Molecule Information

General Information of the Molecule (ID: Mol02038)

• Name: 23S rRNA (cytidine-2'-O)-methyltransferase TlyA (TLYA) ,Campylobacter jejuni
• Synonyms: tlyA; CJJ81176_0616
• Molecule Type: Protein
• Gene Name: TLYA
• Sequence:
  MRFDFFVSKRLNISRNKALELIENEEVLLNGKSFKASFDVKNFLENLKKTQDLNPEDILL
  TDGLKLDLLSEIYVSRAALKLKNFLEENGIEIKHKNCLDIGSSTGGFVQILLENQALKIT
  ALDVGNNQLHLSLRTNEKIILHENTDLRTFKSEEKFELITCDVSFISLINLLYYIDNLAL
  KEIILLFKPQFEVGKNIKRDKKGVLKDDKAILKARMDFEKACAKLGWLLKNTQKSSIKGK
  EGNVEYFYYYIKN
• Function: Catalyzes the 2'-O-methylation at nucleotide C1920 in 23S rRNA. Enhances motility. Enchances biofilm formation. Involved in the assembly of 70S ribosomes. Involved in virulence by promoting adherence and invasion to host cells. Involved in pathogenicity by modulating secretion of host-protective chemokine interleukin 8 (IL-8). Involved in susceptibility to antibiotic capreomycin.
• Uniprot ID: TLYA_CAMJJ

Kingdom: N.A.
Phylum: Proteobacteria
Class: Epsilonproteobacteria
Order: Campylobacterales
Family: Campylobacteraceae
Genus: Campylobacter
Species: Campylobacter jejuni

Type(s) of Resistant Mechanism of This Molecule

  ADTT: Aberration of the Drug's Therapeutic Target

Drug Resistance Data Categorized by Drug

Approved Drug(s) 2 drug(s) in total

Erythromycin

Drug Resistance Data Categorized by Their Corresponding Mechanisms

Aberration of the Drug's Therapeutic Target (ADTT)

Disease Class: Bordetella pertussis infection [1]

• Resistant Disease: Bordetella pertussis infection [ICD-11: 1C12.0]
• Resistant Drug: Erythromycin
• Molecule Alteration: Missense mutation; p.A2047G
• Experimental Note: Identified from the Human Clinical Data
• In Vitro Model: Bordetella pertussis isolate; 1952
• Experiment for Molecule Alteration: Whole genome sequencing assay
• Experiment for Drug Resistance: Disk diffusion assay
• Mechanism Description: All of the strains of B. pertussis resistant to erythromycin in our center had the A2047G mutation of the 23S rRNA gene.

Disease Class: Mycoplasma pneumoniae infection [2]

• Resistant Disease: Mycoplasma pneumoniae infection [ICD-11: 1D01.3]
• Resistant Drug: Erythromycin
• Molecule Alteration: Missense mutation; p.A2063G+p.A2064G+p.A2617G
• Experimental Note: Discovered Using In-vivo Testing Model
• In Vitro Model: Mycoplasma pneumoniae strain; 2014
• Experiment for Drug Resistance: MIC assay
• Mechanism Description: It has been confirmed that drug resistance to macrolide antibiotics of MP is mainly related to the mutation of Gene 23SrRNA in Area V, most commonly in the mutation of A2063G and followed by A2064G and A2617G. Rarely, mutation of ribosomal protein L4 or L22 may induce drug resistance to macrolide antibiotics.

Zithromax

Drug Resistance Data Categorized by Their Corresponding Mechanisms

Aberration of the Drug's Therapeutic Target (ADTT)

Disease Class: Traveler's diarrhea [3]

• Resistant Disease: Traveler's diarrhea [ICD-11: DA90.1]
• Resistant Drug: Zithromax
• Molecule Alteration: Missense mutation; p.A2075G
• Experimental Note: Identified from the Human Clinical Data
• In Vitro Model: Campylobacter jejuni isolates; 197
• In Vitro Model: Campylobacter jejuni ATCC 33560; 197
• Experiment for Molecule Alteration: Gene sequencing assay
• Experiment for Drug Resistance: E-test assay
• Mechanism Description: Point mutation occurred on the 23S rRNA gene at the A2075G transitions, and the number of mutated gene copies was proportional to azithromycin resistance.

References

• Ref 1: Analysis of antibiotic sensitivity and resistance genes of Bordetella pertussis in Chinese children .Medicine (Baltimore). 2021 Jan 15;100(2):e24090. doi: 10.1097/MD.0000000000024090. 10.1097/MD.0000000000024090
• Ref 2: Serological Analysis and Drug Resistance of Chlamydia pneumoniae and Mycoplasma pneumoniae in 4500 Healthy Subjects in Shenzhen, China .Biomed Res Int. 2017;2017:3120138. doi: 10.1155/2017/3120138. Epub 2017 Sep 19. 10.1155/2017/3120138
• Ref 3: Determination of azithromycin heteroresistant Campylobacter jejuni in traveler's diarrhea .Gut Pathog. 2019 May 6;11:19. doi: 10.1186/s13099-019-0301-1. eCollection 2019. 10.1186/s13099-019-0301-1