M6A methyltransferase Mettl3 is essential for neuronal homeostasis and sleep via modulating Npy in mice
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ABSTRACT:
PROVIDER: PRJNA1090068 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR28399482_1.fastq.gz | Fastqsanger.gz | |||
| SRR28399482_2.fastq.gz | Fastqsanger.gz | |||
| SRR28399483_1.fastq.gz | Fastqsanger.gz | |||
| SRR28399483_2.fastq.gz | Fastqsanger.gz | |||
| SRR28399484_1.fastq.gz | Fastqsanger.gz |
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Project description:To unravel the underlying mechanisms how neuronal Mettl3 loss induces the activation of microglia, we performed RNA-sequencing (RNA-seq) with the thalamic tissues of 2- and 4-month-old Ctrl and cKO mice, respectively.
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Project description:All the three enzymes, METTL3, METTL14, and METTL16, belong to methyltransferase like (METTL) family and possess the ability to deposit N6-methyladenosine (m6A) in mRNA. Via immunofluorescence staining and wertern blotting, we discovered either METTL3 or METTL14 mainly localize in nuclear, but METTL16 localizes in both cytosol and nuclei. To compare the m6A methyltransferase activities of the three m6A 'writers' and better understand their differences, MeRIP-seq (m6A-seq) was conducted with poly(A) RNAs isolaed from HEK293T cells with METTL3, 14 and 16 knockout.
2021-10-28 | GSE182607 | GEO
Project description:Sleep is regulated by intricate homeostatic and circadian systems and is influenced by genetic, environmental, and lifestyle factors. However, the roles of the epitranscriptome in sleep-wake regulation remain to be clarified. Here, we find that mice lacking the rRNA methyltransferase Nsun5 exhibit prolonged wakefulness. The absence of Nsun5 decreases 28S rRNA m5C levels, impairing the translational efficiency of nascent proteins associated with myelination, microtubule-based movement, and ribosome binding. This leads to a decreased number of oligodendrocytes and hypomyelination. These deficits result in increased excitability, particularly within the cortex. Notably, restoring myelination properties with clemastine or blocking the abnormally exposed voltage-gated potassium channels rescues the sleep phenotype, suggesting that reduced sleep is associated with hypomyelination. These findings highlight the significant role of epigenetic modifications in sleep regulation and offer broad mechanistic and therapeutic implications for brain disorders involving both myelin and sleep disturbances.
2025-10-01 | GSE276584 | GEO
Project description:Sleep is regulated by intricate homeostatic and circadian systems and is influenced by genetic, environmental, and lifestyle factors. However, the roles of the epitranscriptome in sleep-wake regulation remain to be clarified. Here, we find that mice lacking the rRNA methyltransferase Nsun5 exhibit prolonged wakefulness. The absence of Nsun5 decreases 28S rRNA m5C levels, impairing the translational efficiency of nascent proteins associated with myelination, microtubule-based movement, and ribosome binding. This leads to a decreased number of oligodendrocytes and hypomyelination. These deficits result in increased excitability, particularly within the cortex. Notably, restoring myelination properties with clemastine or blocking the abnormally exposed voltage-gated potassium channels rescues the sleep phenotype, suggesting that reduced sleep is associated with hypomyelination. These findings highlight the significant role of epigenetic modifications in sleep regulation and offer broad mechanistic and therapeutic implications for brain disorders involving both myelin and sleep disturbances.
2025-10-01 | GSE276587 | GEO
Project description:Sleep is regulated by intricate homeostatic and circadian systems and is influenced by genetic, environmental, and lifestyle factors. However, the roles of the epitranscriptome in sleep-wake regulation remain to be clarified. Here, we find that mice lacking the rRNA methyltransferase Nsun5 exhibit prolonged wakefulness. The absence of Nsun5 decreases 28S rRNA m5C levels, impairing the translational efficiency of nascent proteins associated with myelination, microtubule-based movement, and ribosome binding. This leads to a decreased number of oligodendrocytes and hypomyelination. These deficits result in increased excitability, particularly within the cortex. Notably, restoring myelination properties with clemastine or blocking the abnormally exposed voltage-gated potassium channels rescues the sleep phenotype, suggesting that reduced sleep is associated with hypomyelination. These findings highlight the significant role of epigenetic modifications in sleep regulation and offer broad mechanistic and therapeutic implications for brain disorders involving both myelin and sleep disturbances.
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Project description:Neuropeptide Y (NPY) is an endogenous modulator of neuronal activity by regulating GABA and glutamate release. Previously, we found that estradiol modulates NPY expression in the hippocampal dentate gyrus. Here we investigated which estrogen receptor type activation is required for the NPY expression. Further, we determined effects of estrogen receptor activation on NPY release. Finally, we determined the contribution of estrogen-mediated remodeling of the GABAergic and glutamatergic network in relation to changes in coupling with NPY in ovariectomized rats. We found that activation of either estrogen receptor type increases NPY expression as well as NPY release in the dentate gyrus. We also found that compared to OVX rats, estrogen replacement increases the likeness of synergistic/antagonistic coupling between the NPY and GABAergic synapse genes while the glutamatergic synapse genes are less likely coupled with NPY. The data together suggest that estrogen plays a critical role in regulation of activity of the NPY system and its coupling to GABAergic and glutamatergic synapses in female rat dentate gyrus. Two-conditions (E = beta-estradiol replacement vs O = oil) experiment. Biological replicates: 4E, 4O.
2014-08-02 | E-GEOD-60013 | biostudies-arrayexpress
Project description:Determining the methyltransferase activities of METTL3, METTL14, and METTL16
| PRJNA659033 | ENA
Project description:Background: N6-methyladenosine (m6A) RNA modification plays a crucial role in various biological events and is implicated in various metabolic-related diseases. However, its role in MASLD remains unclear. This study aims to investigate the impact of Mettl3 on MASLD through multi-omics analysis, with a focus on exploring its potential mechanisms of action. Methods: MASLD mouse models were established by feeding a high-fat diet for 12 weeks, and Mettl3 stable overexpression AML12 cell models were constructed via lentiviral transfection. Subsequent transcriptomic and proteomic analyses, as well as integrated analysis between different omics datasets, were conducted. Results: Mettl3 expression significantly increased in MASLD mouse models. In the transcriptomic and proteomic analyses, we identified 848 genes with significant inconsistencies between transcriptomic and proteomic datasets. GO/KEGG enrichment terms may involve post-transcriptional modifications, particularly Mettl3-mediated m6A modification. Subsequently, through integrated proteomic analysis of Mettl3-overexpressed AML12 cell models and MASLD mouse models, we selected the top 20 co-upregulated and co-downregulated GO/KEGG terms as the main biological processes influenced by Mettl3 in MASLD. By intersecting with pathways obtained from previous integrated analyses, we identified GO/KEGG terms affected by Mettl3-induced m6A modification. Protein-protein interaction analysis of proteins involved in these pathways highlighted GAPDH, ENO1, and TPI1 as three key hub genes. Conclusion: In MASLD, Mettl3 regulates the glycolytic pathway through m6A modification, influencing the occurrence and development of the disease via the key hub genes GAPDH, ENO1, and TPI1. These findings expand our understanding of MASLD and provide strong evidence for potential therapeutic targets and drug development.
2024-09-20 | PXD050565 | Pride
Project description:Sleep is regulated by intricate homeostatic and circadian systems and is influenced by genetic, environmental, and lifestyle factors. However, the roles of the epitranscriptome in sleep-wake regulation remain to be clarified. Here, we find that mice lacking the rRNA methyltransferase Nsun5 exhibit prolonged wakefulness. The absence of Nsun5 decreases 28S rRNA m5C levels, impairing the translational efficiency of nascent proteins associated with myelination, microtubule-based movement, and ribosome binding. This leads to a decreased number of oligodendrocytes and hypomyelination. These deficits result in increased excitability, particularly within the cortex. Notably, restoring myelination properties with clemastine or blocking the abnormally exposed voltage-gated potassium channels rescues the sleep phenotype, suggesting that reduced sleep is associated with hypomyelination. These findings highlight the significant role of epigenetic modifications in sleep regulation and offer broad mechanistic and therapeutic implications for brain disorders involving both myelin and sleep disturbances.
2024-07-29 | PXD054359 |