GenePage for the citT gene of Escherichia coli K-12

Primary Gene Name: citT
EcoGene Accession Number: EG13538
K-12 Gene Accession Number: ECK0605
MG1655 Gene Identifier: b0612
Gene Name Mnemonic: Citrate
Alternate Gene Symbols: ybdS
Description: Citrate/succinate antiporter; citrate carrier
  # bp Upstream # bp Downstream
MW: 53092.56 ---------487 aa Pre-Run BlastP UniProt
Pre-Run BlastP NR+Env
Left End: 645117
Left Intergenic Region

Name: rna_citT

Length: 113 bp gap

Orientation: Codirectional-

Left_end: 645004

Right_end: 645116

Centisome: 13.90

Genomic Address
Minute or Centisome (%) = 13.90
Right End: 646580
Right Intergenic Region

Name: citT_citG

Length: 50 bp gap

Orientation: Codirectional-

Left_end: 646581

Right_end: 646630

Centisome: 13.93

CitT is an inner membrane protein with 12 TM regions that has been identified as a citate/succcinate antiporter faciltating citrate transport in vivo and in vitro, with additional substrates including C4-dicarboxylates and tricarboxylates (Pos, 1998). CitT is a member of the IT (Ion Transporter) superfamily (Prakash, 2003). CitT belongs to the ST(3) structural class based on hydropathy profile (Lolkema, 2003). 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 utilzation 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 prodcut 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). In addition to its role in citrate utilization, CitAB(DpiBA) may be involved in beta-lactam antibiotic resistance; the citC-T and citAB(dpiBA) operons are induced by beta-lactam treatment and 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, viability 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 (Hirakawa, 2003). Deletion of citAB(dpiBA) did not change the sensitivity to 240 antibiotics and other growth inhibitors; likewise growth was unaltered in 1000 other growth-based 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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