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M6A/m-Seq of mouse adult cortex of Mettl3 cKO or Fto cKO mice

ABSTRACT: m6A/m-Seq of mouse adult cortex of Mettl3 cKO or Fto cKO mice

PROVIDER: PRJNA454049 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7076570_1.fastq.gz	Fastqsanger.gz
	SRR7076570_2.fastq.gz	Fastqsanger.gz
	SRR7076580_1.fastq.gz	Fastqsanger.gz
	SRR7076580_2.fastq.gz	Fastqsanger.gz
	SRR7076571_1.fastq.gz	Fastqsanger.gz

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m6A/m-Seq of mouse adult cortex of Mettl3 cKO or Fto cKO mice

Project description:N6-Methyladenosine (m6A) and N6,2′-O-dimethyladenosine (m6Am) are abundant mRNA modifications that regulate transcript processing and translation. The role of both, here termed m6A/m, in the stress response in the adult brain in vivo are currently unknown. Here, we investigated the effect of gene deletion of Mettl3, a m6A methyltransferase, and Fto, a m6A and m6Am demethlyase, induced in adulthood in excitatory neurons of the neocortex and hippocampus (Camk2a-Cre Mettl3 or Fto cKO) on the cortical epitranscriptome. PolyA-RNA-fragments from 3-5 replicates per group were processed both as m6A/m-sample (RNA immunoprecipiation RIP with an m6A and m6Am antibody) and RNA-input sample.

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mRNA-Seq of mouse Mettl3 cKO and Fto cKO hippocampus after fear conditioning

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Project description:mRNA-Seq of mouse Mettl3 cKO and Fto cKO hippocampus after fear conditioning

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Combined analysis of ribo-seq and rna-seq reveals that Mettl3 regulates embryonic cerebral cortex development in mice by controlling the proliferation and differentiation of neural progenitor cells

Project description:N6-methyladenosine (m6A) is the most important internal messenger RNA (mRNA) modification in mammals. The role of Mettl3, the core component of methyltransferase, and Fto, the demethylase, has not been revealed in the embryonic development of the cerebral cortex in mice. We constructed the conditional knockout of Mettl3 and Fto in the cerebral cortex of mice. We found that Mettl3 deletion causes cell cycle extension of progenitors and massive proliferation of intermediate progenitors at E15.5, which lead to a fold structure of cortex, while Fto deletion hardly altered cell numbers or morphology. Meanwhile, both transcriptome sequence (RNA-Seq) and ribosome profiling (Ribo-Seq) of Mettl3-deleted cortex mRNAs in E15.5 revealed that the differential genes were enriched in cell differentiation, neurogenesis, neuron differentiation, cell proliferation, and cell cycle. Moreover, deleted Mettl3 but not Fto significantly upregulated Ythdf1 and Ythdf2, which caused a substantial change in gene translation efficiency. Our findings indicate cortex m6A represents a novel layer of complexity in gene expression regulation and provide a new mechanism of precisely programmed RNA maturation.

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