Mycobacterium tuberculosis alr with mutation conferring resistance to cycloserine

Accession ARO:3004947
CARD Short NameMtub_alr_DCS
DefinitionMutations in the alr mutation contribute to or confer resistance to cycloserine.
AMR Gene Familycycloserine resistant alr
Drug Classcycloserine-like antibiotic
Resistance Mechanismantibiotic target alteration
Classification9 ontology terms | Show
Parent Term(s)2 ontology terms | Show
+ confers_resistance_to_antibiotic cycloserine [Antibiotic]
+ cycloserine resistant alr [AMR Gene Family]
Publications

Nakatani Y, et al. 2017. Antimicrob Agents Chemother 61(12): Role of Alanine Racemase Mutations in Mycobacterium tuberculosis d-Cycloserine Resistance. (PMID 28971867)

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 alr with mutation conferring resistance to cycloserine 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: protein variant model

SpeciesNCBI ChromosomeNCBI PlasmidNCBI WGSNCBI GIGRDI-AMR2
No prevalence data


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): 750


>gb|NP_217940.1|-|Mycobacterium tuberculosis alr with mutation conferring resistance to cycloserine [Mycobacterium tuberculosis H37Rv]
MKRFWENVGKPNDTTDGRGTTSLAMTPISQTPGLLAEAMVDLGAIEHNVRVLREHAGHAQLMAVVKADGYGHGATRVAQTALGAGAAELG
VATVDEALALRADGITAPVLAWLHPPGIDFGPALLADVQVAVSSLRQLDELLHAVRRTGRTATVTVKVDTGLNRNGVGPAQFPAMLTALR
QAMAEDAVRLRGLMSHMVYADKPDDSINDVQAQRFTAFLAQAREQGVRFEVAHLSNSSATMARPDLTFDLVRPGIAVYGLSPVPALGDMG
LVPAMTVKCAVALVKSIRAGEGVSYGHTWIAPRDTNLALLPIGYADGVFRSLGGRLEVLINGRRCPGVGRICMDQFMVDLGPGPLDVAEG
DEAILFGPGIRGEPTAQDWADLVGTIHYEVVTSPRGRITRTYREAENR


>gb|NC_000962.3|-|3840194-3841420|Mycobacterium tuberculosis alr with mutation conferring resistance to cycloserine [Mycobacterium tuberculosis H37Rv]
GTGAAACGGTTCTGGGAGAATGTCGGAAAGCCAAACGACACGACAGATGGGCGGGGCACGACTTCGTTGGCCATGACACCGATATCCCAG
ACACCTGGCCTCCTCGCCGAGGCCATGGTGGATCTGGGCGCTATTGAACACAACGTGCGGGTGCTGCGTGAGCACGCCGGCCACGCGCAG
CTGATGGCGGTGGTCAAGGCCGACGGCTACGGTCACGGTGCTACGCGCGTCGCCCAAACCGCCCTGGGAGCCGGTGCGGCCGAACTCGGC
GTCGCCACCGTCGACGAGGCGCTAGCGCTGCGCGCTGATGGCATTACCGCACCGGTGCTGGCCTGGCTGCATCCGCCCGGCATCGACTTC
GGGCCCGCGCTGCTGGCCGACGTGCAGGTCGCGGTGTCCTCGCTGCGCCAACTCGACGAACTGTTGCACGCGGTGCGCCGGACCGGCCGG
ACGGCGACGGTGACCGTCAAGGTGGATACCGGGCTGAACCGCAATGGCGTGGGACCGGCACAATTCCCGGCCATGCTGACCGCGTTACGC
CAAGCCATGGCCGAGGACGCCGTCCGGCTGCGGGGGCTGATGTCGCATATGGTTTACGCCGACAAGCCTGACGATTCCATCAACGATGTT
CAGGCCCAACGGTTTACCGCCTTTCTGGCGCAGGCCCGCGAACAAGGGGTGCGGTTCGAGGTGGCGCATCTATCGAACTCATCAGCAACT
ATGGCGCGCCCCGACCTGACGTTCGACCTGGTGCGGCCGGGCATCGCGGTGTATGGGCTAAGCCCGGTACCCGCCCTCGGTGACATGGGG
CTGGTGCCGGCGATGACCGTGAAATGTGCTGTTGCGCTGGTGAAATCGATTCGTGCGGGGGAGGGCGTGTCGTATGGGCACACATGGATC
GCGCCACGCGACACCAATCTGGCGCTGCTGCCGATCGGTTACGCAGACGGCGTGTTCCGGTCGCTGGGCGGGCGGCTGGAGGTGCTGATC
AACGGCAGACGATGCCCCGGTGTGGGGCGGATCTGCATGGACCAGTTCATGGTCGACCTGGGCCCCGGGCCGCTTGATGTGGCCGAAGGC
GACGAGGCGATTTTGTTCGGGCCGGGCATCCGGGGTGAGCCCACGGCTCAGGACTGGGCCGATCTTGTCGGCACCATCCACTACGAAGTG
GTCACCAGCCCGCGAGGACGTATCACCAGGACCTATCGCGAGGCTGAAAACCGTTGA

Curator Acknowledgements
Curator Description Most Recent Edit