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A Method for Measuring RNA N6-methyladenosine Modifications in Cells and Tissues
Published on: December 5, 2016
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Synaptic N6-methyladenosine (m6A) epitranscriptome reveals functional partitioning of localized transcripts
Daria Merkurjev1, Wan-Ting Hong2, Kei Iida3
1Statistics Department, University of California at Los Angeles, Los Angeles, CA, USA.
Nature Neuroscience
|June 29, 2018
Summary
Synaptic RNA modifications, specifically N6-methyladenosine (m6A) epitranscriptome, are crucial for regulating local protein synthesis and synaptic function. Disrupting m6A regulation leads to synaptic dysfunction and altered neuronal communication.
Area of Science:
- Neuroscience
- Molecular Biology
- Epigenetics
Background:
- Synaptic function relies on localized protein synthesis regulated by mRNA.
- Enzyme-mediated mRNA modifications influence cellular mRNA turnover, but their role at synapses is unknown.
Purpose of the Study:
- To investigate the role of N6-methyladenosine (m6A) modifications in regulating the synaptic transcriptome.
- To characterize the synaptic m6A epitranscriptome (SME) and its functional implications.
Main Methods:
- Developed low-input m6A-sequencing for synaptosomal RNA.
- Analyzed m6A sites in healthy adult mouse forebrain synaptosomes.
- Utilized knockdown of m6A readers in hippocampal neurons to assess functional consequences.
Main Results:
- Identified 4,469 enriched m6A sites in 2,921 genes, defining the SME.
- The SME is enriched in pathways related to synapse modulation and neurodevelopmental/neuropsychiatric diseases.
- Knockdown of m6A readers impaired synaptic function, affecting spine morphology, synaptic transmission, PSD-95 clustering, and GluA1 surface expression.
Conclusions:
- Synaptic mRNA chemical modifications, particularly m6A, are critical regulators of synaptic function.
- The SME plays a significant role in maintaining synaptic plasticity and neuronal health.
- Dysregulation of the synaptic m6A epitranscriptome may contribute to neurological disorders.
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