GenePage for the citA gene of Escherichia coli K-12

Primary Gene Name: citA
EcoGene Accession Number: EG13646
K-12 Gene Accession Number: ECK0612
MG1655 Gene Identifier: b0619
Gene Name Mnemonic: Citrate
Alternate Gene Symbols: criS(S.f.); dpiB; mpdB; ybeP
Description: Sensor histidine kinase for the citCDEFXGT operon; citrate-binding; two-component system, with CitB; citrate-independent beta-lactam-induction
  # bp Upstream # bp Downstream
MW: 61684.09 ---------552 aa Pre-Run BlastP UniProt
Pre-Run BlastP NR+Env
Left End: 652235
Left Intergenic Region

Name: citC_citA

Length: 378 bp gap

Orientation: Divergent

Left_end: 651857

Right_end: 652234

Centisome: 14.04

Genomic Address
Minute or Centisome (%) = 14.05
Right End: 653893
Right Intergenic Region

Name: citA_citB

Length: 32 bp overlap

Orientation: Codirectional+

Left_end: 653862

Right_end: 653893

Centisome: 14.09

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-utilization (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). Deletion of citAB(dpiBA) did not change the sensitivity to 240 antibiotics and other growth inhibitors; likewise phenotypes were unaltered in ~1000 other assays such as various carbon and nitrogen source utilizations; the anaerobic utilization of citrate was not tested (Zhou, 2003). In vivo overproduced CitAB(DpiBA) stimulates the citC promoter and represses the appY promoter (Ingmar, 1998). Among other functions, the global transcriptional regulator AppY stimulates expression of the anaerobically-induced energy metabolism operons hyaA-F and cbdABX-appA (Brøndsted, 1996; Atlung, 1996; Atlung, 1997). Overproduced CitA(DpiB) destabilizes pSC101 (and other) plasmid inheritance, hence the synonyms dpiAB, and induces the SOS repsonse, acting by CitB(DpiA) binding to the AT-rich plasmid ori region and the chromosomal origin, respectively; citAB(dpiBA) mutants have no effect on plasmid inheritance (Ingmer, 1998; Miller, 2003). The citA(criR) gene was identified as a transcriptional regulator of the ipa pathogenicity island in Shigella flexneri, but E. coli K-12 does not have the ipa genes (Qi, 1996; Walker, 2002). ChiX(RybC,MicM) regulates citAB(dpiBA) mRNA; citAB(dpiBA) mRNA may be a ChiX trap-mRNA (also called an RNA decoy) (Mandin, 2009).

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