GenePage for the citG gene of Escherichia coli K-12

Primary Gene Name: citG
EcoGene Accession Number: EG13539
K-12 Gene Accession Number: ECK0606
MG1655 Gene Identifier: b0613
Gene Name Mnemonic: Citrate
Alternate Gene Symbols: ybdT
Description: 2-(5''-triphosphoribosyl)-3'-dephosphocoenzyme-A synthase
  # bp Upstream # bp Downstream
MW: 31644.44 ---------292 aa Pre-Run BlastP UniProt
Pre-Run BlastP NR+Env
Left End: 646631
Left Intergenic Region

Name: citT_citG

Length: 50 bp gap

Orientation: Codirectional-

Left_end: 646581

Right_end: 646630

Centisome: 13.93

Genomic Address
Minute or Centisome (%) = 13.93
Right End: 647509
Right Intergenic Region

Name: citG_citX

Length: 26 bp overlap

Orientation: Codirectional-

Left_end: 647484

Right_end: 647509

Centisome: 13.95

The N-terminal periplasmic sensor domain of CitA functions as a high-affinity citrate receptor (Kaspar, 2002). E. coli cannot use citrate as a carbon and energy source for aerobic growth like Klebsiella does (Koser, 1924). Citrate can be catabolized during anaerobic growth in the presence of an oxidizable co-substrate such as glucose, lactose or glycerol; the co-substrate provides needed reducing power (Lütgens, 1980). Aerobic utilization of citrate is blocked by low CitT transporter expression, which can be overcome using a plasmid-encoded transporter (Pos, 1998). In addition to inducing the cit operon and citAB, adding citrate to anaerobic cultures up-regulates the mdh gene needed to convert the oxoaloacetate product to malate (Yamamoto, 2008). The cytoplasmic transmitter domain of autophosphorylated CitA transphosphorylates the CitB receiver domain, causing the CitB DNA-binding output HTH domain to bind to the citCDEFXGT-citAB divergent promoter region and activate transcription of both operons; the reduction of CitA Cys529 is essential for autophosphorylation, perhaps acting as an oxygen-sensing inhibition mechanism restricting cit gene expression to the anaerobic growth conditions that enable citrate-glucose co-fermentation (Yamamoto, 2008; Yamamoto, 2009). CitAB(DpiBA) has been reported to be involved in beta-lactam antibiotic resistance; the citC-T and citAB(dpiBA) operons are induced by beta-lactam treatment and by shifting an ftsI(ts) strain to the non-permissive temperature, in a citB(dpiA)-independent mechanism; both treatments also induce the lexA-, recA-dependent SOS response, dependent upon the citB(dpiA) induction, and lexA or recA mutants block the SOS-dependent antibiotic-induced induction of the cit genes; the antibiotic MICs are not affected by citA or citB mutations; the plating efficiency of a citB(dpiA) mutant is reduced 10-fold as compared to wildtype cells after overnight antibiotic exposure in liquid cultures (Miller, 2004). Plasmid-based overexpression of CitB(DpiA) increases fosfomycin resistance, but has no effect on beta-lactam resistance (Hirakawa, 2003a; Hirakawa, 2003b).

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