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A novel m6A reader Prrc2a controls oligodendroglial specification and myelination
Rong Wu1, Ang Li2,3, Baofa Sun2,3
1The Brain Science Center, Beijing Institute of Basic Medical Sciences, 100850, Beijing, China.
Cell Research
|December 6, 2018
Summary
Researchers discovered Prrc2a, a novel N6-methyladenosine (m6A) reader, crucial for oligodendrocyte development and myelination. Its absence causes hypomyelination and neurological deficits in mice, highlighting a new therapeutic target for related diseases.
Area of Science:
- Neuroscience
- Molecular Biology
- Epigenetics
Background:
- N6-methyladenosine (m6A) is a key mRNA modification influencing cell development.
- The role of m6A in mammalian glial development, particularly oligodendrocytes, is largely unknown.
Purpose of the Study:
- To investigate the function of m6A modifications in mammalian glial development.
- To identify novel m6A-binding proteins involved in oligodendrocyte specification and myelination.
Main Methods:
- Utilized Nestin-Cre mediated knockout mouse models to study Prrc2a function.
- Performed transcriptome-wide RNA-seq, m6A-RIP-seq, and Prrc2a RIP-seq.
- Analyzed oligodendrocyte progenitor cell (OPC) proliferation and fate determination.
Main Results:
- Identified Prrc2a as a novel m6A reader essential for oligodendrocyte specification and myelination.
- Prrc2a knockout led to hypomyelination, reduced lifespan, and neurological defects.
- Prrc2a stabilizes Olig2 mRNA in an m6A-dependent manner, regulating oligodendrocyte development.
Conclusions:
- Prrc2a plays a critical role in mammalian oligodendrocyte development by regulating Olig2 mRNA stability.
- This study reveals a novel m6A-dependent mechanism in glial development.
- Findings suggest Prrc2a as a potential therapeutic target for hypomyelination-related neurological disorders.
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