| Accession | ARO:3000814 |
| CARD Short Name | MexT |
| Definition | MexT is a LysR-type transcriptional activator that positively regulates the expression of MexEF-OprN, OprD, and MexS. |
| AMR Gene Family | resistance-nodulation-cell division (RND) antibiotic efflux pump |
| Drug Class | phenicol antibiotic, diaminopyrimidine antibiotic, fluoroquinolone antibiotic |
| Resistance Mechanism | antibiotic efflux |
| Efflux Component | efflux pump complex or subunit conferring antibiotic resistance |
| Efflux Regulator | protein(s) and two-component regulatory system modulating antibiotic efflux |
| Resistomes with Sequence Variants | Pseudomonas aeruginosag+p+wgs, Pseudomonas fluorescensg |
| Classification | 14 ontology terms | Show + process or component of antibiotic biology or chemistry + mechanism of antibiotic resistance + determinant of antibiotic resistance + antibiotic molecule + antibiotic efflux [Resistance Mechanism] + phenicol antibiotic [Drug Class] + diaminopyrimidine antibiotic [Drug Class] + efflux pump complex or subunit conferring antibiotic resistance [Efflux Component] + chloramphenicol [Antibiotic] + trimethoprim [Antibiotic] + resistance-nodulation-cell division (RND) antibiotic efflux pump [AMR Gene Family] + fluoroquinolone antibiotic [Drug Class] + MexEF-OprN + ciprofloxacin [Antibiotic] |
| Parent Term(s) | 4 ontology terms | Show + protein(s) and two-component regulatory system modulating antibiotic efflux [Efflux Regulator] + regulates MexEF-OprN + part_of MexEF-OprN with MexT mutation conferring resistance to chloramphenicol, ciprofloxacin, and trimethoprim + part_of MexEF-OprN with MexS mutations conferring resistance to chloramphenicol, ciprofloxacin, and trimethoprim |
| Publications | Kohler T, et al. 1999. J Bacteriol 181(20): 6300-6305. Characterization of MexT, the regulator of the MexE-MexF-OprN multidrug efflux system of Pseudomonas aeruginosa. (PMID 10515918) Maseda H, et al. 2000. FEMS Microbiol Lett 192(1): 107-112. Variation of the mexT gene, a regulator of the MexEF-oprN efflux pump expression in wild-type strains of Pseudomonas aeruginosa. (PMID 11040437) Richardot C, et al. 2016. Antimicrob. Agents Chemother. 60(4):2302-10 Amino Acid Substitutions Account for Most MexS Alterations in Clinical nfxC Mutants of Pseudomonas aeruginosa. (PMID 26833155) |
Prevalence of MexT among the sequenced genomes, plasmids, and whole-genome shotgun assemblies available at NCBI or IslandViewer for 414 important pathogens (see methodological details and complete list of analyzed pathogens). Values reflect percentage of genomes, plasmids, genome islands, or whole-genome shotgun assemblies that have at least one hit to the AMR detection model. Default view includes percentages calculated based on Perfect plus Strict RGI hits. Select the checkbox to view percentages based on only Perfect matches to AMR reference sequences curated in CARD (note: this excludes resistance via mutation as references in protein variant models are often wild-type, sensitive sequences).
| Species | NCBI Chromosome | NCBI Plasmid | NCBI WGS | NCBI GI | GRDI-AMR2 |
|---|---|---|---|---|---|
| Pseudomonas aeruginosa | 92.33% | 0.29% | 96.37% | 0% | 0% |
| Pseudomonas fluorescens | 2.78% | 0% | 0% | 0% | 0% |
Model Type: protein overexpression model
Model Definition: Protein Overexpression Models (POM) are similar to Protein Variant Models (PVM) in that they include a protein reference sequence, a curated BLASTP bitscore cut-off, and mapped resistance variants. Whereas PVMs are designed to detect AMR acquired via mutation of house-keeping genes or antibiotic targets, reporting only those with curated mutations conferring AMR, POMs are restricted to regulatory proteins and report both wild-type sequences and/or sequences with mutations leading to overexpression of efflux complexes. The former lead to efflux of antibiotics at basal levels, while the latter can confer clinical resistance. POMs include a protein reference sequence (often from wild-type alleles), a curated bit-score cut-off, and mapped resistance variants. Mapped resistance variants may include any or all of single point mutations, insertions, or deletions curated from the scientific literature. A Perfect RGI match is 100% identical to the wild-type reference protein sequence along its entire length, a Strict RGI match has a BLASTP bit-score above the curated BLASTP cutoff value may or may not contain at least one curated mutation from amongst the mapped resistance variants, while a Loose RGI match has a bit-score less than the curated BLASTP bit-score cut-off may or may not contain at least one curated mutation from amongst the mapped resistance variants.
Bit-score Cut-off (blastP): 500
PubMed: mutation data hand curated from the scientific literature, evaluated as conferring resistance (R). CRyPTIC: mutation data acquired from the CRyPTIC catalog, evaluated as resistant (R), susceptible (S), or undetermined (U). ReSeqTB: mutation data acquired from the ReSeqTB catalog, evaluated as conferring resistance (Minimal, Moderate, High), not conferring resistance (None), or Indeterminate. WHO: mutation data acquired from the WHO 2023 catalog, evaluated as resistant (R), susceptible (S), or undetermined (U).| Mutation | Mutation type | PubMed |
|---|---|---|
| Y138D | single resistance variant | PMID:26833155 |
| G258D | single resistance variant | PMID:26833155 |
| Curator | Description | Most Recent Edit |
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