Mycobacterium tuberculosis rpsL mutations conferring resistance to Streptomycin

Accession ARO:3003395
Synonym(s)Rv0682
CARD Short NameMtub_rpsL_STR
DefinitionRibosomal protein S12 stabilizes the highly conserved pseudoknot structure formed by 16S rRNA. Amino acid substitutions in RpsL affect the higher-order structure of 16S rRNA and confer streptomycin resistance by disrupting interactions between 16S rRNA and streptomycin.
AMR Gene Familyantibiotic-resistant rpsL
Drug Classaminoglycoside antibiotic
Resistance Mechanismantibiotic target alteration
Resistomes with Sequence VariantsBifidobacterium bifidumg+wgs, Bifidobacterium breveg+wgs, Bifidobacterium longumg+wgs, Corynebacterium jeikeiumg+wgs, Corynebacterium ulceranswgs, Corynebacterium urealyticumg, Kocuria palustriswgs, Micrococcus luteuswgs, Mycobacterium kansasiig, Mycobacterium tuberculosisg+wgs, Schaalia odontolyticag+wgs, Tropheryma whippleiwgs, Trueperella pyogenesg+wgs
Classification8 ontology terms | Show
Parent Term(s)2 ontology terms | Show
+ confers_resistance_to_antibiotic streptomycin [Antibiotic]
+ antibiotic-resistant rpsL [AMR Gene Family]
Publications

Ballif M, et al. 2012. BMC Microbiol 12: 191. Drug resistance-conferring mutations in Mycobacterium tuberculosis from Madang, Papua New Guinea. (PMID 22943573)

Sreevatsan S, et al. 1996. Antimicrob Agents Chemother 40(4): 1024-1026. Characterization of rpsL and rrs mutations in streptomycin-resistant Mycobacterium tuberculosis isolates from diverse geographic localities. (PMID 8849220)

Okamoto S, et al. 2007. Mol Microbiol 63(4): 1096-1106. Loss of a conserved 7-methylguanosine modification in 16S rRNA confers low-level streptomycin resistance in bacteria. (PMID 17238915)

Finken M, et al. 1993. Mol Microbiol 9(6): 1239-1246. Molecular basis of streptomycin resistance in Mycobacterium tuberculosis: alterations of the ribosomal protein S12 gene and point mutations within a functional 16S ribosomal RNA pseudoknot. (PMID 7934937)

Brzostek A, et al. 2004. Int J Tuberc Lung Dis 8(8): 1032-1035. Molecular characterisation of streptomycin-resistant Mycobacterium tuberculosis strains isolated in Poland. (PMID 15305490)

Nair J, et al. 1993. Mol Microbiol 10(3): 521-527. The rpsL gene and streptomycin resistance in single and multiple drug-resistant strains of Mycobacterium tuberculosis. (PMID 7968530)

Ezewudo M, et al. 2018. Sci Rep 8(1):15382 Integrating standardized whole genome sequence analysis with a global Mycobacterium tuberculosis antibiotic resistance knowledgebase. (PMID 30337678)

Resistomes

Prevalence of Mycobacterium tuberculosis rpsL mutations conferring resistance to Streptomycin among the sequenced genomes, plasmids, and whole-genome shotgun assemblies available at NCBI or IslandViewer for 413 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 (view sequences)

SpeciesNCBI ChromosomeNCBI PlasmidNCBI WGSNCBI GI
Bifidobacterium bifidum7.14%0%6.47%0%
Bifidobacterium breve9.8%0%7.23%0%
Bifidobacterium longum18.95%0%4.03%0%
Corynebacterium jeikeium60%0%31.58%0%
Corynebacterium ulcerans0%0%4.55%0%
Corynebacterium urealyticum100%0%0%0%
Kocuria palustris0%0%5.56%0%
Micrococcus luteus0%0%3.33%0%
Mycobacterium kansasii27.27%0%0%0%
Mycobacterium tuberculosis17.42%0%9.81%0%
Schaalia odontolytica33.33%0%12.5%0%
Tropheryma whipplei0%0%5.88%0%
Trueperella pyogenes13.33%0%8.33%0%
Show Perfect Only


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): 200

Legend:

  • discovered in clinical, agricultural, or environmental isolates

  • discovered via laboratory selection experiments

  • ReSeqTB https://platform.reseqtb.org

Published Variants:

PMID: 22943573K43R K88Q K88R
PMID: 15305490T40I K43R
PMID: 30337678K43R K88R

ReSeqTB:

High ConfidenceK43R K88R

>gb|NP_215196.1|+|Mycobacterium tuberculosis rpsL mutations conferring resistance to Streptomycin [Mycobacterium tuberculosis H37Rv]
MPTIQQLVRKGRRDKISKVKTAALKGSPQRRGVCTRVYTTTPKKPNSALRKVARVKLTSQ
VEVTAYIPGEGHNLQEHSMVLVRGGRVKDLPGVRYKIIRGSLDTQGVKNRKQARSRYGAK
KEKG



>gb|NC_000962.3|+|781560-781934|Mycobacterium tuberculosis rpsL mutations conferring resistance to Streptomycin [Mycobacterium tuberculosis H37Rv]
ATGCCAACCATCCAGCAGCTGGTCCGCAAGGGTCGTCGGGACAAGATCAGTAAGGTCAAGACCGCGGCTCTGAAGGGCAGCCCGCAGCGT
CGTGGTGTATGCACCCGCGTGTACACCACCACTCCGAAGAAGCCGAACTCGGCGCTTCGGAAGGTTGCCCGCGTGAAGTTGACGAGTCAG
GTCGAGGTCACGGCGTACATTCCCGGCGAGGGCCACAACCTGCAGGAGCACTCGATGGTGCTGGTGCGCGGCGGCCGGGTGAAGGACCTG
CCTGGTGTGCGCTACAAGATCATCCGCGGTTCGCTGGATACGCAGGGTGTCAAGAACCGCAAACAGGCACGCAGCCGTTACGGCGCTAAG
AAGGAGAAGGGCTGA