The genetic analysis of 16 recessive pca mutants in Aspergillus niduluns deficient in the metabolism of protocatechuic acid (PCA) has revealed seven functional genes. The seven gene loci are distributed over three chromosomes: pcaA, pcaC and pcaD on linkage group 11; pcaE, pcaF and pcaC on group V, and pcaB on group VIII, where it shows linkage (recombination frequency (RF) = 6.9%) to the qut gene cluster controlling the degradation of quinic acid to PCA. Only two of the pca gene loci are closely linked: pcaE and pcoC (RF = 043%).The properties of the 4uz and pca mutants clearly demonstrate the separate identity and regulation of the converging pathways from quinate or benzoate to PCA, which in tun is oxidatively degraded through P-ketoadipate to TCA intermediates. Similarly, the mutants are not affected in the metabolism of salicylate to catechol and its oxidation to P-ketoadipate, although two genes (pcaA and pcaF) are required for the further metabolism of P-ketoadipate. Catechol dioxygenase is induced by growth in the presence of salicylate, and PCA dioxygenase by benzoate or quinate. Three groups of pca mutants (pcaB, pcaD and pcaE) are deficient in the induction of PCA oxygenase and accumulate PCA when grown in the presence of quinate or benzoate. All three pcaE mutants and the single pcaA strain totally lack PCA oxygenase activity, while a single pcaB mutant strain has properties tentatively suggesting a positive role in the induction of the PCA pathway.