Activity of a plasmid-borne leu-500 promoter depends on the transcription and translation of an adjacent gene.
leu-500 is a chromosomal promoter mutation in Salmonella typhimurium that normally causes the promoter to be inactive in the initiation of RNA synthesis. But in a strain that has mutations in topA, the gene encoding DNA topoisomerase I, the mutant promoter becomes active. We show that the leu-500 promoter can function on a plasmid when it is adjacent to the tetracycline-resistance gene tetA. Activation of the leu-500 promoter requires that the tetA gene is transcribed and translated and that the host cell is topA. We propose that the A----G mutation in the -10 region of the leu-500 promoter is compensated by local negative supercoiling arising from transcription of the tetA gene, which may reach elevated levels in a topA background, provided that diffusional dissipation is reduced due to anchoring of the TetA peptide in the membrane. This is a clear example of the modulation of the activity of a promoter by the activity of another promoter in cis, when they can be coupled through the topology of the template.[1]References
- Activity of a plasmid-borne leu-500 promoter depends on the transcription and translation of an adjacent gene. Chen, D., Bowater, R., Dorman, C.J., Lilley, D.M. Proc. Natl. Acad. Sci. U.S.A. (1992) [Pubmed]
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