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Published on: March 20, 2014
RACK7 Interacts with PRC2 Complex to Regulate Astrocyte Development
Fangfang Jiao1,2, Tianxiang Tang3, Bowen Wang4
1Center for Medical Research and Innovation, Shanghai Pudong Hospital, Fudan University Pudong Medical Center, and the Shanghai Key Laboratory of Medical Epigenetics, the International Co-laboratory of Medical Epigenetics and Metabolism, Ministry of Science and Technology, Institutes of Biomedical Sciences, Fudan University, Shanghai, 200032, China.
Abstract:
Dysregulation of epigenetic mechanisms plays a crucial role in brain development and disease. Emerging largely evidence suggests that Receptor for Activated C-kinase 7 (RACK7), an epigenetic reader protein, may play a role in brain development and neural developmental disease, but in vivo explorations are still lacking. Here, a Rack7 conditional knock-out mouse model is established and shows that Rack7-deficient mice exhibit overt developmental defects associated with aberrant astrocyte development. Mechanistically, it is found that RACK7 interacts with the histone H3 lysine 27 (H3K27) methyltransferase, i.e., the Polycomb Repressive Complex 2 (PRC2) complex, to establish the genomic locations of Suppressor of Zeste 12 homolog (SUZ12) and H3K27 methylation. Deletion of Rack7 in astrocytes leads to a remarkable decrease of H3K27me3 chromatin localization genome-wide. Furthermore, RACK7 works together with H3K27me3 to prevent overactivation of the Wnt signaling pathway and other astrocyte differentiation genes are found. Collectively, this study provides new insights into the cellular and molecular mechanisms underlying brain development regulated by RACK7.
Insights
Receptor for Activated C-kinase 7 (RACK7) is crucial for normal brain development. Loss of RACK7 in mice causes developmental defects by disrupting astrocyte development and gene regulation.
Area of Science:
- Neuroscience
- Epigenetics
- Developmental Biology
Background:
- Epigenetic mechanisms are vital for brain development and disease.
- Receptor for Activated C-kinase 7 (RACK7), an epigenetic reader, is implicated in neural development, but in vivo data is limited.
Purpose of the Study:
- To investigate the in vivo role of RACK7 in brain development.
- To elucidate the molecular mechanisms by which RACK7 regulates astrocyte development and neural function.
Main Methods:
- Established a conditional knock-out mouse model for Rack7.
- Utilized molecular biology techniques to examine RACK7 interactions with epigenetic modifiers.
- Analyzed gene expression and chromatin localization in Rack7-deficient astrocytes.
Main Results:
- Rack7-deficient mice displayed significant developmental defects and aberrant astrocyte development.
- RACK7 was found to interact with the Polycomb Repressive Complex 2 (PRC2) to regulate H3K27 methylation.
- Deletion of Rack7 led to reduced H3K27me3 chromatin localization and dysregulated Wnt signaling pathway.
- RACK7 and H3K27me3 collaborate to control astrocyte differentiation genes.
Conclusions:
- RACK7 plays a critical role in regulating astrocyte development and brain formation.
- The study reveals a novel mechanism involving RACK7, PRC2, and H3K27 methylation in neural development.
- Findings provide new insights into the molecular basis of neural developmental disorders.
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