GenePage for the dctR gene of Escherichia coli K-12

Primary Gene Name: dctR
EcoGene Accession Number: EG11889
K-12 Gene Accession Number: ECK3491
MG1655 Gene Identifier: b3507
Gene Name Mnemonic: Dicarboxylate transport regulator
Alternate Gene Symbols: yhiF
Description: Putative LuxR family repressor for C4-dicarboxylate transport
  # bp Upstream # bp Downstream
MW: 20408.21 ---------176 aa Pre-Run BlastP UniProt
Pre-Run BlastP NR+Env
Left End: 3654683
Left Intergenic Region

Name: slp_dctR

Length: 155 bp gap

Orientation: Codirectional+

Left_end: 3654528

Right_end: 3654682

Centisome: 78.73

Genomic Address
Clockwise
Minute or Centisome (%) = 78.74
Right End: 3655213
Right Intergenic Region

Name: dctR_yhiD

Length: 41 bp gap

Orientation: Convergent

Left_end: 3655214

Right_end: 3655254

Centisome: 78.75

A dctR mutation reverses the succinate growth defect of an atp operon deletion resulting in a Suc+ growth phenotype; DctA overproduction also confers Suc+ to the atp deletion strain; cloned dctR complements the dctR mutant Suc+ phenotype restoring the Suc- phenotype conferred by the atp deletion; it was proposed that DctR(YhiF) is a repressor for the dctA gene and that yhiF be renamed as DctR (Boogerd, 1998). E. coli K-12 has other known and putative dicarboxylate transporters such as DcuAB, CitT and YbhI that were not tested for suppression of the Suc- phenotype, and DctR was not shown to be a dctA repressor, so DctR could be repressing a dicarboxylate transporter gene other than dctA. dctR and slp are in the AFI 12 gene acid fitness island and their roles in acids resistance are to counter the effects of organic acids in spent medium; a slp-dctR(yhiF) double mutant, but not either single mutant, loses protection against metabolites that are toxic at pH 2.5 including formate, succinate, and lactate, but not acetate; the double mutant phenotype can be complemented by a yhiF clone but complementation by a slp clone was not tested; this implies that Slp and DctR provide redundant protection; the protective role for DctR during the acid resistance response may be repression of one or more C4-dicarboxylate importers; a dctA mutant did not alter the slp-dctR phenotype, indicating that other C4-dicarboxylate importers in addition to or instead of DctA may be repressed by DctR (Mates, 2007). Overexpression of DctR causes filamentous biofilm formation (Tenorio, 2003). DctR is possibly involved in the regulation of type III secretion systems in enterohemorrhagic E. coli O157:H7 (Tatsuno, 2003). dctR is part of the EvgAS regulon (Masuda, 2002). Greater than 92% of the upstream slp mRNA is monocistronic and it is not known if all dctR expression is based on readthrough of the slp terminator or if dctR also has its own promoter (Alexander, 1994; Tucker, 2003).

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BamHI EcoRI HindIII