Molecule Information

General Information of the Molecule (ID: Mol00781)

• Name: Aminoglycoside 2'-N-acetyltransferase (A2NA) ,Mycolicibacterium fortuitum
• Synonyms: AAC(2')-Ib
• Molecule Type: Protein
• Gene Name: aac
• Gene ID: 29426913
• Sequence:
  MPFQDVSAPVRGGILHTARLVHTSDLDQETREGARRMVIEAFEGDFSDADWEHALGGMHA
  FICHHGALIAHAAVVQRRLLYRDTALRCGYVEAVAVREDWRGQGLATAVMDAVEQVLRGA
  YQLGALSASDTARGMYLSRGWLPWQGPTSVLQPAGVTRTPEDDEGLFVLPVGLPAGMELD
  TTAEITCDWRDGDVW
• Function: Confers resistance to gentamicin, tobramycin, dibekacin, netilmicin, and 6'-N-ethylnetilmicin.
• Uniprot ID: AAC2_MYCFO

Kingdom: N.A.
Phylum: Actinobacteria
Class: Actinomycetia
Order: Corynebacteriales
Family: Mycobacteriaceae
Genus: Mycolicibacterium
Species: Mycolicibacterium fortuitum

Type(s) of Resistant Mechanism of This Molecule

  DISM: Drug Inactivation by Structure Modification

Drug Resistance Data Categorized by Drug

Approved Drug(s) 7 drug(s) in total

Aminodeoxykanamycin

Drug Resistance Data Categorized by Their Corresponding Mechanisms

Drug Inactivation by Structure Modification (DISM)

Disease Class: Mycobacterium fortuitum infection [1]

• Resistant Disease: Mycobacterium fortuitum infection [ICD-11: 1B2Z.2]
• Resistant Drug: Aminodeoxykanamycin
• Molecule Alteration: Expression; Inherence
• Experimental Note: Identified from the Human Clinical Data
• In Vitro Model: Escherichia coli XL1-Blue; 562
• In Vitro Model: Streptomyces lividans strain 1326; 1200984
• In Vitro Model: Mycolicibacterium fortuitum strain FC1k; 1766
• In Vitro Model: Mycolicibacterium smegmatis strain mc2 155; 246196
• Experiment for Molecule Alteration: Southern blot hybridizations assay
• Experiment for Drug Resistance: Twofold dilution of antibiotics assay
• Mechanism Description: Thirty-four environmental and clinical isolates belonging to theM. fortuitumcomplex were chosen for the present study. The MICs of gentamicin varied, ranging from 2 to 16mg/ml. Crude extracts of all 34 strains were shown to have AAC activity. Acetylation of gentamicin, tobramycin, and kanamycins A and B was found for all the strains, showing a substrate profile consistent with the presence of an AAC(3) activity. Environmental isolateM. fortuitumFC1k was chosen for further studies because of its high level of AAC activity and the level of resistance to gentamicin (MIC, 16mg/ml).

Dibekacin

Drug Resistance Data Categorized by Their Corresponding Mechanisms

Drug Inactivation by Structure Modification (DISM)

Disease Class: Mycobacterium smegmatis infection [1]

• Resistant Disease: Mycobacterium smegmatis infection [ICD-11: 1B2Z.3]
• Resistant Drug: Dibekacin
• Molecule Alteration: Expression; Acquired
• Experimental Note: Identified from the Human Clinical Data
• In Vitro Model: Escherichia coli XL1-Blue; 562
• In Vitro Model: Streptomyces lividans strain 1326; 1200984
• In Vitro Model: Mycolicibacterium fortuitum strain FC1k; 1766
• In Vitro Model: Mycolicibacterium smegmatis strain mc2 155; 246196
• Experiment for Molecule Alteration: Southern blot hybridizations assay
• Experiment for Drug Resistance: Twofold dilution of antibiotics assay
• Mechanism Description: The aac(2')-Ib gene cloned in a mycobacterial plasmid and introduced in Mycobacterium smegmatis conferred resistance to gentamicin, tobramycin, dibekacin, netilmicin, and 6'-N-ethylnetilmicin.

Gentamicin B

Drug Resistance Data Categorized by Their Corresponding Mechanisms

Drug Inactivation by Structure Modification (DISM)

Disease Class: Mycobacterium fortuitum infection [1]

• Resistant Disease: Mycobacterium fortuitum infection [ICD-11: 1B2Z.2]
• Resistant Drug: Gentamicin B
• Molecule Alteration: Expression; Inherence
• Experimental Note: Identified from the Human Clinical Data
• In Vitro Model: Escherichia coli XL1-Blue; 562
• In Vitro Model: Streptomyces lividans strain 1326; 1200984
• In Vitro Model: Mycolicibacterium fortuitum strain FC1k; 1766
• In Vitro Model: Mycolicibacterium smegmatis strain mc2 155; 246196
• Experiment for Molecule Alteration: Southern blot hybridizations assay
• Experiment for Drug Resistance: Twofold dilution of antibiotics assay
• Mechanism Description: Thirty-four environmental and clinical isolates belonging to theM. fortuitumcomplex were chosen for the present study. The MICs of gentamicin varied, ranging from 2 to 16mg/ml. Crude extracts of all 34 strains were shown to have AAC activity. Acetylation of gentamicin, tobramycin, and kanamycins A and B was found for all the strains, showing a substrate profile consistent with the presence of an AAC(3) activity. Environmental isolateM. fortuitumFC1k was chosen for further studies because of its high level of AAC activity and the level of resistance to gentamicin (MIC, 16mg/ml).

Disease Class: Mycobacterium smegmatis infection [1]

• Resistant Disease: Mycobacterium smegmatis infection [ICD-11: 1B2Z.3]
• Resistant Drug: Gentamicin B
• Molecule Alteration: Expression; Acquired
• Experimental Note: Identified from the Human Clinical Data
• In Vitro Model: Escherichia coli XL1-Blue; 562
• In Vitro Model: Streptomyces lividans strain 1326; 1200984
• In Vitro Model: Mycolicibacterium fortuitum strain FC1k; 1766
• In Vitro Model: Mycolicibacterium smegmatis strain mc2 155; 246196
• Experiment for Molecule Alteration: Southern blot hybridizations assay
• Experiment for Drug Resistance: Twofold dilution of antibiotics assay
• Mechanism Description: The aac(2')-Ib gene cloned in a mycobacterial plasmid and introduced in Mycobacterium smegmatis conferred resistance to gentamicin, tobramycin, dibekacin, netilmicin, and 6'-N-ethylnetilmicin.

Gentamicin C

Drug Resistance Data Categorized by Their Corresponding Mechanisms

Drug Inactivation by Structure Modification (DISM)

Disease Class: Mycobacterium fortuitum infection [1]

• Resistant Disease: Mycobacterium fortuitum infection [ICD-11: 1B2Z.2]
• Resistant Drug: Gentamicin C
• Molecule Alteration: Expression; Inherence
• Experimental Note: Identified from the Human Clinical Data
• In Vitro Model: Escherichia coli XL1-Blue; 562
• In Vitro Model: Streptomyces lividans strain 1326; 1200984
• In Vitro Model: Mycolicibacterium fortuitum strain FC1k; 1766
• In Vitro Model: Mycolicibacterium smegmatis strain mc2 155; 246196
• Experiment for Molecule Alteration: Southern blot hybridizations assay
• Experiment for Drug Resistance: Twofold dilution of antibiotics assay
• Mechanism Description: Thirty-four environmental and clinical isolates belonging to theM. fortuitumcomplex were chosen for the present study. The MICs of gentamicin varied, ranging from 2 to 16mg/ml. Crude extracts of all 34 strains were shown to have AAC activity. Acetylation of gentamicin, tobramycin, and kanamycins A and B was found for all the strains, showing a substrate profile consistent with the presence of an AAC(3) activity. Environmental isolateM. fortuitumFC1k was chosen for further studies because of its high level of AAC activity and the level of resistance to gentamicin (MIC, 16mg/ml).

Disease Class: Mycobacterium smegmatis infection [1]

• Resistant Disease: Mycobacterium smegmatis infection [ICD-11: 1B2Z.3]
• Resistant Drug: Gentamicin C
• Molecule Alteration: Expression; Acquired
• Experimental Note: Identified from the Human Clinical Data
• In Vitro Model: Escherichia coli XL1-Blue; 562
• In Vitro Model: Streptomyces lividans strain 1326; 1200984
• In Vitro Model: Mycolicibacterium fortuitum strain FC1k; 1766
• In Vitro Model: Mycolicibacterium smegmatis strain mc2 155; 246196
• Experiment for Molecule Alteration: Southern blot hybridizations assay
• Experiment for Drug Resistance: Twofold dilution of antibiotics assay
• Mechanism Description: The aac(2')-Ib gene cloned in a mycobacterial plasmid and introduced in Mycobacterium smegmatis conferred resistance to gentamicin, tobramycin, dibekacin, netilmicin, and 6'-N-ethylnetilmicin.

Kanamycin

Drug Resistance Data Categorized by Their Corresponding Mechanisms

Drug Inactivation by Structure Modification (DISM)

Disease Class: Mycobacterium fortuitum infection [1]

• Resistant Disease: Mycobacterium fortuitum infection [ICD-11: 1B2Z.2]
• Resistant Drug: Kanamycin
• Molecule Alteration: Expression; Inherence
• Experimental Note: Identified from the Human Clinical Data
• In Vitro Model: Escherichia coli XL1-Blue; 562
• In Vitro Model: Streptomyces lividans strain 1326; 1200984
• In Vitro Model: Mycolicibacterium fortuitum strain FC1k; 1766
• In Vitro Model: Mycolicibacterium smegmatis strain mc2 155; 246196
• Experiment for Molecule Alteration: Southern blot hybridizations assay
• Experiment for Drug Resistance: Twofold dilution of antibiotics assay
• Mechanism Description: Thirty-four environmental and clinical isolates belonging to theM. fortuitumcomplex were chosen for the present study. The MICs of gentamicin varied, ranging from 2 to 16mg/ml. Crude extracts of all 34 strains were shown to have AAC activity. Acetylation of gentamicin, tobramycin, and kanamycins A and B was found for all the strains, showing a substrate profile consistent with the presence of an AAC(3) activity. Environmental isolateM. fortuitumFC1k was chosen for further studies because of its high level of AAC activity and the level of resistance to gentamicin (MIC, 16mg/ml).

Netilmicin

Drug Resistance Data Categorized by Their Corresponding Mechanisms

Drug Inactivation by Structure Modification (DISM)

Disease Class: Mycobacterium smegmatis infection [1]

• Resistant Disease: Mycobacterium smegmatis infection [ICD-11: 1B2Z.3]
• Resistant Drug: Netilmicin
• Molecule Alteration: Expression; Acquired
• Experimental Note: Identified from the Human Clinical Data
• In Vitro Model: Escherichia coli XL1-Blue; 562
• In Vitro Model: Streptomyces lividans strain 1326; 1200984
• In Vitro Model: Mycolicibacterium fortuitum strain FC1k; 1766
• In Vitro Model: Mycolicibacterium smegmatis strain mc2 155; 246196
• Experiment for Molecule Alteration: Southern blot hybridizations assay
• Experiment for Drug Resistance: Twofold dilution of antibiotics assay
• Mechanism Description: The aac(2')-Ib gene cloned in a mycobacterial plasmid and introduced in Mycobacterium smegmatis conferred resistance to gentamicin, tobramycin, dibekacin, netilmicin, and 6'-N-ethylnetilmicin.

Tobramycin

Drug Resistance Data Categorized by Their Corresponding Mechanisms

Drug Inactivation by Structure Modification (DISM)

Disease Class: Mycobacterium fortuitum infection [1]

• Resistant Disease: Mycobacterium fortuitum infection [ICD-11: 1B2Z.2]
• Resistant Drug: Tobramycin
• Molecule Alteration: Expression; Inherence
• Experimental Note: Identified from the Human Clinical Data
• In Vitro Model: Escherichia coli XL1-Blue; 562
• In Vitro Model: Streptomyces lividans strain 1326; 1200984
• In Vitro Model: Mycolicibacterium fortuitum strain FC1k; 1766
• In Vitro Model: Mycolicibacterium smegmatis strain mc2 155; 246196
• Experiment for Molecule Alteration: Southern blot hybridizations assay
• Experiment for Drug Resistance: Twofold dilution of antibiotics assay
• Mechanism Description: Thirty-four environmental and clinical isolates belonging to theM. fortuitumcomplex were chosen for the present study. The MICs of gentamicin varied, ranging from 2 to 16mg/ml. Crude extracts of all 34 strains were shown to have AAC activity. Acetylation of gentamicin, tobramycin, and kanamycins A and B was found for all the strains, showing a substrate profile consistent with the presence of an AAC(3) activity. Environmental isolateM. fortuitumFC1k was chosen for further studies because of its high level of AAC activity and the level of resistance to gentamicin (MIC, 16mg/ml).

Disease Class: Mycobacterium smegmatis infection [1]

• Resistant Disease: Mycobacterium smegmatis infection [ICD-11: 1B2Z.3]
• Resistant Drug: Tobramycin
• Molecule Alteration: Expression; Acquired
• Experimental Note: Identified from the Human Clinical Data
• In Vitro Model: Escherichia coli XL1-Blue; 562
• In Vitro Model: Streptomyces lividans strain 1326; 1200984
• In Vitro Model: Mycolicibacterium fortuitum strain FC1k; 1766
• In Vitro Model: Mycolicibacterium smegmatis strain mc2 155; 246196
• Experiment for Molecule Alteration: Southern blot hybridizations assay
• Experiment for Drug Resistance: Twofold dilution of antibiotics assay
• Mechanism Description: The aac(2')-Ib gene cloned in a mycobacterial plasmid and introduced in Mycobacterium smegmatis conferred resistance to gentamicin, tobramycin, dibekacin, netilmicin, and 6'-N-ethylnetilmicin.

Investigative Drug(s) 1 drug(s) in total

6'-N-Ethylnetilmicin

Drug Resistance Data Categorized by Their Corresponding Mechanisms

Drug Inactivation by Structure Modification (DISM)

Disease Class: Mycobacterium smegmatis infection [1]

• Resistant Disease: Mycobacterium smegmatis infection [ICD-11: 1B2Z.3]
• Resistant Drug: 6'-N-Ethylnetilmicin
• Molecule Alteration: Expression; Acquired
• Experimental Note: Identified from the Human Clinical Data
• In Vitro Model: Escherichia coli XL1-Blue; 562
• In Vitro Model: Streptomyces lividans strain 1326; 1200984
• In Vitro Model: Mycolicibacterium fortuitum strain FC1k; 1766
• In Vitro Model: Mycolicibacterium smegmatis strain mc2 155; 246196
• Experiment for Molecule Alteration: Southern blot hybridizations assay
• Experiment for Drug Resistance: Twofold dilution of antibiotics assay
• Mechanism Description: The aac(2')-Ib gene cloned in a mycobacterial plasmid and introduced in Mycobacterium smegmatis conferred resistance to gentamicin, tobramycin, dibekacin, netilmicin, and 6'-N-ethylnetilmicin.

References

• Ref 1: Characterization of the chromosomal aminoglycoside 2'-N-acetyltransferase gene from Mycobacterium fortuitum. Antimicrob Agents Chemother. 1996 Oct;40(10):2350-5. doi: 10.1128/AAC.40.10.2350.