
Publications about nucleosomes. Maintained by @TeifLab. Also see @TF_binding_bot, @CTCF_papers, @cfDNA_papers, @generegulation. @nucleosome_bot@genomic.social
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ALT Figure 1. (A) Classical gel electrophoresis experiments showing mono-, di-, tri-, tetra-, and further multinucleosome bands upon chromatin digestion. (B) The nucleosome repeat length (NRL) is defined as the genomic distance between the centres of two neighbouring nucleosomes.

ALT Figure 2. Nucleosome mapping using MNase-seq versus ATAC-seq. (A) In MNase-seq, nucleosomes in both open and tightly packed genomic regions are accessible to digestion. MNase preferentially cleaves DNA between nucleosomes and digests DNA until it encounters a histone octamer, which provides a footprint of nucleosome-protected DNA regions. (B) Bulk MNase-seq results in averaged maps across millions of cells, effectively capturing all possible nucleosome positioning configurations. (C) Single-cell MNase-seq (scMNase-seq) results in a noisier and sparser signal. The resulting footprints still represent nucleosome-protected regions, but not all nucleosomes are represented. (D) In ATAC-seq, open regions can be accessed by the enzyme Tn5 transposase, which can insert primers in regions free from the binding of nucleosomes and transcription factors (TFs). (E) For open chromatin regions, nucleosome maps can be obtained from ATAC-seq similar to MNase-seq. (F) Closed, tightly packed chromatin...

ALT Figure 5. Molecular mechanisms affecting nucleosome spacing. (A) Linker histones H1 and nonhistone chromatin proteins which compete with H1s and modulate nucleosome spacing through structural and electrostatic mechanisms. (B) Chromatin remodellers actively reposition nucleosomes following context-dependent rules. (C) Cell state-dependent chromatin boundaries formed by CTCF and other structural proteins, as well as associated recruitment of chromatin remodellers which space nucleosomes. (D) Gene activity associated with remodeller action and RNA polymerases transcribing through the nucleosomes, leading to smaller distances between nucleosomes in regulatory regions and gene bodies. (E) DNA sequence repeats of different types.
![Figure 6. Examples of NRL changes in biological systems. (A) Cell differentiation leads to NRL changes between different cell types, e.g. mouse dorsal root ganglia neurons (NRL ∼165 bp) versus cortical astrocytes (NRL ∼183 bp) [175]. Schematic cell shapes are adapted from an image created in BioRender (https://BioRender.com/89trj2t). (B) Paired normal versus tumour breast tissues show NRL shortening in cancer (figure adapted from [36] under the CC BY 4.0 licence (https://creativecommons.org/licenses/by/4.0/)). (C) Nucleosome positioning derived from cfDNA of human volunteers shows NRL increase with age (figure reprinted from [79] under the CC BY 4.0 licence (https://creativecommons.org/licenses/by/4.0/)).](https://pbs.twimg.com/media/HCuDTNuWAAEOTC5.png?name=small&format=webp)
ALT Figure 6. Examples of NRL changes in biological systems. (A) Cell differentiation leads to NRL changes between different cell types, e.g. mouse dorsal root ganglia neurons (NRL ∼165 bp) versus cortical astrocytes (NRL ∼183 bp) [175]. Schematic cell shapes are adapted from an image created in BioRender (https://BioRender.com/89trj2t). (B) Paired normal versus tumour breast tissues show NRL shortening in cancer (figure adapted from [36] under the CC BY 4.0 licence (https://creativecommons.org/licenses/by/4.0/)). (C) Nucleosome positioning derived from cfDNA of human volunteers shows NRL increase with age (figure reprinted from [79] under the CC BY 4.0 licence (https://creativecommons.org/licenses/by/4.0/)).

ALT Figure 5 from Jacob et al, 2024. NRL shortening as a novel breast cancer marker. A–E) NRL values calculated for each individual sample from this study inside different types of genomic regions. A) Transcriptionally active A-compartments of chromatin annotated in breast cancer MCF-7 cells; B) Regions surrounding gene promoters. C Genomic regions around Alu repeats; D) Regions enriched with H1X linker histones in breast cancer T47D cells; E) Differentially methylated DNA regions annotated based on cell lines MCF-10A, MCF-7 and MDA-MB-231. Open squares—average NRL values for a given condition; horizontal lines—median values. The colours of the points are assigned per sample as in Fig. 3A. F) A scheme of the change of nucleosome compaction in breast cancer tissues. DNA (black) is wrapped around histone octamers (grey) in contact with linker histones (blue). MNase used in this study or apoptotic nucleases present in situ (orange) cut DNA not protected by nucleosomes and linker histones.

ALT Chromatin organization is essential for DNA packaging and gene regulation in eukaryotic genomes. While significant progresses have been made, the exact atomistic arrangement of nucleosomes remains controversial. Using a well-calibrated residue-level coarse-grained model and advanced dynamics modeling techniques, particularly the non-Markovian dynamics model, we map the free energy landscape of tetra-nucleosome systems, identify both metastable conformations and intermediate states in folding pathways, and quantify the folding kinetics. Our findings show that chromatin with 10n base pairs (bp) DNA linker lengths favor zigzag fibril structures. However, longer linker lengths destabilize this conformation. When the linker length is 10n+5 bp, chromatin loses unique conformations, favoring a dynamic ensemble of structures resembling folding intermediates. Embedding the tetra-nucleosome in a nucleosome condensate similarly shifts stability towards folding intermediates...

ALT Chromatin plays a pivotal role in genome expression, maintenance, and replication. To better understand chromatin organization, we developed a novel proximity-tagging method which assigns unique DNA barcodes to molecules that associate in 3D space. Using this method – Proximity Copy Paste (PCP) – we mapped the connectivity of individual nucleosomes in Saccharomyces cerevisiae. We show that chromatin is predominantly organized into regularly spaced nucleosome arrays whose properties differ according to transcriptional activity. Additionally, by mapping long-range, multi-way interactions we provide evidence that metaphase chromosomes are compacted by arrayed cohesin hubs. Using single-molecule nuclease footprinting data we define distinct chromatin states within a mixed population to show that noncanonical nucleosomes are a stable feature of chromatin. PCP is a versatile method allowing the connectivity of individual molecules to be mapped at high-resolution.

ALT a. Mean trajectories of Pol II transcription through a nucleosome. All traces were aligned when Pol II reached the entry of the 1st nucleosome encountered (t = 0), with the shaded regions representing 30% of the standard deviation. The left panel shows data from the singlenucleosome template (left; N = 86 for -TFIIS, N = 215 for +TFIIS). The right panel shows data from the first nucleosome on the chromatin template (right; N = 99 for -TFIIS; N = 302 for +TFIIS). b. Pol II nucleosome-passage rate. The mean passage rates under torsion were obtained from data shown in a, with the torque value being the torque experienced by Pol II when encountering the nucleosome dyad. The mean passage rates under zero-torsion of the single-nucleosome template were obtained from data shown in Supplementary Fig. 8. The error bars represent the SEMs.















