Identity
Canonical name: Quinate. 1
Type: Compound. 1
Known aliases: No aliases were reported in the document. 1
Stable external identifier: No stable external identifier was reported in the document. 1
Evidence from ADP1 studies
Quinate was one of 8 carbon sources used for mutant growth-fitness measurements in acinetobacter-baylyi-adp1. 1
Pairwise mutant-fitness correlation between quinate and urea was r = 0.11, indicating an almost uncorrelated relationship in this dataset. 1 Urea fitness was weakly correlated with the other tested conditions, with correlations of r = 0.12-0.28, while the mean pairwise correlation across the 8 carbon sources was 0.44. 1 The weak quinate–urea relationship supports the hypothesis that urea catabolism involves a largely independent set of genes, although this interpretation is based on the ADP1-centered dataset. 1
The deletion-collection analysis refines this correlation-based picture by classifying quinate as a robust condition: only 1.6% of genes showed severe defects at growth ratio < 0.5, and the mean growth ratio was 1.36. 2 The analysis identified a 24-gene module with extreme quinate-specific defects, including aromatic degradation pathway genes, while scores were near zero on other conditions. 2
Quinate-specific genes included pcaC, pcaG, pcaH, pcaB, quiA, quiB, pqqC, and pqqD, linking quinate fitness to quinate-degradation-pathway and pqq-biosynthesis. 2 The quinate-specific set also included NADH-ubiquinone oxidoreductase subunits; this suggests the hypothesis that aromatic catabolism creates distinctive electron-transport-chain demands, rather than establishing that mechanism. 2
The new 51-gene support-network analysis supports and extends this pathway-specific interpretation: it assigns 44/51 genes to aromatic degradation, Complex I, iron acquisition, or PQQ biosynthesis, with the pathway converting quinate through protocatechuate and β-ketoadipate to succinyl-CoA and acetyl-CoA. 3 Complex I accounts for 21/51 genes, and FBA (flux-balance analysis) measured fluxes of 0.55 versus 0.31, or 1.76× higher on aromatic substrates, while predicting 0% essentiality; observed quinate-specific defects in 10/13 Complex I operon subunits therefore refine the earlier respiratory-demand hypothesis and expose a model blind spot. 3
The respiratory-chain wiring analysis supports and mechanistically refines this interpretation: quinate generated 4 total NADH, or 0.57 NADH per carbon, and required Complex I, whereas cytochrome bo3, cytochrome bd, succinate dehydrogenase, and the other listed respiratory components were dispensable. 4 Complex I had a growth ratio of 0.37 on quinate, compared with 1.44 on glucose and 0.49 on acetate. 4 The report proposes that quinate-ring cleavage produces succinyl-CoA and acetyl-CoA simultaneously, creating a concentrated TCA-cycle NADH burst that may exceed NDH-2 reoxidation capacity; this is a biochemical hypothesis based on theoretical stoichiometry, not measured flux distributions. 4 This condition-specific configuration supports the earlier hypothesis that aromatic catabolism creates distinctive electron-transport-chain demands, while refining it from a general pathway association to a proposed NADH-flux-capacity mechanism. 4
The network also supports roles for PQQ and iron supply in quinate catabolism, while the PQQ dependency is not exclusive to quinate because PQQ-biosynthesis genes also appeared as glucose-specific in the deletion-phenotype study. 3 Co-fitness correlations assign the previously unknown proteins ACIAD3137 and ACIAD2176 to candidate Complex I-associated functions at r > 0.98, although the analysis used only 8 conditions and the assignments may be indirect. 3
These findings contribute to condition-specific-fitness and are documented in Acinetobacter baylyi ADP1 Data Explorer, ADP1 Deletion Collection Phenotype Analysis, Aromatic Catabolism Support Network in ADP1, and Condition-Specific Respiratory Chain Wiring in ADP1. 1,2,3,4