TY - JOUR
AU - Gicquel, Brigitte
AB - BACTERIAL resistance to antibiotics is often plasmid-mediated and the associated resistance genes encoded by transposable elements. Mycobacteria, including the human pathogens Mycobacterium tuberculosis and M. leprae, are resistant to many antibiotics, and their cell-surface structure is believed to be largely responsible for the wide range of resistance phenotypes. Antibiotic-resistance plasmids have so far not been implicated in resistance of mycobacteria to antibiotics. Nevertheless, antibiotic-modifying activities such as aminoglycoside acetyltransferases1 and phosphotransferases1 have been detected in fast-growing species2,3. β-lactamases have also been found in most fast- and slow-growing mycobacteria. To date no mycobacterial antibiotic-resistance genes have been isolated and characterized. We now report the isolation, cloning and sequencing of a genetic region responsible for resistance to sulphonamides in M. fortuitum. This region also contains an open reading frame homologous to one present in Tn1696
4 (member of the Tn21 family) which encodes a site-specific integrase5,6. The mycobacterial resistance element is flanked by repeated sequences of 880 base pairs similar to the insertion elements of the IS6 family found in Gram+ and Gram- bacteria. The insertion element is shown to transpose to different sites in the chromosome of a related fast-growing species, M. smegmatis. The characterization of this element should permit transposon mutagenesis in the analysis of mycobacterial virulence and related problems.
TI - Transposition of an antibiotic resistance element in mycobacteria
JF - Nature
DO - 10.1038/345739a0
DA - 1990-06-21
UR - https://www.deepdyve.com/lp/springer-journals/transposition-of-an-antibiotic-resistance-element-in-mycobacteria-Kw66c6E7h0
SP - 739
EP - 743
VL - 345
IS - 6277
DP - DeepDyve
ER -