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Gene Review:

benR - AraC family transcriptional regulator

Pseudomonas putida KT2440

Jeffrey, W.H. et al., Cowles, C.E. et al., Retallack, D.M. et al.

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High impact information on benR

Here we identified a gene, benR, as a regulator of benzoate, methylbenzoate, and 4-HBA degradation genes [1].
A benR mutant isolated by random transposon mutagenesis was unable to grow on benzoate [1].
An additional seven genes located adjacent to benR were inferred to be involved in benzoate degradation based on their deduced amino acid sequences [1].
Southern hybridizations demonstrated that DNA encoding the benzoate dioxygenase structural genes showed homology to DNA encoding toluate dioxygenase from the TOL plasmid pWW0, but benR did not show homology to xylS [2].
Each operon was found to be controlled by an AraC family transcriptional activator, located immediately upstream of the first structural gene in each respective operon (antR or benR) [3].

Biological context of benR

The results obtained when xylS was substituted for benR strongly suggest an isofunctional regulatory mechanism between the TOL plasmid lower-pathway genes (via the OP2 promoter) and chromosomal benABC [2].

References

BenR, a XylS homologue, regulates three different pathways of aromatic acid degradation in Pseudomonas putida. Cowles, C.E., Nichols, N.N., Harwood, C.S. J. Bacteriol. (2000) [Pubmed]
Characterization of Pseudomonas putida mutants unable to catabolize benzoate: cloning and characterization of Pseudomonas genes involved in benzoate catabolism and isolation of a chromosomal DNA fragment able to substitute for xylS in activation of the TOL lower-pathway promoter. Jeffrey, W.H., Cuskey, S.M., Chapman, P.J., Resnick, S., Olsen, R.H. J. Bacteriol. (1992) [Pubmed]
Identification of anthranilate and benzoate metabolic operons of Pseudomonas fluorescens and functional characterization of their promoter regions. Retallack, D.M., Thomas, T.C., Shao, Y., Haney, K.L., Resnick, S.M., Lee, V.D., Squires, C.H. Microbial cell factories [electronic resource]. (2006) [Pubmed]

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