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Dissection of Xenopus laevis Neural Crest for in vitro Explant Culture or in vivo Transplantation
Published on: March 4, 2014
A PHD12-Snail2 repressive complex epigenetically mediates neural crest epithelial-to-mesenchymal transition
Pablo H Strobl-Mazzulla1, Marianne E Bronner
1Biología del Desarrollo, Instituto de Investigaciones Biotecnológicas-Instituto Tecnológico de Chascomús, Consejo Nacional de Investigaciones Científicas y Técnicas-Universidad Nacional de San Martín, 7130 Chascomús, Argentina.
The Journal of Cell Biology
|September 19, 2012
Summary
The adaptor protein PHD12 is crucial for neural crest cell migration by interacting with Snail2 and HDAC to repress Cadherin6b transcription during epithelial to mesenchymal transition (EMT). This reveals a novel mechanism regulating neural crest development.
Area of Science:
- Developmental Biology
- Cell Biology
- Molecular Biology
Background:
- Neural crest cells undergo epithelial to mesenchymal transition (EMT) for migration.
- Snail2 is a transcriptional repressor involved in neural crest EMT through an unknown mechanism.
Purpose of the Study:
- To elucidate the mechanism by which Snail2 regulates neural crest EMT.
- To identify novel proteins involved in neural crest emigration and Cadherin6b regulation.
Main Methods:
- Knockdown experiments (PHD12, Snail2)
- In vivo protein interaction studies
- Chromatin immunoprecipitation (ChIP)
- Histone acetylation analysis
Main Results:
- PHD12 is highly expressed before neural crest EMT and its loss mimics Snail2 knockdown.
- PHD12 and Snail2 interact with Sin3A/HDAC complex at the Cad6b promoter.
- PHD12 recruitment to the Cad6b promoter leads to histone deacetylation and transcriptional repression.
Conclusions:
- PHD12 is a key regulator of neural crest EMT, working in concert with Snail2.
- A novel Snail2-PHD12-Sin3A-HDAC complex is formed at the Cad6b promoter to control neural crest emigration.
- This study reveals the molecular mechanism of Snail2-mediated repression during neural crest development.
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