Summary: The genetic analysis of 16 recessive mutants in deficient in the metabolism of protocatechuic acid (PCA) has revealed seven functional genes. The seven gene loci are distributed over three chromosomes: and on linkage group II; and on group V, and on group VIII, where it shows linkage [recombination frequency (RF) = 6·9%] to the gene cluster controlling the degradation of quinic acid to PCA. Only two of the gene loci are closely linked: and (RF = 0·8%). The properties of the and mutants clearly demonstrate the separate identity and regulation of the converging pathways from quinate or benzoate to PCA, which in turn is oxidatively degraded through β-ketoadipate to TCA intermediates. Similarly, the mutants are not affected in the metabolism of salicylate to catechol and its oxidation to β-ketoadipate, although two genes ( and ) are required for the further metabolism of β-ketoadipate. Catechol dioxygenase is induced by growth in the presence of salicylate, and PCA dioxygenase by benzoate or quinate. Three groups of mutants ( and ) are deficient in the induction of PCA oxygenase and accumulate PCA when grown in the presence of quinate or benzoate. All three mutants and the single strain totally lack PCA oxygenase activity, while a single mutant strain has properties tentatively suggesting a positive role in the induction of the PCA pathway.


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