Supercoiling is the process of twisting the DNA double helix into a tight coil, condensing it to a smaller volume and thus allowing large bacterial genomes to fit within small prokaryotic cells. The more tightly coiled a DNA domain is wound, the more transcription will be suppressed. However, there will still be stochastic transcripts, due to the nature of transcription.
There is some evidence to suggest that negative supercoiling can support in the unwinding (or melting) of promoter sequences. This can increase transcriptional activity of a given gene or operon, making it easier for RNA polymerase to bind.
Topoisomerases are a group of enzymes that induce supercoils into the DNA. This is done with the GyrB/GyrA complex of topoisomerase II (also called gyrase). GyrB forms a double strand (ds) break in the DNA, through which one strand is passed by GyrA. GyrB then re-ligates the ds break, and a negative supercoil has been formed in the DNA. Typically, negative supercoils are induced in the DNA. Topoisomerases I, III, and IV form positive supercoils, and are used to ‘unwind’ the DNA to make it more transcriptionally active.
Quinolone antibiotics, such as ciprofloxacin, stabilise the GyrB/GyrA complex, preventing the supercoiling of DNA and leading to the subsequent death of the cell.
Topoisomerases can undergo mutation that still allows them to form supercoils in the DNA, while preventing quinolone antibiotics from binding. This allows a bacterium to become resistant. Through horizontal gene transfer, this mutation can rapidly spread throughout the bacterial population.