title: Mab_3168c, a putative acetyltransferase, enhances adherence, intracellular survival and antimicrobial resistance of Mycobacterium abscessus.
abstract: Mycobacterium abscessus is a non-tuberculous mycobacterium. It can cause diseases in both immunosuppressed and immunocompetent patients and is highly resistant to multiple antimicrobial agents. M. abscessus displays two different colony morphology types: smooth and rough morphotypes. Cells with a rough morphotype are more virulent. The purpose of this study was to identify genes responsible for M. abscessus morphotype switching. With transposon mutagenesis, a mutant with a Tn5 inserted into the promoter region of the mab_3168c gene was found to switch its colonies from a rough to a smooth morphotype. This mutant had a higher sliding motility but a lower ability to form biofilms, aggregate in culture, and survive inside macrophages. Results of bioinformatic analyses suggest that the putative Mab_3168c protein is a member of the GCN5-related N-acetyltransferase superfamily. This prediction was supported by the demonstration that the mab_3168c gene conferred M. abscessus and M. smegmatis cells resistance to amikacin. The multiple roles of mab_3168c suggest that it could be a potential target for development of therapeutic regimens to treat diseases caused by M. abscessus.
authors.affiliation: Institute of Microbiology and Immunology, School of Life Science, National Yang-Ming University, Taipei, Taiwan, ROC.
authors.forename: Sheng-Hui
authors.initials: SH
authors.lastname: Tsai
authors.forename: Gwan-Han
authors.initials: GH
authors.lastname: Shen
authors.forename: Chao-Hsiung
authors.initials: CH
authors.lastname: Lin
authors.forename: Jiue-Ru
authors.initials: JR
authors.lastname: Liau
authors.forename: Hsin-Chih
authors.initials: HC
authors.lastname: Lai
authors.forename: Shiau-Ting
authors.initials: ST
authors.lastname: Hu
mesh_terms: D000123:Acetyltransferases / Q000235:genetics* / Q000378:metabolism*; D000583:Amikacin / Q000494:pharmacology; D000890:Anti-Infective Agents / Q000494:pharmacology; D018441:Biofilms / Q000254:growth & development; D019295:Computational Biology / Q000379:methods; D004352:Drug Resistance, Microbial / Q000235:genetics*; D057927:Hydrophobic and Hydrophilic Interactions / Q000187:drug effects; D008264:Macrophages / Q000378:metabolism; D009113:Muramidase / Q000187:drug effects / Q000235:genetics / Q000378:metabolism; D009154:Mutation / Q000235:genetics; D009161:Mycobacterium / Q000187:drug effects / Q000201:enzymology* / Q000235:genetics / Q000378:metabolism; D009165:Mycobacterium Infections, Nontuberculous / Q000188:drug therapy / Q000201:enzymology* / Q000235:genetics / Q000378:metabolism; D009170:Nontuberculous Mycobacteria / Q000187:drug effects / Q000201:enzymology* / Q000235:genetics / Q000378:metabolism; D011401:Promoter Regions, Genetic / Q000235:genetics
chemical_list: D000890:Anti-Infective Agents; D000583:Amikacin; D000123:Acetyltransferases; D009113:Muramidase