Deletions of Tn916-like transposons are implicated in tetM-mediated resistance in pathogenic Neisseria
- PMID: 7934821
- DOI: 10.1111/j.1365-2958.1993.tb01956.x
Deletions of Tn916-like transposons are implicated in tetM-mediated resistance in pathogenic Neisseria
Abstract
Using the tetM-containing conjugative transposon Tn916 as a mutagenesis tool, we identified two distinct classes of transposon insertions in the meningococcal chromosome. Class I insertions have an intact copy of Tn916 that appears to have transposed by a novel recombinational mechanism, similar to the transposition of conjugative transposons in Gram-positive bacteria. Class II insertions were characterized by deletions of Tn916 but preservation of the tetM determinant. In addition, we identified Class II Tn916-like insertions in the naturally occurring 25.2 MDa tetM-containing plasmids of both Neisseria meningitidis and Neisseria gonorrhoeae. The turncated Tn916-like insertions appeared to be present in the same site in these two plasmids; however, the deletions of the transposon were different. Plasmid sequence adjacent to the truncated transposon in the 25.2 MDa plasmids was found in a tetracycline-sensitive N. gonorrhoeae 24.5 MDa conjugative plasmid. These data suggest that the 25.2 MDa plasmids are the result of one or a series of Class II Tn916-like insertions into 24.5 MDa conjugative plasmids. Class II insertions of Tn916-like transposons are implicated in the dissemination of tetM resistance in pathogenic Neisseria.
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