Synergistic regulation of the expression of various genes in a catabolic pathway is crucial for the degradation, survival, and adaptation of microorganisms in polluted environments. However, how a single regulator accurately regulates and controls differential transcriptions of various catabolic genes to ensure metabolic safety remains largely unknown. Here, a LysR-type transcriptional regulator (LTTR), OdcR, encoded by the regulator gene odcR, was confirmed to be essential for 3,5-dibromo-4-hydroxybenozate (DBHB) catabolism and simultaneously activated the transcriptions of a gene with unknown function, orf419, and three genes, odcA, odcB, and odcC, involved in the DBHB catabolism in Pigmentiphaga sp. strain H8. OdcB further metabolized the highly toxic intermediate 2,6-dibromohydroquinone, which was produced from DBHB by OdcA. The upregulated transcriptional level of odcB was 7- to 9-fold higher than that of orf419, odcA, or odcC in response to DBHB. Through an electrophoretic mobility shift assay and DNase I footprinting assay, DBHB was found to be the effector and essential for OdcR binding to all four promoters of orf419, odcA, odcB, and odcC. A single nucleotide mutation in the regulatory binding site (RBS) of the promoter of odcB (
Keywords: 2,6-dibromohydroquinone toxicity; 3,5-dibromo-4-hydroxybenzoate; LysR-type transcriptional regulator; activator; differential transcription; metabolic safety.