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Epigenetic and transcriptional landscapes during cerebral cortex development in a microcephaly mouse model [RRBS/oxRRBS]

ABSTRACT: Epigenetic and transcriptional landscapes during cerebral cortex development in a microcephaly mouse model [RRBS/oxRRBS]

PROVIDER: PRJNA889392 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR21862119_1.fastq.gz	Fastqsanger.gz
	SRR21862119_2.fastq.gz	Fastqsanger.gz
	SRR21862120_1.fastq.gz	Fastqsanger.gz
	SRR21862120_2.fastq.gz	Fastqsanger.gz
	SRR21862121_1.fastq.gz	Fastqsanger.gz

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Epigenetic and transcriptional landscapes during cerebral cortex development in a microcephaly mouse model [RRBS/oxRRBS]

Project description:The cerebral cortex is a pivotal structure that is integral to advanced brain functions within the mammalian central nervous system. Patterns of DNA methylation and hydroxymethylation play important roles in regulating cerebral cortex development. However, it remains unclear whether abnormal cerebral cortex development, such as microcephaly, could rescale the epigenetic landscape, potentially contributing to dysregulated gene expression during brain development. In this study, we characterize and compare the DNA methylome/hydroxymethylome and transcriptome profiles of the cerebral cortex across several developmental stages in wild-type (WT) mice and Mcph1 knockout (Mcph1-del) mice with severe microcephaly. Intriguingly, we discover a global reduction of 5'- hydroxymethylcytosine (5hmC) level, primarily in TET1-binding regions, in Mcph1-del mice compared to WT mice during juvenile and adult stages. Notably, genes exhibiting diminished 5hmC levels and concurrently decreased expression are essential for neurodevelopment and brain functions. Additionally, genes displaying a delayed accumulation of 5hmC in Mcph1-del mice are significantly associated with the establishment and maintenance of the nervous system during the adult stage. These findings reveal that aberrant cerebral cortex development in early stages can profoundly alter the epigenetic regulation program, which provides new insights into the molecular mechanisms underpinning diseases related to cerebral cortex development.

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Epigenetic and transcriptional landscapes during cerebral cortex development in a microcephaly mouse model

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Epigenetic and transcriptional landscapes during cerebral cortex development in a microcephaly mouse model [RNA-seq]

Project description:Epigenetic and transcriptional landscapes during cerebral cortex development in a microcephaly mouse model [RNA-seq]

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Expression data from mouse cerebral cortex

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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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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