Accession ARO:3000862
CARD Short Namesgm
DefinitionSgm, or sisomicin-gentamicin methyltransferase, methylates G1405 of 16S rRNA to confer resistance to various aminoglycosides.
AMR Gene Family16S rRNA methyltransferase (G1405)
Drug Classaminoglycoside antibiotic
Resistance Mechanismantibiotic target alteration
Classification11 ontology terms | Show
Parent Term(s)12 ontology terms | Show
+ confers_resistance_to_antibiotic dibekacin [Antibiotic]
+ confers_resistance_to_antibiotic amikacin [Antibiotic]
+ confers_resistance_to_antibiotic gentamicin C [Antibiotic]
+ confers_resistance_to_antibiotic sisomicin [Antibiotic]
+ confers_resistance_to_antibiotic netilmicin [Antibiotic]
+ confers_resistance_to_antibiotic kanamycin A [Antibiotic]
+ confers_resistance_to_antibiotic tobramycin [Antibiotic]
+ confers_resistance_to_antibiotic isepamicin [Antibiotic]
+ confers_resistance_to_antibiotic G418 [Antibiotic]
+ confers_resistance_to_antibiotic arbekacin [Antibiotic]
+ confers_resistance_to_antibiotic gentamicin B [Antibiotic]
+ 16S rRNA methyltransferase (G1405) [AMR Gene Family]
Publications

Husain N, et al. 2010. Nucleic Acids Res 38(12): 4120-4132. Structural basis for the methylation of G1405 in 16S rRNA by aminoglycoside resistance methyltransferase Sgm from an antibiotic producer: a diversity of active sites in m7G methyltransferases. (PMID 20194115)

Resistomes

Prevalence of sgm 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 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|WP_063978071.1|+|sgm [Micromonospora zionensis]
MTAPAADDRIDEIERAITKSRRYQTVAPATVRRLARAALVAARGDVPDAVKRTKRGLHEIYGAFLPPSPPNYAALLRHLDSAVDAGDDEA
VRAALLRAMSVHISTRERLPHLDEFYRELFRHLPRPNTLRDLACGLNPLAAPWMGLPAETVYIASDIDARLVGFVDEALTRLNVPHRTNV
ADLLEDRLDEPADVTLLLKTLPCLETQQRGSGWEVIDIVNSPNIVVTFPTKSLGQRSKGMFQNYSQSFESQARERSCRIQRLEIGNELIY
VIQK


>gb|NG_050600.1|+|101-925|sgm [Micromonospora zionensis]
ATGACGGCACCTGCGGCCGACGACCGTATCGACGAGATTGAGCGGGCCATCACCAAGAGCAGGCGTTACCAGACGGTGGCGCCGGCCACC
GTGCGCCGCCTGGCCCGCGCTGCTCTCGTCGCCGCGCGGGGTGACGTGCCCGACGCGGTGAAGCGCACCAAGCGGGGTCTGCACGAGATC
TACGGCGCCTTCCTGCCGCCCAGCCCTCCCAACTACGCAGCGTTGCTGCGGCACCTGGACTCGGCAGTGGACGCCGGTGACGACGAGGCG
GTTCGAGCGGCCCTACTTCGCGCTATGTCCGTACATATCTCCACCCGCGAGCGATTGCCGCACCTCGACGAGTTCTACCGGGAACTCTTC
CGGCACCTCCCCCGACCGAACACGCTGCGTGACCTCGCCTGTGGTCTCAACCCCCTGGCCGCGCCCTGGATGGGCCTGCCCGCCGAGACC
GTCTACATCGCCTCGGACATCGACGCCCGCCTGGTCGGCTTCGTGGACGAGGCCCTGACCCGACTCAATGTTCCACATCGGACGAACGTG
GCCGACCTGCTCGAGGACCGTCTTGACGAGCCGGCCGACGTCACGCTATTGCTGAAGACGCTGCCCTGTCTGGAGACTCAGCAACGAGGA
TCGGGCTGGGAAGTGATTGACATTGTCAACTCGCCGAATATCGTGGTAACCTTCCCGACCAAGTCTCTCGGTCAGCGATCGAAGGGGATG
TTTCAGAACTATTCACAGAGTTTTGAGTCCCAGGCCAGAGAGCGGTCATGCCGTATTCAGCGACTGGAGATTGGCAACGAGCTGATTTAC
GTCATTCAGAAATAG