Molecular Biology

Mapping Supercoils

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Science  08 Mar 2013:
Vol. 339, Issue 6124, pp. 1127
DOI: 10.1126/science.339.6124.1127-c

During transcription, the two strands of double-helical DNA must be locally separated, so that the RNA polymerase can transcribe the DNA, and then the helix must be resealed again. Opening the two strands and then moving this opening along the DNA as the template DNA strand is fed through the polymerase causes the helix ahead of the opening to be overwound (positively supercoiled) and the helix behind the opening to be under-wound (negatively supercoiled). Either state has the potential to generate a topological impediment to transcription. Kouzine et al. developed a method using the DNA crosslinking agent psoralen to map transcription-dependent supercoiling across the genome of human tissue culture cells. They find that, on average, negative supercoiling is prominent up to 1.5 kb upstream of the transcription start sites (TSSs) of moderately or strongly activated genes. Dynamic supercoiling was not associated with enhancers, regardless of the distance from their associated promoters. Topoisomerase I and II, enzymes that can dissipate supercoils, were found to act redundantly at moderately active genes, whereas topoisomerase II acted preferentially at the TSS of highly active genes. The results suggest that dynamic supercoiling is caused by frictional restriction of DNA twist diffusion and that it does not seem to be confined by fixed boundaries in chromatin.

Nat. Struct. Mol. Biol. 20, 10.1038/nsmb.2517 (2013).

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