| 10629187 |
Jaspers MC, Suske WA, Schmid A, Goslings DA, Kohler HP, van der Meer JR: HbpR, a new member of the XylR/DmpR subclass within the NtrC family of bacterial transcriptional activators, regulates expression of 2-hydroxybiphenyl metabolism in Pseudomonas azelaica HBP1. J Bacteriol. 2000 Jan;182(2):405-17.
The regulation of 2-hydroxybiphenyl and 2,2'-dihydroxybiphenyl degradation in Pseudomonas azelaica is mediated by the regulatory gene, hbpR. The hbpR gene encodes a 63-kDa protein belonging to the NtrC family of prokaryotic transcriptional activators and having the highest homology to members of the XylR/DmpR subclass. Disruption of the hbpR gene in P. azelaica and complementation in trans showed that the HbpR protein was the key regulator for 2-hydroxybiphenyl metabolism. Induction experiments with P. azelaica and Escherichia coli containing luxAB-based transcriptional fusions revealed that HbpR activates transcription from a promoter (P (hbpC)) in front of the first gene for 2-hydroxybiphenyl degradation, hbpC, and that 2-hydroxybiphenyl itself is the direct effector for HbpR-mediated activation. Of several compounds tested, only the pathway substrates 2-hydroxybiphenyl and 2,2'-dihydroxybiphenyl and structural analogs like 2-aminobiphenyl and 2-hydroxybiphenylmethane were effectors for HbpR activation. HbpR is therefore, to our knowledge, the first regulator of the XylR/DmpR class that recognizes biaromatic but not monoaromatic structures. Analysis of a spontaneously occurring mutant, P. azelaica HBP1 Prp, which can grow with the non-wild-type effector 2-propylphenol, revealed a single mutation in the hbpR gene (T613C) leading to a Trp--> Arg substitution at amino acid residue 205. P. azelaica HBP1 derivative strains without a functional hbpR gene constitutively expressed the genes for 2-hydroxybiphenyl degradation when complemented in trans with the hbpR-T613C gene. This suggests the importance of this residue, which is conserved among all members of the XylR/DmpR subclass, for interdomain repression. |
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