Neural crest cells arise from the border of the neural plate and epidermal 
ectoderm, migrate extensively and differentiate into diverse cell types during 
vertebrate embryogenesis. Although much has been learnt about growth factor 
signals and gene regulatory networks that regulate neural crest development, 
limited information is available on how epigenetic mechanisms control this 
process. In this study, we show that Polycomb repressive complex 2 (PRC2) 
cooperates with the transcription factor Snail2/Slug to modulate neural crest 
development in Xenopus. The PRC2 core components Eed, Ezh2 and Suz12 are 
expressed in the neural crest cells and are required for neural crest marker 
expression. Knockdown of Ezh2, the catalytic subunit of PRC2 for histone H3K27 
methylation, results in defects in neural crest specification, migration and 
craniofacial cartilage formation. EZH2 interacts directly with Snail2, and 
Snail2 fails to expand the neural crest domains in the absence of Ezh2. 
Chromatin immunoprecipitation analysis shows that Snail2 regulates EZH2 
occupancy and histone H3K27 trimethylation levels at the promoter region of the 
Snail2 target E-cadherin. Our results indicate that Snail2 cooperates with EZH2 
and PRC2 to control expression of the genes important for neural crest 
specification and migration during neural crest development.