Modulation of histone levels in gut enterocytes by rapamycin treatment alters chromatin organisation and induces intestinal autophagy through transcriptional regulation to prevent age-related decline in the intestine and extend lifespan.

Computer simulations considering actions of the intranuclear enzyme, Topoisomerase-II, in a mechanistic scheme elucidated a capability of enzymes to contribute to controlling chromatin spatial organizations and discovered new characteristic features in eu- and heterochromatin organization caused by the enzymatic activity.

Terminal selectors reorganize postmitotic neuronal chromatin to select cis-regulatory elements during 5-HT neuron maturation.

Computer simulations show transitions between novel types of chromatin organization (peripheral, central, conventional) depending on chromatin interactions with itself, the lamin and nuclear hydration, measured in recent experiments.

Structural models of the chromatin remodeling enzyme Chd1 in solution and when bound to chromatin indicate that conformational changes to both the enzyme and the nucleosome occur upon nucleotide dependent engagement.

The physicochemical interactions among wild-type nucleosomes hold substantial significance and play a role in chromatin folding under physiological salt concentrations.

Seemingly contradictory findings of single-molecule and in vivo experiments on a major mechanism of chromosome organization are reconciled by computationally investigating mechanisms of loop extrusion that are consistent with both.

The PBAF chromatin-remodelling complex is essential for the proliferation of melanocytes and melanoma cells and is recruited to critical regulatory elements by physical and functional interactions with MITF, a transcription factor and master regulator of melanoma.

The physical distance between genes in individual cells is the major factor driving co-transcriptional bursts, showing a significant degree of correlation for distances below 400 nm.

Single-molecule imaging of CTCF and cohesin in live cells suggests that chromatin loops are dynamic structures that frequently form and fall apart.