Neural crest cell-specific inactivation ofNipblorMau2during mouse development results in a late onset of craniofacial defects

genesis ◽  
2014 ◽  
Vol 52 (7) ◽  
pp. 687-694 ◽  
Author(s):  
Terence Gordon Smith ◽  
Steve Laval ◽  
Fangli Chen ◽  
Matthew James Rock ◽  
Tom Strachan ◽  
...  
PLoS Genetics ◽  
2010 ◽  
Vol 6 (3) ◽  
pp. e1000878 ◽  
Author(s):  
Satoshi Kurosaka ◽  
N. Adrian Leu ◽  
Fangliang Zhang ◽  
Ralph Bunte ◽  
Sougata Saha ◽  
...  

2010 ◽  
Vol 344 (1) ◽  
pp. 467
Author(s):  
Samantha Brugmann ◽  
Nancy C. Allen ◽  
Aaron W. James ◽  
Zesemayat Mekonnen ◽  
Elena Madan ◽  
...  

2018 ◽  
Author(s):  
Hana Kim ◽  
Ingeborg M. Langohr ◽  
Mohammad Faisal ◽  
Margaret McNulty ◽  
Caitlin Thorn ◽  
...  

AbstractIn the current study, we examined the role of Ezh2 as an epigenetic modifier for the enteric neural crest cell development through H3K27me3. Ezh2 conditional null mice were viable up to birth, but died within the first hour of life. In addition to craniofacial defects, Ezh2 conditional null mice displayed reduced number of ganglion cells in the enteric nervous system. RT-PCR and ChIP assays indicated aberrant up-regulation of Zic1, Pax3, and Sox10 and loss of H3K27me3 marks in the promoter regions of these genes in the myenteric plexus. Overall, these results suggest that Ezh2 is an important epigenetic modifier for the enteric neural crest cell development through repression of Zic1, Pax3, and Sox10.


2011 ◽  
Vol 356 (1) ◽  
pp. 197
Author(s):  
Dennis A. Ridenour ◽  
Rebecca McLennan ◽  
Jessica M. Teddy ◽  
Katherine W. Prather ◽  
Craig L. Semerad ◽  
...  

1981 ◽  
Vol 82 (1) ◽  
pp. 86-94 ◽  
Author(s):  
Jeanne Loring ◽  
Bengt Glimelius ◽  
Carol Erickson ◽  
James A. Weston

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