MabUL3168c, a Putative Acetyltransferase, Enhances Adherence, Intracellular Survival and Antimicrobial Resistance of Mycobacterium abscessus. e67563

• Published in: PloS one 2013-06, Vol.8 (6)
• Main Authors: Tsai, Sheng-Hui, Shen, Gwan-Han, Lin, Chao-Hsiung, Liau, Jiue-Ru, Lai, Hsin-Chih, Hu, Shiau-Ting
• Format: Article
• Language: English
• Subjects: Acetyltransferase; Mycobacterium
• ISSN: 1932-6203
• DOI: 10.1371/journal.pone.0067563

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 mabUL3168c 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 MabUL3168c protein is a member of the GCN5-related N-acetyltransferase superfamily. This prediction was supported by the demonstration that the mabUL3168c gene conferred M. abscessus and M. smegmatis cells resistance to amikacin. The multiple roles of mabUL3168c suggest that it could be a potential target for development of therapeutic regimens to treat diseases caused by M. abscessus.