Salmonella serovars soxS with mutation conferring antibiotic resistance

Accession ARO:3003383
CARD Short NameSent_soxS_MULT
DefinitionSoxS is a global regulator that up-regulates the expression of AcrAB efflux genes. It also reduces OmpF expression to decrease cell membrane permeability.
AMR Gene Familyresistance-nodulation-cell division (RND) antibiotic efflux pump, major facilitator superfamily (MFS) antibiotic efflux pump, ATP-binding cassette (ABC) antibiotic efflux pump, General Bacterial Porin with reduced permeability to beta-lactams
Drug Classtetracycline antibiotic, penam, fluoroquinolone antibiotic, cephalosporin, disinfecting agents and antiseptics, rifamycin antibiotic, phenicol antibiotic, glycylcycline, cephamycin, penem, carbapenem, monobactam
Resistance Mechanismantibiotic efflux, reduced permeability to antibiotic, antibiotic target alteration
Efflux Componentefflux pump complex or subunit conferring antibiotic resistance
Efflux Regulatorprotein(s) and two-component regulatory system modulating antibiotic efflux
Classification46 ontology terms | Show
+ process or component of antibiotic biology or chemistry
+ antibiotic molecule
+ beta-lactam antibiotic
+ mechanism of antibiotic resistance
+ cephem
+ determinant of antibiotic resistance
+ antibiotic efflux [Resistance Mechanism]
+ tetracycline antibiotic [Drug Class]
+ reduced permeability to antibiotic [Resistance Mechanism]
+ penam [Drug Class]
+ fluoroquinolone antibiotic [Drug Class]
+ cephalosporin [Drug Class]
+ disinfecting agents and antiseptics [Drug Class]
+ efflux pump complex or subunit conferring antibiotic resistance [Efflux Component]
+ rifamycin antibiotic [Drug Class]
+ phenicol antibiotic [Drug Class]
+ protein modulating permeability to antibiotic
+ glycylcycline [Drug Class]
+ antibiotic target alteration [Resistance Mechanism]
+ resistance-nodulation-cell division (RND) antibiotic efflux pump [AMR Gene Family]
+ cephamycin [Drug Class]
+ major facilitator superfamily (MFS) antibiotic efflux pump [AMR Gene Family]
+ tigecycline [Antibiotic]
+ norfloxacin [Antibiotic]
+ penem [Drug Class]
+ ampicillin [Antibiotic]
+ mutation conferring antibiotic resistance
+ triclosan [Antibiotic]
+ carbapenem [Drug Class]
+ ATP-binding cassette (ABC) antibiotic efflux pump [AMR Gene Family]
+ General Bacterial Porin (GBP)
+ rifampin [Antibiotic]
+ tetracycline [Antibiotic]
+ cefalotin [Antibiotic]
+ monobactam [Drug Class]
+ ciprofloxacin [Antibiotic]
+ chloramphenicol [Antibiotic]
+ antibiotic resistant gene variant or mutant
+ AcrAB-TolC
+ PatA-PatB
+ protein(s) and two-component regulatory system modulating antibiotic efflux [Efflux Regulator]
+ QepA1
+ General Bacterial Porin with reduced permeability to beta-lactams [AMR Gene Family]
+ mutant efflux regulatory protein conferring antibiotic resistance
+ soxRS
+ porin OmpF
Parent Term(s)2 ontology terms | Show
+ soxS
+ confers_resistance_to_antibiotic ciprofloxacin [Antibiotic]
Publications

O'Regan E, et al. 2009. Antimicrob Agents Chemother 53(3): 1080-1087. Multiple regulatory pathways associated with high-level ciprofloxacin and multidrug resistance in Salmonella enterica serovar enteritidis: involvement of RamA and other global regulators. (PMID 19104017)

Resistomes

Prevalence of Salmonella serovars soxS with mutation conferring antibiotic resistance among the sequenced genomes, plasmids, and whole-genome shotgun assemblies available at NCBI or IslandViewer for 377 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).

Prevalence: protein variant model

SpeciesNCBI ChromosomeNCBI PlasmidNCBI WGSNCBI GI
No prevalence data


Detection Models

Model Type: protein variant model

Model Definition: Protein Variant Models (PVM) perform a similar search as Protein Homolog Models (PHM), i.e. detect protein sequences based on their similarity to a curated reference sequence, but secondarily screen query sequences for curated sets of mutations to differentiate them from antibiotic susceptible wild-type alleles. PVMs are designed to detect AMR acquired via mutation of house-keeping genes or antibiotic targets, e.g. a mutated gyrase resistant to aminocoumarin antibiotics. PVMs include a protein reference sequence (often from antibiotic susceptible 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 Strict RGI match has a BLASTP bit-score above the curated BLASTP cutoff value and contains 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 but still contains at least one curated mutation from amongst the mapped resistance variants.

Bit-score Cut-off (blastP): 215

Legend:

  • discovered in clinical, agricultural, or environmental isolates

  • discovered via laboratory selection experiments

  • ReSeqTB https://platform.reseqtb.org

Published Variants:


>gb|AAL23089.1|-|Salmonella serovars soxS with mutation conferring antibiotic resistance [Salmonella enterica subsp. enterica serovar Typhimurium str. LT2]
MSHQQIIQTLIEWIDEHIDQPLNIDVVAKKSGYSKWYLQRMFRTVTHQTLGEYIRQRRLL
LAAVELRTTERPIFDIAMDLGYVSQQTFSRVFRREFDRTPSDYRHRL



>gb|AE006468.2|-|4503986-4504309|Salmonella serovars soxS with mutation conferring antibiotic resistance [Salmonella enterica subsp. enterica serovar Typhimurium str. LT2]
ATGTCGCATCAGCAGATAATTCAGACCCTTATCGAATGGATTGATGAACATATCGACCAACCGCTAAACATTGATGTGGTGGCAAAAAAA
TCGGGCTACTCCAAGTGGTATTTGCAGCGGATGTTTCGTACGGTAACGCATCAAACATTAGGCGAGTATATTCGCCAGCGCCGTCTCCTG
TTGGCGGCCGTTGAGCTACGAACGACCGAGCGCCCGATTTTTGATATCGCGATGGACCTGGGCTATGTATCGCAGCAAACCTTCTCGCGT
GTATTCCGCCGCGAGTTCGATCGCACTCCCAGCGATTACCGTCACCGCCTGTAG