The structure of the chromatin remodeller CHD4 bound to a nucleosome reveals differences to the known Chd1-nucleosome complex and maps cancer mutations.

In fusion-positive rhabdomyosarcoma, CHD4 positively regulates super-enhancer-mediated gene expression by allowing a chromatin architecture at these cis-regulatory regions, which is permissive to the binding of the transcription factor PAX3-FOXO1.

The unwrapping two turns of DNA on Chd1-bound nucleosomes cause the histone H3 tail and ubiquitin to be re-positioned.

Neural crest cells differentiated from patient-derived cells with mutations in the chromatin remodeler CHD7 show defective delamination, migration and motility in vitro, and defective migration in chick embryos.

Inositol polyphosphate multikinase physically binds to the core subunits of SWI/SNF complex and plays an important role in regulating BRG1 occupancy and BRG-mediated chromatin accessibility in mouse embryonic stem cells.

Network propagation connects TWIST1 with epigenetic regulators CHD7, CHD8, and WHSC1, which collectively promote the bias toward neural crest while suppressing neural stem cell programmes, and subsequently enhance ectomesenchyme potential.

The ATP-dependent chromatin remodeler Chd1 controls nucleosome turnover to allow RNA Polymerase to transcribe in vivo.

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.

Single-cell screens during human cardiomyocyte (CM) differentiation reveal that perturbation of congenital heart defect-linked enhancers/genes causes deficient CM differentiation.

Combined evidence of human genetics, in vitro cardiomyocyte differentiation, and mouse model indicates that SORBS2 is a regulator of second heart field development and its deficiency causes seemingly opposite atrial septal defects.