Regulation of the early steps of 3-phenylpropionate catabolism in Escherichia coli.

Microbial catabolism of phenylpropanoid compounds plays a key role in the degradation of aromatic molecules originating from the degradation of proteins and plant constituents. In this study, the regulation of the early steps in the utilisation of 3-phenylpropionate, a phenylpropanoid compound, was investigated. Expression of the hcaA gene product, which is involved in 3-phenylpropionate catabolism in Escherichia coli, was positively regulated by HcaR, a regulatory protein similar to members of the LysR regulators family. Remarkably, the expression of hcaA in the presence of 3-phenylpropionate was sharply and transiently induced at the end of the exponential growth phase. This occurred in a rpoS-independent manner. This transient induction was also mediated by HcaR. The expression of this positive regulator is negatively autoregulated, as for other members of the LysR family. The expression of hcaR is strongly repressed in the presence of glucose. Glucose-dependent repression of hcaR expression could only be partially overcome by adding exogenous cAMP.

Pyrophosphate increases the efficiency of enterobactin-dependent iron uptake in Escherichia coli.

Exogenous inorganic pyrophosphate increases the biomass yield of Escherichia coli. In this report, we show that the effect of pyrophosphate is related to iron uptake. We have found that addition of pyrophosphate, ammonium iron (III) citrate or iron (III) chloride, in M63 minimal medium containing 1.7 microM of iron, causes an increase in growth yield. In contrast to iron chloride or ammonium iron (III) citrate, exogenous pyrophosphate is deleterious to strains unable to synthesize enterobactin. Thus the positive effect of pyrophosphate is related to the enterobactin uptake system expressed in a low iron content medium. Pyrophosphate in minimal medium has a repressing effect on the expression of Fur-regulated genes. In iron rich medium where enterobactin synthesis is strongly decreased, addition of pyrophosphate increases expression of Fur-regulated genes. Furthermore, this latter regulatory effect of pyrophosphate in iron-rich medium is enhanced in the absence of enterobactin synthesis. It has also been shown that addition of pyrophosphate protects the cell against the oxidative stress caused by the presence of hydrogen peroxide in an iron-rich containing medium. These results indicate that pyrophosphate acts as an iron-chelating agent, could trigger the enterobactin-dependent iron uptake system and could promote an increased binding of iron to enterobactin.