N6-methyladenosine (m6A) dysregulation contributes to network excitability in temporal lobe epilepsy
Analogous to DNA methylation and protein phosphorylation, it is now well understood that RNA is also subject to extensive processing and modification. N6-methyladenosine (m6A) is the most abundant internal RNA modification and regulates RNA fate in several ways, including stability and translational...
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| Published in | JCI insight Vol. 10; no. 14 |
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| Main Authors | , , , , , , , , , , , , , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
American Society for Clinical Investigation
22.07.2025
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| Abstract | Analogous to DNA methylation and protein phosphorylation, it is now well understood that RNA is also subject to extensive processing and modification. N6-methyladenosine (m6A) is the most abundant internal RNA modification and regulates RNA fate in several ways, including stability and translational efficiency. The role of m6A in both experimental and human epilepsy remains unknown. Here, we used transcriptome-wide m6A arrays to obtain a detailed analysis of the hippocampal m6A-ome from both mouse and human epilepsy samples. We combined this with human proteomic analyses and show that epileptic tissue displays disrupted metabolic and autophagic pathways that may be directly linked to m6A processing. Specifically, our results suggest that m6A levels inversely correlate with protein pathway activation. Finally, we show that elevated levels of m6A decrease seizure susceptibility and severity in mice. Together, our findings indicate that m6A represents an additional layer of gene regulation complexity in epilepsy and may contribute to the pathomechanisms that drive the development and maintenance of hyperexcitable brain networks. |
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| AbstractList | Analogous to DNA methylation and protein phosphorylation, it is now well understood that RNA is also subject to extensive processing and modification. N6-methyladenosine (m6A) is the most abundant internal RNA modification and regulates RNA fate in several ways, including stability and translational efficiency. The role of m6A in both experimental and human epilepsy remains unknown. Here, we used transcriptome-wide m6A arrays to obtain a detailed analysis of the hippocampal m6A-ome from both mouse and human epilepsy samples. We combined this with human proteomic analyses and show that epileptic tissue displays disrupted metabolic and autophagic pathways that may be directly linked to m6A processing. Specifically, our results suggest that m6A levels inversely correlate with protein pathway activation. Finally, we show that elevated levels of m6A decrease seizure susceptibility and severity in mice. Together, our findings indicate that m6A represents an additional layer of gene regulation complexity in epilepsy and may contribute to the pathomechanisms that drive the development and maintenance of hyperexcitable brain networks. Analogous to DNA methylation and protein phosphorylation, it is now well understood that RNA is also subject to extensive processing and modification. N 6 -methyladenosine (m 6 A) is the most abundant internal RNA modification and regulates RNA fate in several ways, including stability and translational efficiency. The role of m 6 A in both experimental and human epilepsy remains unknown. Here, we used transcriptome-wide m 6 A arrays to obtain a detailed analysis of the hippocampal m 6 A-ome from both mouse and human epilepsy samples. We combined this with human proteomic analyses and show that epileptic tissue displays disrupted metabolic and autophagic pathways that may be directly linked to m 6 A processing. Specifically, our results suggest that m 6 A levels inversely correlate with protein pathway activation. Finally, we show that elevated levels of m 6 A decrease seizure susceptibility and severity in mice. Together, our findings indicate that m 6 A represents an additional layer of gene regulation complexity in epilepsy and may contribute to the pathomechanisms that drive the development and maintenance of hyperexcitable brain networks. This study reveals dysregulated m6A patterning in temporal lobe epilepsy, and links altered m6A to changes in protein expression, neuronal structure and seizure susceptibility across models. Analogous to DNA methylation and protein phosphorylation, it is now well understood that RNA is also subject to extensive processing and modification. N6-methyladenosine (m6A) is the most abundant internal RNA modification and regulates RNA fate in several ways, including stability and translational efficiency. The role of m6A in both experimental and human epilepsy remains unknown. Here, we used transcriptome-wide m6A arrays to obtain a detailed analysis of the hippocampal m6A-ome from both mouse and human epilepsy samples. We combined this with human proteomic analyses and show that epileptic tissue displays disrupted metabolic and autophagic pathways that may be directly linked to m6A processing. Specifically, our results suggest that m6A levels inversely correlate with protein pathway activation. Finally, we show that elevated levels of m6A decrease seizure susceptibility and severity in mice. Together, our findings indicate that m6A represents an additional layer of gene regulation complexity in epilepsy and may contribute to the pathomechanisms that drive the development and maintenance of hyperexcitable brain networks.Analogous to DNA methylation and protein phosphorylation, it is now well understood that RNA is also subject to extensive processing and modification. N6-methyladenosine (m6A) is the most abundant internal RNA modification and regulates RNA fate in several ways, including stability and translational efficiency. The role of m6A in both experimental and human epilepsy remains unknown. Here, we used transcriptome-wide m6A arrays to obtain a detailed analysis of the hippocampal m6A-ome from both mouse and human epilepsy samples. We combined this with human proteomic analyses and show that epileptic tissue displays disrupted metabolic and autophagic pathways that may be directly linked to m6A processing. Specifically, our results suggest that m6A levels inversely correlate with protein pathway activation. Finally, we show that elevated levels of m6A decrease seizure susceptibility and severity in mice. Together, our findings indicate that m6A represents an additional layer of gene regulation complexity in epilepsy and may contribute to the pathomechanisms that drive the development and maintenance of hyperexcitable brain networks. |
| Author | Villalba Benito, Leticia Brett, Francesca M. Jimenez-Mateos, Eva M. Kh. A.E. Alkhayyat, Mohammad Huang, Yifan Cryan, Jane Sullivan, Mairéad Casillas-Espinosa, Pablo M. Harnett, Aileen Tran, Cindy Srinivas, Sujithra Henshall, David C. Mathoux, Justine Auer, Theresa Glennon, Jeffrey C. Farrell, Michael A. Kesavan, Jaideep Delanty, Norman Wilson, Marc-Michel Litovskich, Gabrielle Sanz-Rodriguez, Amaya Lacey, Austin O’Brien, Donncha F. Brennan, Gary P. Liu, Zining Canavan, Mary |
| AuthorAffiliation | 5 Department of Neuroscience, Central Clinical School, Monash University, Melbourne, Victoria, Australia 13 Translational Immunopathology, School of Biochemistry and Immunology and School of Medicine, Trinity College Dublin, Dublin, Ireland 6 UCD School of Medicine, University College Dublin, Belfield, Dublin, Ireland 1 Department of Physiology and Medical Physics, RCSI University of Medicine and Health Sciences, Dublin, Ireland 8 Department of Neurology 10 Department of Neurosurgery, Beaumont Hospital Dublin, Dublin, Ireland 3 UCD School of Biomolecular and Biomedical Science, University College Dublin, Belfield, Dublin 4, Ireland 9 Department of Neuropathology, and 11 Department of Neurology, The Alfred Hospital, Commercial Road, Melbourne, Victoria, Australia 12 Discipline of Physiology, School of Medicine, Trinity College Dublin, The University of Dublin, Dublin, Ireland 2 FutureNeuro Research Ireland Centre for Translational Brain Science, and 7 School of Pharmacy and Biomolecular Sciences, |
| AuthorAffiliation_xml | – name: 4 UCD Conway Institute, University College Dublin, Dublin, Ireland – name: 3 UCD School of Biomolecular and Biomedical Science, University College Dublin, Belfield, Dublin 4, Ireland – name: 2 FutureNeuro Research Ireland Centre for Translational Brain Science, and – name: 6 UCD School of Medicine, University College Dublin, Belfield, Dublin, Ireland – name: 7 School of Pharmacy and Biomolecular Sciences, RCSI University of Medicine and Health Sciences, Dublin, Ireland – name: 11 Department of Neurology, The Alfred Hospital, Commercial Road, Melbourne, Victoria, Australia – name: 5 Department of Neuroscience, Central Clinical School, Monash University, Melbourne, Victoria, Australia – name: 13 Translational Immunopathology, School of Biochemistry and Immunology and School of Medicine, Trinity College Dublin, Dublin, Ireland – name: 9 Department of Neuropathology, and – name: 10 Department of Neurosurgery, Beaumont Hospital Dublin, Dublin, Ireland – name: 12 Discipline of Physiology, School of Medicine, Trinity College Dublin, The University of Dublin, Dublin, Ireland – name: 1 Department of Physiology and Medical Physics, RCSI University of Medicine and Health Sciences, Dublin, Ireland – name: 8 Department of Neurology |
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| Keywords | Cell biology Epigenetics Neuroscience Mouse models Epilepsy |
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| Snippet | Analogous to DNA methylation and protein phosphorylation, it is now well understood that RNA is also subject to extensive processing and modification.... Analogous to DNA methylation and protein phosphorylation, it is now well understood that RNA is also subject to extensive processing and modification. N 6... |
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| SubjectTerms | Adenosine - analogs & derivatives Adenosine - genetics Adenosine - metabolism Animals Disease Models, Animal Epilepsy, Temporal Lobe - genetics Epilepsy, Temporal Lobe - metabolism Epilepsy, Temporal Lobe - physiopathology Female Gene Expression Regulation Hippocampus - metabolism Humans Male Mice Mice, Inbred C57BL Proteomics Transcriptome |
| Title | N6-methyladenosine (m6A) dysregulation contributes to network excitability in temporal lobe epilepsy |
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