2004/06/16 by Farshid Mohammad-Rafiee, Mohammad-Rafiee, Farshid, Igor M. Kulić +5
Biochemistry, Genetics and Molecular Biology · #Biomolecules (q-bio.BM) #DNA and Nucleic Acid Chemistry #FOS: Biological sciences #Genomics and Chromatin Dynamics #RNA Interference and Gene Delivery #Subcellular Processes (q-bio.SC) #q-bio.BM #q-bio.SC
paper · pdf · doi:10.48550/arxiv.q-bio/0406037
23 pages, 4 figures, submitted to J. Mol. Biol
arxiv created 2004/06/16 · openalex publication_date 2004/06/16 · arxiv updated 2009/12/01 · openalex created_date 2025/10/10 · openalex updated_date 2026/07/28
Histone octamers show a heat-induced mobility along DNA. Recent theoretical studies have established two mechanisms that are qualitatively and quantitatively compatible with in vitro experiments on nucleosome sliding: Octamer repositiong through one-basepair twist defects and through ten-basepair bulge defects. A recent experiment demonstrated that the repositioning is strongly suppressed in the presence of minor-groove binding DNA ligands. In the present study we give a quantitative theory for nucleosome repositioning in the presence of such ligands. We show that the experimentally observed octamer mobilities are consistent with the picture of bound ligands blocking the passage of twist defects through the nucleosome. This strongly supports the model of twist defects inducing a corkscrew motion of the nucleosome as the underlying mechanism of nucleosome sliding. We provide a theoretical estimate of the nucleosomal mobility without adjustable parameters, as a function of ligand concentration, binding affinity, binding site orientiation, temperature and DNA anisotropy. Having this mobility at hand we speculate about the interaction between a nucleosome and a transcribing RNA polymerase and suggest a novel mechanism that might account for polymerase induced nucleosome repositioning.