TL;DR
An optimized low-input Cleavage Under Targets and Release Using Nuclease (CUT&RUN) workflow tailored for fluorescence-activated cell sorting (FACS) isolated NCCs from zebrafish embryos is presented and can also offer insights into epigenetic dysregulation associated with disease.
Increasing global chromatin accessibility alone was insufficient to enhance global transcription and could even reduce it, and the transcriptional response depended on the mechanism of chromatin perturbation.
These findings reveal a previously unrecognized role for PRCs in establishing TAD-scale repressive chromatin domains during neuronal maturation, thereby safeguarding neuronal identity from external stimuli through broad silencing of alternative cell fate programs.
Ch chromatin polyvalency model is established as a multi-layered, hierarchical repression mechanism that governs temporal control of gene expression during embryogenesis and disrupts temporal control of polyvalent gene activation.
This protocol outlines how to map dynamic changes in enhancer and SE usage during human trophoblast differentiation using human trophoblast stem cells and their subsequent differentiation into more specialized cell types.
It is shown that loss of default neural differentiation capacity and failure to form brain organoids are linked to erosion of bivalent chromatin marks at developmental gene loci, independent of DNA methylation, driving acquisition of a posterior epiblast-like state and premature developmental gene expression.
This approach uncovers epigenomic priming of basal cells in the mammary gland and captures the dynamics of basal-to-luminal transdifferentiation, suggesting that epigenomic and transcriptional remodeling do not occur in complete synchrony during cell-fate conversion.
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