ArticleJournal of cellular and molecular medicine2021
Conditional deficiency of m6A methyltransferase Mettl14 in substantia nigra alters dopaminergic neuron function.
Article in Journal of cellular and molecular medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 37 citations in OpenAlex.
- Interaction between N6-methyladenosine (mGenes & diseases · 2026Review
- Loss of METTL14 in dopaminergic neurons disrupts ER homeostasis via m6A-dependent regulation of Atp2a3 mRNA: Implications for Parkinson's Disease.NPJ Parkinson's disease · 2026Article
- Astrocytic Mettl14 depletion enhances cognitive function by attenuating astrogliosis via the DUSP1/MAPK pathway in APP/PS1 mice: targeting neuroinflammation in Alzheimer's disease.Molecular psychiatry · 2026Article
- SPI1 Promotes TNF-α-Induced Epithelial-Mesenchymal Transition-Like Changes in Retinal Pigment Epithelial Cells: Implications for the Pathogenesis of Age-Related Macular Degeneration.Journal of ophthalmology · 2026Article
- The mCells · 2025Review
- RNA methylation modifications in neurodegenerative diseases: Focus on their enzyme system.Journal of advanced research · 2025Review
- N6-methyladenosine methylation: a novel key to unlocking mental disorders.The international journal of neuropsychopharmacology · 2025Review
- Circadian clock dysfunction in Parkinson's disease: mechanisms, consequences, and therapeutic strategy.NPJ Parkinson's disease · 2025Review
- The Role ofBiomolecules · 2025Review
- Environmental Exposure, Epitranscriptomic Perturbations, and Human Diseases.Environmental science & technology · 2025Review
- IGF2BP2 Regulates the Progression of Alzheimer's Disease Through m6A-Mediated NLRP3 Inflammasome.Immunity, inflammation and disease · 2025Article
- Dioxinodehydroeckol: A Potential Neuroprotective Marine Compound Identified by In Silico Screening for the Treatment and Management of Multiple Brain Disorders.Molecular biotechnology · 2024Article
- Research progress of neural stem cells as a source of dopaminergic neurons for cell therapy in Parkinson's disease.Molecular biology reports · 2024Review
- Emerging Role of Environmental Epitranscriptomics and RNA Modifications in Parkinson's Disease.Journal of Parkinson's disease · 2024Review
- METTL14 Regulates the m6A Modification of TRAF6 to Suppress Mitochondrial Dysfunction and Ferroptosis in Dopaminergic Neurons via the cGAS-STING Pathway.Current molecular medicine · 2024Article
- Emerging Roles for DNA 6mA and RNA m6A Methylation in Mammalian Genome.International journal of molecular sciences · 2023Review
- The RNA m6A modification might participate in microglial activation during hypoxic-ischemic brain damage in neonatal mice.Human genomics · 2023Article
- In Search of a Function for the N6-Methyladenosine in Epitranscriptome, Autophagy and Neurodegenerative Diseases.Neurology international · 2023Review
- Upregulation of UBR1 m6A Methylation by METTL14 Inhibits Autophagy in Spinal Cord Injury.eNeuro · 2023Article
- m6A methylation: Critical roles in aging and neurological diseases.Frontiers in molecular neuroscience · 2023Review
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
N6-Methyladenosine (m6A) is the most prevalent internal modification in messenger RNAs (mRNAs) of eukaryotes and plays a vital role in post-transcriptional regulation. Recent studies demonstrated that m6A is essential for the normal function of the central nervous system (CNS), and the deregulation of m6A leads to a series of CNS diseases. However, the functional consequences of m6A deficiency within the dopaminergic neurons of adult brain are elusive. To evaluate the necessity of m6A in dopaminergic neuron functions, we conditionally deleted Mettl14, one of the most important part of m6A methyltransferase complexes, in the substantia nigra (SN) region enriched with dopaminergic neurons. By using rotarod test, pole test, open-field test and elevated plus maze, we found that the deletion of Mettl14 in the SN region induces impaired motor function and locomotor activity. Further molecular analysis revealed that Mettl14 deletion significantly reduced the total level of m6A in the mRNA isolated from SN region. Tyrosine hydroxylase (TH), an essential enzyme for dopamine synthesis, was also down-regulated upon Mettl14 deletion, while the activation of microglia and astrocyte was enhanced. Moreover, the expression of three essential transcription factors in the regulation of TH including Nurr1, Pitx3 and En1, with abundant m6A-binding sites on their RNA 3'-untranslated regions (UTR), was significantly decreased upon Mettl14 deletion in SN. Our finding first confirmed the significance of m6A in maintaining normal dopaminergic function in the SN of adult mouse.
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