Abstract
In 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.
Highlights
Accepted: August 20, 2018Published: August 31, 2018
To characterize the function of Enhancer of Zeste homolog 2 (Ezh2) during mouse neural crest cells (NCCs) development, the mutant mice homozygous for the two loxP sites flanking exon 15 through 18 in 129P2/OlaHsd background were backcrossed with the Wnt1-Cre line in the 129/B6 mixed background, generating the Ezh2 homozygous mice in NCC (Ezh2flox/flox;Wnt1-CreT/+; hereafter referred to as ‘Ezh2 null’ mice)
The results suggest a role for Ezh2 as an epigenetic modifier for the development of ENCC in regulating the repression of Pax3, Zic1, and Sox10 during the development of the ENCCs
Summary
Data Availability Statement: All relevant data are within the paper and its Supporting information files. Hox genes, which are critical for body segmentation and axial patterning [6, 7], affect the development of NCCs [8] Mutations in these genes can lead to neurocristopathies, which encompass a wide range of congenital diseases of neural crest cell origin. Function of Ezh in enteric neural crest cell development to be associated with the neurocristopathies, the penetrance for the mutant allele of these genes varies, suggesting a multigenic and potentially epigenetic involvement in manifestation of these disorders. In vitro culture of these BA1 cells demonstrated that differentiation factors such as GFAP and NF160 were properly expressed in Ezh conditional null cells [8] These mutant NCCs have not been examined in later stages of embryonic development in vivo. Our results suggest a unique epigenetic role of Ezh in enteric neural crest cell development
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