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Transcriptome-wide maps of m6A methylation in mouse embryonic and postnatal cerebral cortex

ABSTRACT: Transcriptome-wide maps of m6A methylation in mouse embryonic and postnatal cerebral cortex

PROVIDER: PRJNA595356 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10677746_1.fastq.gz	Fastqsanger.gz
	SRR10677746_2.fastq.gz	Fastqsanger.gz
	SRR10677747_1.fastq.gz	Fastqsanger.gz
	SRR10677747_2.fastq.gz	Fastqsanger.gz
	SRR10677748_1.fastq.gz	Fastqsanger.gz

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Transcriptome-wide maps of m6A methylation in mouse embryonic and postnatal cerebral cortex

Project description:We report the applicatin of Methylation RNA Immunoprecipitation with Next Generation Sequencing (MeRIP-seq) technology for high-throughput status of m6A methylation modifications in mouse embryonic and postnatal cerebral cortices. By data analysis, we provided the distinct status of m6A methylation between embryonic and postnatal cortices.

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Project description:Differential gene expression of cerebral cortex might be responsible for distinct neurovascular developments between different mouse strains We used Affymetrix microarray to explore the global gene expression patterns of mouse cerebral cortex of different mouse strains at two developmental stages Cerebral cortex from two mouse strains [C57BL/6J(B6) and C3H/J (C3H)] at post-natal day 1 (p1) and post-natal 11 weeks (11 wk) were harvested for microarray experiments

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Gene expression in the mouse cerebral cortex exposed to Bisphenol A (BPA) during development.

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Metabolomic signature of mouse cerebral cortex following Toxoplasma gondii infection

Project description:BACKGROUND: The protozoan parasite Toxoplasma gondii infects and alters the neurotransmission in cerebral cortex and other brain regions, leading to neurobehavioral and neuropathologic changes in humans and animals. However, the molecules that contribute to these changes remain largely unknown.METHODS: We have investigated the impact of T. gondii infection on the overall metabolism of mouse cerebral cortex. Mass-spectrometry-based metabolomics and multivariate statistical analysis were employed to discover metabolomic signatures that discriminate between cerebral cortex of T. gondii-infected and uninfected control mice.RESULTS: Our results identified 73, 67 and 276 differentially abundant metabolites, which were involved in 25, 37 and 64 pathways at 7, 14 and 21 days post-infection (dpi), respectively. Metabolites in the unsaturated fatty acid biosynthesis pathway were upregulated as the infection progressed, indicating that T. gondii induces the biosynthesis of unsaturated fatty acids to promote its own growth and survival. Some of the downregulated metabolites were related to pathways, such as steroid hormone biosynthesis and arachidonic acid metabolism. Nine metabolites were identified as T. gondii responsive metabolites, namely galactosylsphingosine, arachidonic acid, LysoSM(d18:1), L-palmitoylcarnitine, calcitetrol, 27-Deoxy-5b-cyprinol, L-homophenylalanine, oleic acid and ceramide (d18:1/16:0).CONCLUSIONS: Our data provide novel insight into the dysregulation of the metabolism of the mouse cerebral cortex during T. gondii infection and have important implications for studies of T. gondii pathogenesis.

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