Disease relevance of ampC

• ampC cephalosporinase of Escherichia coli K-12 has a different evolutionary origin from that of beta-lactamases of the penicillinase type [1].
• Comparison of the overlapping frd and ampC operons of Escherichia coli with the corresponding DNA sequences in other gram-negative bacteria [2].
• The major exception is Salmonella typhimurium LT2, which shows a strong homology to the E. coli frd probe but none to the E. coli ampC probe [2].
• ampC beta-lactamase hyperproduction in Escherichia coli: natural ampicillin resistance generated by horizontal chromosomal DNA transfer from Shigella [3].
• The cloned Citrobacter freundii ampC beta-lactamase is inducible in the presence of its regulatory gene ampR in Escherichia coli (Lindberg et al., 1985) [4].

High impact information on ampC

• Addition of the muropeptide, anhMurNAc-tripeptide, which accumulates in beta-lactamase-overproducing mutants, counteracts the negative effect of UDP-MurNAc-pentapeptide, restoring the innate ability of AmpR to induce ampC expression in vitro [5].
• The murein precursor, UDP-MurNAc-pentapeptide, decreases AmpR-mediated transcriptional activation in vitro, but has no effect on an AmpR(G102E) mutant that mediates constitutive activation of ampC in vivo [5].
• Insertion of IS2 creates a novel ampC promoter in Escherichia coli [6].
• In vitro transcription revealed that the transcription initiation site in the ampC::IS2 mutants was identical with that of ampC wild-type promoter [6].
• The insertion of IS2 in orientation II created a novel promoter in which the -35 region and the 17 bp long spacing sequence between the two consensus sequences are present in IS2 DNA, whereas the -10 region from the original ampC promoter is retained [6].

Chemical compound and disease context of ampC

• Six ampicillin-resistant clinical isolates of Escherichia coli that hyperproduced the chromosomal ampC beta-lactamase were studied [3].
• CONCLUSIONS: Cefoxitin resistance in E. coli N99-0001 was due to overexpression of ampC caused by an increase in promoter strength [7].
• Mutation of the ampC and/or ampH genes in E. coli lacking PBPs 1a and 5 produced morphologically aberrant cells, particularly in cell filaments induced by aztreonam [8].
• The MICs of cefpirome and cefepime of E. coli harboring ampC and ampR genes from CHE were 100--200 times higher than those of E. coli harboring ampC and ampR genes from OUDhyp [9].
• DNA sequencing data showed that five clinical isolates of Escherichia coli with reduced susceptibility to ceftazidime, ceftriaxone, and cefotaxime contain an ampC gene that is preceded by a strong promoter [10].

Biological context of ampC

• Evidence is presented that the ampC attenuator serves as the terminator for transcription of this preceding operon [11].
• The nucleotide sequence was determined for two proteins that were shown to be encoded by a DNA segment preceding the ampC gene [11].
• A 1536-nucleotide-long sequence that carries the ampC beta-lactamase gene of the Escherichia coli K-12 chromosome has been determined [1].
• Accordingly, a G.C insertion in the promoter gave both increased transcription of ampC and a frameshift in this overlapping gene, resulting in readthrough proteins [11].
• The ampC beta-lactamase with a substrate specificity for cephalosporins showed no significant sequence homologies with beta-lactamases of the penicillinase type or with D-alanine carboxypeptidases [1].

Associations of ampC with chemical compounds

• This suggests that the deletion, confirmed by sequencing of the ampC gene, is involved in resistance to cefepime and cefpirome [9].
• Eleven cefoxitin-resistant, AmpC PCR-negative isolates had ampC promoter region mutations [12].

Other interactions of ampC

• Overlap between ampC and frd operons on the Escherichia coli chromosome [11].
• We have isolated mutants, containing alterations in a novel E. coli gene, ampG, in which a cloned C. freundii ampC gene is unable to respond to beta-lactam inducers [13].
• In contrast to Escherichia coli which expresses ampC constitutively from a promoter located in the upstream frdD gene, E. cloacae displays inducible ampC expression [14].
• DNA sequencing between ampC and sugE at the 94.5 min region of the E. coli chromosome revealed an open reading frame specifying 177 amino acid residues [15].
• Neither the parental phenotype of E. cloacae 55M nor the wild-type phenotype of E. cloacae 55 could be restored in E. cloacae 55M-L by the introduction of functional ampR, ampC, or ampD genes [16].

Analytical, diagnostic and therapeutic context of ampC

• METHODS: Plasmid analysis, PCR for beta-lactamases, and sequencing of the ampC genes was carried out [7].
• An RT-PCR method was developed to determine relative ampC expression [7].
• PCR and sequence analysis of the ampC promoter region revealed 51 different promoter or attenuator variants and 14 wild-type promoters [17].
• These beta-lactamases were further characterized by isoelectric focusing (IEF) and PCR, and bla(TEM), bla(OXA-1), bla(SHV) and ampC genes were detected [18].

References