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Updated: Jul 1, 2025

Characterizing RNA Modifications in Single Neurons Using Mass Spectrometry

Characterizing RNA Modifications in Single Neurons Using Mass Spectrometry

Published on: April 21, 2022

m6A RNA methylation regulates mitochondrial function.

Michael Kahl^1,2, Zhaofa Xu^1,2, Saravanan Arumugam^1,2

¹Departments of Pediatrics, Neurology and Neuroscience, Northwestern University Feinberg School of Medicine, 303 East Superior Street, Chicago, IL 60611, United States.

Human Molecular Genetics

|March 14, 2024

Summary

N6-methyladenosine (m6A) RNA methylation regulates mitochondrial function by enhancing the translation of nuclear-encoded mitochondrial proteins. Loss of m6A impairs energy metabolism and mitochondrial respiration, impacting neuronal health.

Keywords:

m6A RNA methylation metabolomics mitochondria neurological disease transcriptomics

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A Method for Measuring RNA N6-methyladenosine Modifications in Cells and Tissues

A Method for Measuring RNA N6-methyladenosine Modifications in Cells and Tissues

Published on: December 5, 2016

Area of Science:

Molecular Biology
Cellular Biology
Neuroscience

Background:

N6-methyladenosine (m6A) is a key RNA modification regulating RNA biology.
Mitochondrial function is critical, especially in high-energy demand neuronal cells.
The role of RNA methylation in mitochondrial regulation remained largely unknown.

Purpose of the Study:

To investigate the role of m6A RNA methylation in regulating mitochondrial function in neuronal cells.
To elucidate the molecular mechanisms by which m6A affects mitochondrial activity.

Main Methods:

Conditional genetic knockout of Mettl14 (Methyltransferase like 14) in mice.
Metabolomic analysis and m6A-Seq (RNA methylation profiling).
Assessment of mitochondrial respiration, membrane potential, and protein expression.

Main Results:

Mettl14 knockout led to m6A depletion and downregulated energy metabolism metabolites.
m6A-Seq revealed enrichment of methylation on mitochondria-related RNAs.
Loss of m6A reduced mitochondrial respiratory capacity, membrane potential, and electron transport chain complex activity by decreasing translational efficiency.

Conclusions:

m6A RNA methylation is a novel regulator of mitochondrial function, essential for promoting the translation of nuclear-encoded mitochondrial proteins.
This pathway is crucial for maintaining cellular energy homeostasis and neuronal function.
Dysregulation of m6A-mediated mitochondrial regulation may contribute to neurodegenerative diseases.