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Related Experiment Video

Updated: Jun 19, 2026

Streamlined 3D Cerebellar Differentiation Protocol with Optional 2D Modification

Streamlined 3D Cerebellar Differentiation Protocol with Optional 2D Modification

Published on: December 9, 2017

An EED/PRC2-H19 Loop Regulates Cerebellar Development.

Pei-Pei Liu^1,2,3, Xiao Han^2,4,5, Xiao Li^1,2,3

¹Key Laboratory of Organ Regeneration and Reconstruction, State Key Laboratory of Stem Cell and Reproductive Biology, Institute of Zoology, Chinese Academy of Sciences, Beijing, 100101, China.

Advanced Science (Weinheim, Baden-Wurttemberg, Germany)

|November 5, 2024

Summary

Embryonic ectoderm development (EED) protein is crucial for cerebellar development. Its absence causes motor deficits by overactivating the H19 gene, revealing a critical EED-H19 feedback loop.

Keywords:

EED, H19, Motor movement, PRC2 cerebellum

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Published on: September 16, 2022

Area of Science:

Neuroscience
Developmental Biology
Epigenetics

Background:

The embryonic ectoderm development (EED) protein is a key component of polycomb repressive complex 2 (PRC2), involved in epigenetic regulation.
The specific role of EED in cerebellar development has not been previously elucidated.

Purpose of the Study:

To investigate the function of EED in cerebellar development.
To understand the molecular mechanisms underlying EED's role in the cerebellum.

Main Methods:

Utilized EED deletion models in neural stem cells and cerebellar granule cell progenitors in mice.
Performed joint transcriptomic and ChIP-seq profiling in cerebellar granule cells.
Investigated the interplay between EED, H19 long non-coding RNA, and histone modifications (H3K27ac, H3K27me3).

Main Results:

EED deletion led to reduced cerebellar granule cell progenitor proliferation, increased cell death, cerebellar hypoplasia, and motor deficits.
EED ablation resulted in the overactivation of the H19 long non-coding RNA.
EED regulates H19 expression in an H3K27me3-dependent manner, and H19 deletion impacts EED expression and epigenetic profiles.
H19 upregulation was identified as the cause of cerebellar defects in EED mutant mice.

Conclusions:

EED plays a vital role in cerebellar morphogenesis and development by regulating gene expression critical for cerebellar granule cell progenitors.
A negative feedback loop between EED and H19 is established, which is essential for controlling cerebellar development and preventing hypoplasia and motor deficits.