Disease relevance of tfdR

• Within the 5.9-kb DNA region between the tfdR and tfdK genes on the 2,4-dichlorophenoxyacetic acid (2,4-D) catabolic plasmid pJP4 from Ralstonia eutropha JMP134, we identified five open reading frames (ORFs) with significant homology to the genes for chlorocatechol and chlorophenol metabolism (tfdCDEF and tfdB) already present elsewhere on pJP4 [1].
• Analysis of duplicated gene sequences associated with tfdR and tfdS in Alcaligenes eutrophus JMP134 [2].

High impact information on tfdR

• Expression of tfdR and tfdS, the (identical) regulatory genes for the tfd pathway remained low and essentially unchanged during the entire adaptation phase [3].
• The deduced amino acid sequence of tfdR indicates that it is a member of the LysR-type activators [4].
• Regulation of these operons by two unlinked genes, tfdR and tfdS, has been proposed [4].
• One reason why the tfd(II) genes do not disappear from plasmid pJP4 might be the necessity for keeping the regulatory genes for the 2,4-D pathway expression tfdR and tfdS [1].
• The tfdR gene product can successfully take over the role of the insertion element-inactivated TfdT protein as a transcriptional activator of the tfdCDEF gene cluster, which encodes chlorocatechol degradation in Ralstonia eutropha JMP134(pJP4) [5].

Biological context of tfdR

• The deduced amino acid sequence of the incomplete ORF, situated divergently from tfdR, indicates similarity to chloromuconate cycloisomerases produced by genes tfdD and tcbD of plasmids pJP4 and pP51, respectively [2].
• Physical and DNA sequence analyses revealed that the tfdR and tfdS genes were identical and were located within a longer inverted repeat of 1592 bp [4].

Analytical, diagnostic and therapeutic context of tfdR

• Purification and crystallization of a LysR-type transcriptional regulator CBNR from Ralstonia eutropha NH9 [6].

References