|  Help  |  About  |  Contact Us

Publication : Repressor element 1 silencing transcription factor couples loss of pluripotency with neural induction and neural differentiation.

First Author  Soldati C Year  2012
Journal  Stem Cells Volume  30
Issue  3 Pages  425-34
PubMed ID  22162260 Mgi Jnum  J:190511
Mgi Id  MGI:5448940 Doi  10.1002/stem.1004
Citation  Soldati C, et al. (2012) Repressor element 1 silencing transcription factor couples loss of pluripotency with neural induction and neural differentiation. Stem Cells 30(3):425-34
abstractText  Neural differentiation of embryonic stem cells (ESCs) requires coordinated repression of the pluripotency regulatory program and reciprocal activation of the neurogenic regulatory program. Upon neural induction, ESCs rapidly repress expression of pluripotency genes followed by staged activation of neural progenitor and differentiated neuronal and glial genes. The transcriptional factors that underlie maintenance of pluripotency are partially characterized whereas those underlying neural induction are much less explored, and the factors that coordinate these two developmental programs are completely unknown. One transcription factor, REST (repressor element 1 silencing transcription factor), has been linked with terminal differentiation of neural progenitors and more recently, and controversially, with control of pluripotency. Here, we show that in the absence of REST, coordination of pluripotency and neural induction is lost and there is a resultant delay in repression of pluripotency genes and a precocious activation of both neural progenitor and differentiated neuronal and glial genes. Furthermore, we show that REST is not required for production of radial glia-like progenitors but is required for their subsequent maintenance and differentiation into neurons, oligodendrocytes, and astrocytes. We propose that REST acts as a regulatory hub that coordinates timely repression of pluripotency with neural induction and neural differentiation.
Quick Links:
 
Quick Links:
 

Expression

Publication --> Expression annotations

 

Other

3 Bio Entities

0 Expression