Fig. 6: Model for how transcription-driven positive DNA supercoiling may cause the disassembly of H-NS:DNA complexes.

The model posits that H-NS:DNA complexes exist in vivo in the form of H-NS-bound negatively supercoiled DNA. The H-NS filament follows the path of the righthanded plectoneme bridging sequences from its two arms. During transcription of a neighboring gene, frictional resistance to the rotation of the transcription complex around the DNA axis forces the DNA axis to rotate on itself, thereby generating positive supercoils. This effect is amplified by the association of the leading ribosome with the elongation complex and even more so by the co-transcriptional anchoring of a nascent polypeptide to the cell membrane (see text). If not relaxed by DNA gyrase, positive supercoils diffuse along the DNA and merge with the H-NS-bound negatively supercoiled plectoneme. Rotation of the DNA axis causes the plectoneme to unroll. Unrolling breaks the H-NS bridges resulting in the release of H-NS dimers.