TWIST1 and chromatin regulatory proteins interact to guide neural crest cell differentiation.

Autor:	Fan X; Embryology Unit, Children's Medical Research Institute, The University of Sydney, Sydney, Australia.; The University of Sydney, School of Medical Sciences, Faculty of Medicine and Health, Sydney, Australia., Masamsetti VP; Embryology Unit, Children's Medical Research Institute, The University of Sydney, Sydney, Australia., Sun JQ; Embryology Unit, Children's Medical Research Institute, The University of Sydney, Sydney, Australia., Engholm-Keller K; Synapse Proteomics Group, Children's Medical Research Institute, The University of Sydney, Sydney, Australia., Osteil P; Embryology Unit, Children's Medical Research Institute, The University of Sydney, Sydney, Australia., Studdert J; Embryology Unit, Children's Medical Research Institute, The University of Sydney, Sydney, Australia., Graham ME; Synapse Proteomics Group, Children's Medical Research Institute, The University of Sydney, Sydney, Australia., Fossat N; Embryology Unit, Children's Medical Research Institute, The University of Sydney, Sydney, Australia.; The University of Sydney, School of Medical Sciences, Faculty of Medicine and Health, Sydney, Australia., Tam PP; Embryology Unit, Children's Medical Research Institute, The University of Sydney, Sydney, Australia.; The University of Sydney, School of Medical Sciences, Faculty of Medicine and Health, Sydney, Australia.
Jazyk:	angličtina
Zdroj:	ELife [Elife] 2021 Feb 08; Vol. 10. Date of Electronic Publication: 2021 Feb 08.
DOI:	10.7554/eLife.62873
Abstrakt:	Protein interaction is critical molecular regulatory activity underlining cellular functions and precise cell fate choices. Using TWIST1 BioID-proximity-labeling and network propagation analyses, we discovered and characterized a TWIST-chromatin regulatory module (TWIST1-CRM) in the neural crest cells (NCC). Combinatorial perturbation of core members of TWIST1-CRM: TWIST1, CHD7, CHD8, and WHSC1 in cell models and mouse embryos revealed that loss of the function of the regulatory module resulted in abnormal differentiation of NCCs and compromised craniofacial tissue patterning. Following NCC delamination, low level of TWIST1-CRM activity is instrumental to stabilize the early NCC signatures and migratory potential by repressing the neural stem cell programs. High level of TWIST1 module activity at later phases commits the cells to the ectomesenchyme. Our study further revealed the functional interdependency of TWIST1 and potential neurocristopathy factors in NCC development. Competing Interests: XF, VM, JS, KE, PO, JS, MG, NF, PT No competing interests declared (© 2021, Fan et al.)
Databáze:	MEDLINE
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