Disease relevance of pcaR

• Characterization of the pcaR regulatory gene from Pseudomonas putida, which is required for the complete degradation of p-hydroxybenzoate [1].
• The pcaR gene product, when overexpressed in Escherichia coli, possessed a specific affinity for the pcaIJ promoter region and demonstrated that the entire PcaR protein was required for this function [1].

High impact information on pcaR

• DNA sequencing, mutational analysis, and complementation studies revealed that pcaR encodes a regulatory protein required for induction of at least four of the enzymes of the beta-ketoadipate pathway and that pcaF encodes beta-ketoadipyl-coenzyme A thiolase, the last enzyme in the pathway [2].
• Insertional inactivation mutagenesis, using Tn5 and mini-Tn5 transposons, was used to locate, clone, and sequence this pcaR regulatory gene [1].
• Fusion analyses showed that pcaI and pcaJ constitute an operon which requires beta-ketoadipate or its nonmetabolizable analog, adipate, as well as the pcaR regulatory gene for induction [3].
• An additional P. putida gene, pcaR, was shown to be required for expression of the pca structural genes in response to beta-ketoadipate [4].
• The regulatory pcaR gene is located about 15 kbp upstream from the pcaBDC operon [4].

Biological context of pcaR

• Comparisons of the pcaIJ and pcaR promoter regions revealed conservation of a 15-bp sequence centered around the -10 region in both sequences [1].

References