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Hippocampal epitranscriptomic (m6A) in IA-KA mouse model of Temporal Lobe Epilepsy

ABSTRACT: Hippocampal epitranscriptomic (m6A) in IA-KA mouse model of Temporal Lobe Epilepsy

PROVIDER: PRJNA1253760 | ENA |

REPOSITORIES: ENA

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			Action	DRS
		Other
	SRR33242800.fastq.gz	Fastqsanger.gz
	SRR33242801.fastq.gz	Fastqsanger.gz
	SRR33242802.fastq.gz	Fastqsanger.gz
	SRR33242803.fastq.gz	Fastqsanger.gz

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Hippocampal epitranscriptomic (m6A) in IA-KA mouse model of Temporal Lobe Epilepsy

Project description:RNA is subject to extensive processing and modification. N6-methyladenosine (m6A) is the most abundant internal modification and regulates RNA fate in several ways including stability and translational efficiency. Here, we provide a detailed analysis of the m6A-ome in hippocampus of a mouse model of temporal lobe epilepsy during epileptogenesis and into the epilepsy stage of the disease. Our results suggest that m6A represents a novel layer of complexity in gene regulation in epilepsy.

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Hippocampal epitranscriptomic (m6A) in human model of Temporal Lobe Epilepsy

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Project description: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 use transcriptome-wide m6A arrays to obtain a detailed analysis of the hippocampal m6A-ome from human temporal lobe epilepsy samples. We show that epileptic tissue displays disrupted metabolic and autophagic pathways which may be directly linked to m6A-processing. Together our findings indicate that m6A represents a novel layer of gene regulation complexity in epilepsy and may contribute to the pathomechanisms which drive the development and maintenance of hyperexcitable brain networks.

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