Molecular mechanism for the enhancement of arbekacin resistance in a methicillin-resistant Staphylococcus aureus.
We have clinically isolated a methicillin-resistant Staphylococcus aureus (MRSA) K-1 which exhibits enhanced arbekacin (Abk) resistance. In this study, we investigated a molecular mechanism for the overproduction of a bifunctional enzyme catalyzing both 2"-O-phosphorylation and 6'-N-acetylation of aminoglycoside antibiotics that is encoded by aacA-aphD and designated [AAC(6')/APH(2")] and is expressed in MRSA K-1. The sequence analysis of the 5'-adjacent region of the aacA-aphD structural gene in MRSA K-1 showed that 12 bp are deleted from the aacA-aphD promoter region when compared with that in MRSA B-26, which exhibits lower resistance to Abk than K-1. By artificially deleting the 12 bp from the corresponding region in MRSA B-26, we confirmed that the strain increases Abk resistance to the same level as seen in MRSA K-1, which suggests that the 12 bp deletion from the 5'-adjacent region of the aacA-aphD structural gene created a strong promoter to overexpress the bifunctional enzyme.[1]References
- Molecular mechanism for the enhancement of arbekacin resistance in a methicillin-resistant Staphylococcus aureus. Matsuo, H., Kobayashi, M., Kumagai, T., Kuwabara, M., Sugiyama, M. FEBS Lett. (2003) [Pubmed]
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