Abstract
Medium-chain-length-polyhydroxyalkanoic acids (MCL-PHAs) formed in Pseudomonas spp. have a rather broad distribution of monomer-units whose precursors are supplied via beta-oxidation degradation of MCL fatty acids fed as the carbon source and/or via PhaG enzyme catalyzing the acyl-group transfer from 3-hydroxyacyl-ACPs derived from acetyl-CoA to coenzyme A. It was found that salicylic acid (SA), in a concentration dependent manner, suppressed the accumulation of PHA in Pseudomonas fluorescens BM07 from fructose as well as shifted the distribution of monomer-units derived from a MCL fatty acid co-added as carbon source (e.g., 11-phenoxyundecanoic acid (11-POU)) to longer monomer-units. Both SA and acrylic acid were found to induce high accumulations of 3-ketohexanoic acid in BM07 wild-type cells grown with n-hexanoic acid as well as to inhibit the formation of acetyl-CoA from acetoacetyl-CoA by BM07 cell extract, suggesting that 3-ketoacyl-CoA thiolase is their common beta-oxidation target. The structural motif of acrylic acid present in the molecular structure of SA may self-explain the similar actions of the two inhibitors. A comparison of monomer modulation between BM07 wild-type and DeltaphaG mutant cells grown on the mixtures of fructose and 11-POU revealed that both PhaG and beta-oxidation inhibitor may play a critical role in the synthesis of PHA with longer side-chain omega-functional substitutions.
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