Decreased of Oct4 gene expression levels correlate with a drop in competence to maintain pluripotency transcriptional regulatory networks. This downregulation is associated with chromatin accessibility changes at pluripotency genes regulatory elements, contributing to pluripotency exit. However, I proved that cranial neural crest cells naturally reactivate pluripotency programs to expand their differentiation potential.
The molecular mechanisms regulating pluripotency programs dynamic expression in cranial neural crest cells are still unknown.
Using in vivo and in vitro models to label and isolate cells repressing or reactivating pluripotency programs, we are using single-cell transcriptomics and chromatin accessibility assays to uncover the molecular mechanisms controlling cranial neural crest cells pluripotency programs activation and repressions and explore how this return into a precise pluripotency state is regulated.