Helicobacter pylori 16S rRNA mutation conferring resistance to tetracycline

Accession ARO:3003510
DefinitionTetracycline binds tightly to the helix 34 domain in 16S rRNA, where it interferes sterically with the binding of aminoacyl-tRNA to the ribosome A site to block protein synthesis. Mutations in the nucleotide sequence in this domain of Helicobacter pylori can result in resistance against tetracycline.
AMR Gene Family16S rRNA with mutation conferring resistance to tetracycline derivatives
Drug Classtetracycline antibiotic
Resistance Mechanismantibiotic target alteration
Classification11 ontology terms | Show
Parent Term(s)2 ontology terms | Show
+ confers_resistance_to_antibiotic tetracycline [Antibiotic]
+ 16S rRNA with mutation conferring resistance to tetracycline derivatives [AMR Gene Family]
Publications

Dailidiene D, et al. 2002. Antimicrob Agents Chemother 46(12): 3940-3946. Emergence of tetracycline resistance in Helicobacter pylori: multiple mutational changes in 16S ribosomal DNA and other genetic loci. (PMID 12435699)

Trieber CA, et al. 2002. J Bacteriol 184(8): 2131-2140. Mutations in the 16S rRNA genes of Helicobacter pylori mediate resistance to tetracycline. (PMID 11914344)

Resistomes

Prevalence of Helicobacter pylori 16S rRNA mutation conferring resistance to tetracycline among the sequenced genomes, plasmids, and whole-genome shotgun assemblies available at NCBI for 82 important pathogens (see methodological details and complete list of analyzed pathogens). Values reflect percentage of genomes, plasmids, 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: rRNA gene variant model

SpeciesNCBI ChromosomeNCBI PlasmidNCBI WGS
No prevalence data


Detection Models

Model Type: rRNA gene variant model

Model Definition: The rRNA gene variant model is an AMR detection model used to identify ribosomal RNA (rRNA) genes with mutations shown clinically to confer resistance to known antibiotic(s) relative to the wild-type rRNA sequence. Like the protein variant model, rRNA gene variant models detect the presence of an rRNA sequence based on its homolog, and then secondarily search submitted query sequences for a curated mutation. This model includes an rRNA gene reference sequence, a BLASTN bitscore cutoff, and a set of mapped resistance variants. A submitted sequence must have both high homolog to the reference sequence and include a known resistance variant to be detected.

Legend:

  • discovered in clinical, agricultural, or environmental isolates
  • discovered via laboratory selection experiments


Bit-score Cut-off (blastN): 2700

PMID in progress (single): A965G A967C

PMID: 12435699A965G,A967C A965G,G966U
PMID: 11914344A965U,G966U,A967C


>gb|CP003904.1|-|1511157-1512657|Helicobacter pylori 16S rRNA mutation conferring resistance to tetracycline [Helicobacter pylori 26695]
AGGAGGTGATCCAACCGCAGGTTCACTACGGTTACCTTGTTACGACTTCACCCCAGTCGCTGTGTGTGCCGTGGGCAGTAGCCAATTTAG
CATCCTGACTTAAGGCAAACACAACTCCCATGGTGTGACGGGCGGTGAGTACAAGACCCGGGAACGTATTCACCGCAACATGGCTGATTT
GCGATTACTAGCGATTCCAGCTTCATGCAGGCGAGTTGCAGCCTACAATCCGAACTGAGAGGTGTTTTGAAGATTGGCTCCATTCGCAGT
ATTGCTTCTCTTTGTGCACCCCATTGTAGCACGTGTGTAGCCCTAGGCGTAAGGGCCATGATGACTTGACGTCGTCCCCACCTTCCTNCC
CTTACGGAGGCAGTATCCTTAGAGTTCTCAGCATAACCTGTTAGCAACTAAGAAAAGGGGTTGCGCTCGTTGCGGGACTTAACCCAACAT
CTCACGACACGAGCTGACGACAGCCGTGCAGCACCTGTTTTCAAGGTCTGGCAAGCCAGACACTCCACTATTTCTAGCGGATTCTCTCAA
TGTCAAGCCTAGGTAAGGTTCTTCGTGTATCTTCGAATTAAACCACATGCTCCACCGCTTGTGCGGGTCCCCGTCTATTCCTTTGAGTTT
TAATCTTGCGACCGTACTCCCCAGGCGGGATGCTTAATGCGTTAGCTGCATTACTGGAGAGACTAAGCCCTCCAACAACTAGCATCCATC
GTTTAGGGCGTGGACTACCAGGGTATCTAATCCTGTTTGCTCCCCAACMGCTTTCGCGCAATCAGCGTCAGTAATGTTCCAGCAGGTCGC
CTTCGCAATGAGTATTCCTCTTGATCTCTACGGATTTTACCCCTACACCAAGAATTCCACCTACCTCTCCCACACTCTAGAATAGTAGTT
TCAAATGCAGTTCTATGGTTAAGCCATAGGATTTCACACCTGACTGACTATCCCGCCTACGCGCTCTTTACGCCCAGTGATTCCGAGTAA
CGCTTGCACCCTCCGTATTACCGCGGCTGCTGGCACGGAGTTAGCCGGTGCTTATTCGTTAGATACCGTCATTATCTTCTCTAACAAAAG
GAGTTTACAATCCTAAAACCTTCATCCTCCACGCGGCGTTGCTGCTTCAGGGTTTCCCCCATTGAGCAATATTCCCTACTGCTGCCTCCC
GTAGGAGTCTGGACCGTGTCTCAGTTCCAGTGTGTCCGTTCACCCTCTCAGGCCGGATACCCGTCATAGCCTTGGTAAGCCATTACCTTA
CCAACAAGCTGATAGGACATAGGCTGATCTCTTAGCGATAAATCTTTCCCCCGTAGGAGTATCTGGTATTAATCATCGTTTCCAATGGCT
ATCCCAAACTAAGAGGCACATAACCTATGCGTTACTCACCCGTGCGCCACTAATCAGCACTCTAGCAAGCTAGAAGCTTCATCGTTCGAC
TTGCATGTATTAGGCACGCCGCCAGCGTTCACTCTGAGCCAGGATCAAACTCTCCATAAAA