tlrB conferring tylosin resistance

Accession ARO:3001299
CARD Short NameSfra_tlrB_TYL
DefinitionTlrB is a methyltransferase found in Streptomyces fradiae and confers resistance to mycinamicin, tylosin and lincosamides. Specifically, this enzyme adds a methyl group to guanosine 748 (E. coli numbering). TlrB is found in the tylosin biosynthetic cluster and is one mechanism by which S. fradiae protects itself from self-destruction when producing this macrolide.
AMR Gene Familynon-erm 23S ribosomal RNA methyltransferase (G748)
Drug Classlincosamide antibiotic, macrolide antibiotic
Resistance Mechanismantibiotic target alteration
Classification11 ontology terms | Show
Parent Term(s)3 ontology terms | Show
+ confers_resistance_to_antibiotic tylosin [Antibiotic]
+ gene involved in self-resistance to antibiotic
+ non-erm 23S ribosomal RNA methyltransferase (G748) [AMR Gene Family]
Publications

Wilson VT, et al. 1999. J Antibiot (Tokyo) 52(3): 288-296. Molecular analysis of tlrB, an antibiotic-resistance gene from tylosin-producing Streptomyces fradiae, and discovery of a novel resistance mechanism. (PMID 10348045)

Liu M, et al. 2000. Mol Microbiol 37(4): 811-820. The tylosin resistance gene tlrB of Streptomyces fradiae encodes a methyltransferase that targets G748 in 23S rRNA. (PMID 10972803)

Resistomes

Prevalence of tlrB conferring tylosin resistance 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 homolog model

SpeciesNCBI ChromosomeNCBI PlasmidNCBI WGSNCBI GI
No prevalence data


Detection Models

Model Type: protein homolog model

Model Definition: Protein Homolog Models (PHM) detect protein sequences based on their similarity to a curated reference sequence, using curated BLASTP bitscore cut-offs. Protein Homolog Models apply to all genes that confer resistance through their presence in an organism, such as the presence of a beta-lactamase gene on a plasmid. PHMs include a reference sequence and a bitscore cut-off for detection using BLASTP. A Perfect RGI match is 100% identical to the reference protein sequence along its entire length, a Strict RGI match is not identical but the bit-score of the matched sequence is greater than the curated BLASTP bit-score cutoff, Loose RGI matches have a bit-score less than the curated BLASTP bit-score cut-off.

Bit-score Cut-off (blastP): 500


>gb|AAD12162.1|+|tlrB conferring tylosin resistance [Streptomyces fradiae]
MRKNVVRYLRCPHCAAPLRSSDRTLRCENGHTFDVARQGYVNLLRRPTKLAADTTDMVAARAALLDSGHYAPLTERLAGTAGRAAGAGAP
DCVVDIGGGTGHHLARVLEEFEDAEGLLLDMSKPAVRRAARAHPRASSAVADVWDTLPLRDGAAAMALNVFAPRNPPEIRRILRPGGTLL
VVTPQQDHLAELVDALGLLRVRDHKEGRLAEQLAPHFEAVGQERLRTTLRLDHDALGRVVAMGPSSWHQDPDELARRIAELPGIHEVTLS
VTFTVCRPLP


>gb|AF055922.1|+|1788-2630|tlrB conferring tylosin resistance [Streptomyces fradiae]
ATGCGGAAGAACGTCGTGCGATATCTGCGCTGTCCGCACTGCGCAGCCCCTCTGCGGTCATCCGACCGCACCCTCCGCTGCGAAAACGGG
CACACCTTCGACGTCGCCCGGCAGGGCTATGTGAATCTGCTCAGACGCCCGACGAAGCTCGCCGCCGACACCACCGACATGGTCGCCGCC
CGGGCCGCGCTGCTGGACAGCGGGCATTACGCGCCGCTGACCGAGCGGCTGGCCGGGACGGCCGGGCGCGCGGCGGGCGCCGGGGCACCG
GACTGCGTCGTGGACATCGGCGGGGGCACCGGTCACCATCTCGCCCGTGTCCTGGAGGAGTTCGAGGACGCCGAGGGACTCCTGCTGGAC
ATGTCCAAGCCGGCCGTGCGCAGGGCCGCCCGCGCCCATCCCCGGGCCAGCTCCGCCGTCGCCGACGTATGGGACACACTTCCGCTGCGG
GACGGGGCCGCCGCGATGGCCCTCAACGTCTTCGCCCCGCGCAACCCGCCGGAGATCCGCAGGATCCTCCGCCCCGGCGGCACCCTGCTG
GTCGTCACGCCCCAGCAGGACCACCTCGCCGAACTCGTGGACGCGCTGGGGCTGTTGCGCGTACGGGACCACAAGGAGGGCCGGCTGGCC
GAACAGCTCGCGCCGCACTTCGAGGCCGTCGGGCAGGAGCGGCTGCGGACCACTCTCCGCCTCGATCACGACGCGCTCGGCCGGGTGGTC
GCCATGGGGCCCAGTTCCTGGCACCAGGACCCGGATGAACTGGCGCGGCGGATCGCGGAGTTGCCCGGCATCCACGAGGTCACGCTCTCG
GTCACCTTCACCGTCTGCCGCCCTCTGCCCTGA