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We recently identified two aminoglycoside-acetylating genes [\n            <jats:italic>aac(2\u2032)<\/jats:italic>\n            and\n            <jats:italic>eis2<\/jats:italic>\n            ] which, however, do not affect susceptibility to streptomycin. This suggests the existence of a discrete mechanism of streptomycin resistance.\n            <jats:named-content content-type=\"genus-species\">M. abscessus<\/jats:named-content>\n            BLASTP analysis identified MAB_2385 as a close homologue of the 3\u2033-\n            <jats:italic>O<\/jats:italic>\n            -phosphotransferase [APH(3\u2033)] from the opportunistic pathogen\n            <jats:named-content content-type=\"genus-species\">Mycobacterium fortuitum<\/jats:named-content>\n            as a putative streptomycin resistance determinant. Heterologous expression of\n            <jats:italic>MAB_2385<\/jats:italic>\n            in\n            <jats:named-content content-type=\"genus-species\">Mycobacterium smegmatis<\/jats:named-content>\n            increased the streptomycin MIC, while the gene deletion mutant\n            <jats:named-content content-type=\"genus-species\">M. abscessus<\/jats:named-content>\n            \u0394MAB_2385 showed increased streptomycin susceptibility. The MICs of other aminoglycosides were not altered in\n            <jats:named-content content-type=\"genus-species\">M. abscessus<\/jats:named-content>\n            \u0394MAB_2385. This demonstrates that\n            <jats:italic>MAB_2385<\/jats:italic>\n            encodes a specific and prime innate streptomycin resistance determinant in\n            <jats:named-content content-type=\"genus-species\">M. abscessus<\/jats:named-content>\n            . We further explored the feasibility of applying\n            <jats:italic>rpsL<\/jats:italic>\n            -based streptomycin counterselection to generate gene deletion mutants in\n            <jats:named-content content-type=\"genus-species\">M. abscessus<\/jats:named-content>\n            . Spontaneous streptomycin-resistant mutants of\n            <jats:named-content content-type=\"genus-species\">M. abscessus<\/jats:named-content>\n            \u0394MAB_2385 were selected, and we demonstrated that the wild-type\n            <jats:italic>rpsL<\/jats:italic>\n            is dominant over the mutated\n            <jats:italic>\n              rpsL\n              <jats:sup>K43R<\/jats:sup>\n            <\/jats:italic>\n            in merodiploid strains. In a proof of concept study, we exploited this phenotype for construction of a targeted deletion mutant, thereby establishing an\n            <jats:italic>rpsL<\/jats:italic>\n            -based counterselection method in\n            <jats:named-content content-type=\"genus-species\">M. abscessus<\/jats:named-content>\n            .\n          <\/jats:p>","DOI":"10.1128\/aac.01427-17","type":"journal-article","created":{"date-parts":[[2017,10,24]],"date-time":"2017-10-24T00:40:25Z","timestamp":1508805625000},"update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":36,"title":["Molecular Mechanisms of Intrinsic Streptomycin Resistance in Mycobacterium abscessus"],"prefix":"10.1128","volume":"62","author":[{"given":"Michael","family":"Dal Molin","sequence":"first","affiliation":[{"name":"Institut f\u00fcr Medizinische Mikrobiologie, Universit\u00e4t Z\u00fcrich, Z\u00fcrich, 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