Repression of cointegration ability of insertion element IS1 by transcriptional readthrough from flanking regions.
We describe a repression mechanism in which read-through messages transcribed from a gene into an IS1 sequence inhibit its ability to mediate plasmid cointegration. This mechanism was derived from the demonstration that removal of the promoter region of the chloramphenicol resistance gene in transposon Tn9, or introduction of a strong transcription terminator of phage T7 downstream of the chloramphenicol resistance gene, increases the cointegration ability of the downstream IS1 sequence when in a particular orientation. The cointegration ability of an IS1 sequence downstream of the chloramphenicol resistance gene but in an orientation opposite that of the above-mentioned IS1 sequence also can be repressed. Analysis of transcripts synthesized in vitro showed that the transcripts of the chloramphenicol resistance gene were read through into the IS1 sequence located downstream of the gene in either orientation. Repression of this type may be one mechanism that controls the rate of transposition of the IS1 element, which apparently does not encode a structural gene for repressor.
D002701:Chloramphenicol / Q000494:pharmacology; D004251:DNA Transposable Elements; D004352:Drug Resistance, Microbial; D005798:Genes, Bacterial; D009154:Mutation; D010957:Plasmids; D011995:Recombination, Genetic; D014158:Transcription, Genetic
D004251:DNA Transposable Elements; D002701:Chloramphenicol