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Mab_3168c, a Putative Acetyltransferase, Enhances Adherence, Intracellular Survival and Antimicrobial Resistance of Mycobacterium abscessus
Author(s) -
Sheng-Hui Tsai,
Gwan-Han Shen,
Chao-Hsiung Lin,
Jiue-Ru Liau,
HsinChih Lai,
Shiau-Ting Hu
Publication year - 2013
Publication title -
plos one
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.99
H-Index - 332
ISSN - 1932-6203
DOI - 10.1371/journal.pone.0067563
Subject(s) - mycobacterium abscessus , biology , virulence , mycobacterium smegmatis , microbiology and biotechnology , mutant , transposon mutagenesis , monoclonal antibody , mycobacterium , amikacin , gene , antimicrobial , transposable element , genetics , antibody , bacteria , mycobacterium tuberculosis , medicine , tuberculosis , pathology
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 Tn 5 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 .

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