2017).
2. Regulation of Hfq by the RNA CrcZ in Pseudomonas aeruginosa Carbon Catabolite Repression. PLOS Genetics (2014).
3. Regulation of carbohydrate degradation pathways in Pseudomonas involves a versatile set of transcriptional regulators. Microbial Biotechnology (2018).
4. Regulation of Glucose Metabolism in Pseudomonas THE PHOSPHORYLATIVE BRANCH AND ENTNER-DOUDOROFF ENZYMES ARE REGULATED BY A REPRESSOR CONTAINING A SUGAR ISOMERASE DOMAIN*. Journal of Biological Chemistry (2009).
5. Increased airway glucose increases airway bacterial load in hyperglycaemia. Scientific Reports (2016).