Cutibacterium acnes 16S rRNA mutation conferring resistance to tetracycline

Accession ARO:3003499
CARD Short NameCacn_16S_TET
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 for Cutibacterium acnes can result in resistance against tetracycline.
AMR Gene Family16S rRNA with mutation conferring resistance to tetracycline derivatives
Drug Classtetracycline antibiotic
Resistance Mechanismantibiotic target alteration
Resistomes with Sequence VariantsCutibacterium acnesg+wgs
Classification10 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

Ross JI, et al. 1998. Antimicrob Agents Chemother 42(7): 1702-1705. 16S rRNA mutation associated with tetracycline resistance in a gram-positive bacterium. (PMID 9661007)

Resistomes

Prevalence of Cutibacterium acnes 16S rRNA mutation conferring resistance to tetracycline 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).

Prevalence: rRNA gene variant model (view sequences)

SpeciesNCBI ChromosomeNCBI PlasmidNCBI WGSNCBI GIGRDI-AMR2
Cutibacterium acnes5%0%6.35%0%0%
Show Perfect Only


Detection Models

Model Type: rRNA gene variant model

Model Definition: Ribosomal RNA (rRNA) Gene Variant Models (RVM) are similar to Protein Variant Models (PVM), i.e. detect sequences based on their similarity to a curated reference sequence and secondarily screen query sequences for curated sets of mutations to differentiate them from antibiotic susceptible wild-type alleles, except RVMs are designed to detect AMR acquired via mutation of genes encoding ribosomal RNAs (rRNA). RVMs include a rRNA 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 BLASTN bit-score above the curated BLASTN 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 BLASTN bit-score cut-off but still contains at least one curated mutation from amongst the mapped resistance variants.

Bit-score Cut-off (blastN): 2600

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).

MutationMutation typePubMed
g1032csingle resistance variantPMID:9661007


>gb|NR_040847.1|+|1-1486|Cutibacterium acnes 16S rRNA mutation conferring resistance to tetracycline [Cutibacterium acnes]
AGAGTTTGATCCTGGCTCAGGACGAACGCTGGCGGCGTGCTTAACACATGCAAGTCGAACGGAAAGGCCCTGCTTTTGTGGGGTGCTCGA
GTGGCGAACGGGTGAGTAACACGTGAGTAACCTGCCCTTGACTTTGGGATAACTTCAGGAAACTGGGGCTAATACCGGATAGGAGCTCCT
GCTGCATGGTGGGGGTTGGAAAGTTTCGGCGGTTGGGGATGGACTCGCGGCTTATCAGCTTGTTGGTGGGGTAGTGGCTTACCAAGGCTT
TGACGGGTAGCCGGCCTGAGAGGGTGACCGGCCACATTGGGACTGAGATACGGCCCAGACTCCTACGGGAGGCAGCAGTGGGGAATATTG
CACAATGGGCGGAAGCCTGATGCAGCAACGCCGCGTGCGGGATGACGGCCTTCGGGTTGTAAACCGCTTTCGCCTGTGACGAAGCGTGAG
TGACGGTAATGGGTAAAGAAGCACCGGCTAACTACGTGCCAGCAGCCGCGGTGATACGTAGGGTGCGAGCGTTGTCCGGATTTATTGGGC
GTAAAGGGCTCGTAGGTGGTTGATCGCGTCGGAAGTGTAATCTTGGGGCTTAACCCTGAGCGTGCTTTCGATACGGGTTGACTTGAGGAA
GGTAGGGGAGAATGGAATTCCTGGTGGAGCGGTGGAATGCGCAGATATCAGGAGGAACACCAGTGGCGAAGGCGGTTCTCTGGGCCTTTC
CTGACGCTGAGGAGCGAAAGCGTGGGGAGCGAACAGGCTTAGATACCCTGGTAGTCCACGCTGTAAACGGTGGGTACTAGGTGTGGGGTC
CATTCCACGGGTTCCGTGCCGTAGCTAACGCTTTAAGTACCCCGCCTGGGGAGTACGGCCGCAAGGCTAAAACTCAAAGGAATTGACGGG
GCCCCGCACAAGCGGCGGAGCATGCGGATTAATTCGATGCAACGCGTAGAACCTTACCTGGGTTTGACATGGATCGGGAGTGCTCAGAGA
TGGGTGTGCCTCTTTTGGGGTCGGTTCACAGGTGGTGCATGGCTGTCGTCAGCTCGTGTCGTGAGATGTTGGGTTAAGTCCCGCAACGAG
CGCAACCCTTGTTCACTGTTGCCAGCACGTTATGGTGGGGACTCAGTGGAGACCGCCGGGGTCAACTCGGAGGAAGGTGGGGATGACGTC
AAGTCATCATGCCCCTTATGTCCAGGGCTTCACGCATGCTACAATGGCTGGTACAGAGAGTGGCGAGCCTGTGAGGGTGAGCGAATCTCG
GAAAGCCGGTCTCAGTTCGGATTGGGGTCTGCAACTCGACCTCATGAAGTCGGAGTCGCTAGTAATCGCAGATCAGCAACGCTGCGGTGA
ATACGTTCCCGGGGCTTGTACACACCGCCCGTCAAGTCATGAAAGTTGGTAACACCCGAAGCCGGTGGCCTAACCGTTGTGGGGGAGCCG
TCGAAGGTGGGACTGGTGATTAGGACTAAGTCGTAACAAGGTAACC

Curator Acknowledgements
Curator Description Most Recent Edit