cbrB encodes the response regulator output of the CbrA/CbrB two-component system in Pseudomonas putida KT2440. CbrB is an ATP-dependent sigma-N transcriptional activator that directly controls crcZ, crcY, and a broader regulon expressed under poor-carbon conditions, thereby coupling carbon and nitrogen balance to carbon catabolite repression relief and to the activation of catabolic genes. The KT2440 literature consistently studies locus PP_4696 as CbrB, although the current UniProt entry Q88DX2 names the ortholog AlgB based on homology.
| GO Term | Evidence | Action | Reason |
|---|---|---|---|
| GO:0000160 phosphorelay signal transduction system | IEA GO_REF:0000002 | ACCEPT | Summary: This annotation is correct and captures a core biological process for cbrB. CbrB is the cognate response regulator in the CbrA/CbrB two-component system, and biochemical work shows phosphotransfer from CbrA to CbrB. The term remains appropriate even though the seeded evidence was only domain-based. Supporting Evidence: PMID:32214184 the histidine kinase can autophosphorylate and transfer the phosphoryl group to the response regulator CbrB. PMID:23692431 Thus, CbrAB constitute a global signal transduction pathway integrated in a higher regulatory network that also controls catabolite repression through the expression of the two regulatory RNAs CrcZ and CrcY. file:PSEPK/cbrB/cbrB-deep-research-openai.md CbrB is part of the CbrA/CbrB two-component system (TCS), which is exclusive to pseudomonads and responds to carbon/nutrient availability. file:PSEPK/cbrB/cbrB-deep-research-falcon.md Biochemical work shows that **CbrA autophosphorylates and transfers the phosphoryl group to CbrB**, supporting the canonical two-component phosphorelay. |
| GO:0005524 ATP binding | IEA GO_REF:0000002 | KEEP AS NON CORE | Summary: This annotation is likely correct because CbrB contains the characteristic AAA+ sigma-54 activator ATPase region, but it is generic and less informative than the response-regulator and transcription-activator functions. It should be retained as non-core rather than emphasized in the summary of gene function. Supporting Evidence: file:PSEPK/cbrB/cbrB-uniprot.txt DR InterPro; IPR003593; AAA+_ATPase. file:PSEPK/cbrB/cbrB-uniprot.txt KW ATP-binding {ECO:0000256|ARBA:ARBA00022840}; |
| GO:0006355 regulation of DNA-templated transcription | IEA GO_REF:0000002 | MODIFY | Summary: The annotation is directionally correct but too broad. CbrB is not merely a generic transcription regulator; it is a sigma-N-dependent transcriptional activator that directly activates crcZ, crcY, and a larger regulon. A more informative replacement is positive regulation of DNA-templated transcription, with carbon catabolite repression retained as a distinct downstream biological process. Proposed replacements: positive regulation of DNA-templated transcription Supporting Evidence: PMID:23692431 We show that the response regulatory protein CbrB, an activator of Ο(N) -dependent promoters, directly controls the expression of the small RNAs CrcZ and CrcY in P.βputida. PMID:30557364 determined that it directly controls the expression of at least 61 genes file:PSEPK/cbrB/cbrB-deep-research-falcon.md **Primary biological role**: **CbrB is a transcriptional regulatory response regulator that activates Ο54-dependent promoters**, most prominently the **crcZ (and crcY) sRNA expression program**, thereby modulating Hfq/Crc-mediated CCR and nutrient adaptation. |
| GO:0000156 phosphorelay response regulator activity | IDA PMID:32214184 Transport and kinase activities of CbrA of Pseudomonas putid... | NEW | Summary: This missing molecular function should be added. CbrB is explicitly described as the response regulator of the CbrAB system and is the direct phosphorelay acceptor from the histidine kinase CbrA. Supporting Evidence: PMID:23692431 We show that the response regulatory protein CbrB, an activator of Ο(N) -dependent promoters, directly controls the expression of the small RNAs CrcZ and CrcY in P.βputida. PMID:32214184 the histidine kinase can autophosphorylate and transfer the phosphoryl group to the response regulator CbrB. file:PSEPK/cbrB/cbrB-deep-research-falcon.md An independent genome-scale fitness study explicitly labels **cbrB (PP_4696)** as a **Ο54-dependent response regulator** and links it to central carbon metabolism and amino-acid uptake in pseudomonads. |
| GO:0001216 DNA-binding transcription activator activity | IDA PMID:23692431 Transcriptional activation of the CrcZ and CrcY regulatory R... | NEW | Summary: This missing term captures CbrB's direct output function more precisely than the seeded generic transcription annotation. Multiple studies show that CbrB directly binds and activates sigma-N-dependent promoters, especially crcZ and crcY, and broader regulon analyses extend that direct activator role to dozens of genes. Supporting Evidence: PMID:23692431 We show that the response regulatory protein CbrB, an activator of Ο(N) -dependent promoters, directly controls the expression of the small RNAs CrcZ and CrcY in P.βputida. PMID:30557364 CbrB is a quite peculiar ΟN-dependent activator since it is barely dependent on phosphorylation for transcriptional activation. file:PSEPK/cbrB/cbrB-deep-research-openai.md Overall, CbrB functions as a transcriptional activator that directly turns on numerous genes involved in nutrient uptake and metabolism when triggered by its sensor kinase CbrA. file:PSEPK/cbrB/cbrB-deep-research-falcon.md Using a **PcrcZ::luxCDABE** reporter, **ΞcbrB** mutants did not express crcZ unless complemented with plasmid-borne **cbrB**, demonstrating that CbrB is required for crcZ activation under inducing conditions (e.g., histidine as carbon source). |
| GO:0061985 carbon catabolite repression | IMP PMID:23692431 Transcriptional activation of the CrcZ and CrcY regulatory R... | NEW | Summary: This process term should be added because there is direct evidence that CbrB controls carbon catabolite repression through transcriptional activation of the regulatory RNAs crcZ and crcY. That role is central to the biological logic of the CbrAB system in P. putida. Supporting Evidence: PMID:23692431 Thus, CbrAB constitute a global signal transduction pathway integrated in a higher regulatory network that also controls catabolite repression through the expression of the two regulatory RNAs CrcZ and CrcY. PMID:22053874 The CbrA/CbrB two-component system activated crcZ transcription, but had little effect on crcY. file:PSEPK/cbrB/cbrB-deep-research-falcon.md crcZ expression is **(partially) repressed** in LB or succinate (preferred carbon source) and **maximally induced** on less favorable sources such as **L-histidine, L-arginine, and oxaloacetate**. |
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Download this section (compressed HTML)Q: What intracellular signal sensed by the CbrA/CbrB system most directly determines CbrB activity under different carbon and nitrogen regimes?
Q: Which members of the 61-gene direct CbrB regulon are the dominant physiological effectors in vivo, versus downstream consequences of crcZ/crcY-mediated rewiring?
Q: Does PP_4696 have a direct alginate-associated regulatory role in KT2440, or does the UniProt AlgB name mainly reflect orthology to better-studied regulators from other Pseudomonas species?
Experiment: Compare wild type cbrB with phospho-acceptor and ATPase-defective alleles using promoter reporters, ChIP-seq, and RNA-seq under succinate, oxaloacetate, and histidine growth conditions.
Hypothesis: CbrB promoter activation has target-specific dependence on phosphorylation and ATPase activity.
Type: mutational_analysis
Experiment: Quantify CbrA-to-CbrB phosphotransfer and CbrB-dependent promoter activation after perturbing candidate intracellular metabolites that track carbon/nitrogen imbalance.
Hypothesis: The upstream signal sensed through CbrA/CbrB is intracellular rather than extracellular histidine itself.
Type: biochemical_assay
Experiment: Rebuild clean chromosomal cbrB loss-of-function and truncation alleles in otherwise isogenic backgrounds and measure biofilm formation, dispersal, lapD/lapG status, and crcZ/crcY expression.
Hypothesis: Reported biofilm phenotypes attributed to cbrB include indirect effects from secondary mutations or downstream circuitry.
Type: phenotype_analysis
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