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Vitamin D modulates cortical transcriptome in an Mecp2 heterozygous Rett syndrome mouse model

ABSTRACT: Vitamin D modulates cortical transcriptome in an Mecp2 heterozygous Rett syndrome mouse model

PROVIDER: PRJNA749001 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15215900.fastq.gz	Fastqsanger.gz
	SRR15215901.fastq.gz	Fastqsanger.gz
	SRR15215902.fastq.gz	Fastqsanger.gz
	SRR15215903.fastq.gz	Fastqsanger.gz
	SRR15215904.fastq.gz	Fastqsanger.gz

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Vitamin D modulates cortical transcriptome in an Mecp2 heterozygous Rett syndrome mouse model

Project description:We investigated whether dietary vitamin D supplementation can rescue the expression of genes that are dysregulated within the neocortex of Mecp2+/- mice, and whether vitamin D deficiency further exacerbates transcriptome disruptions in these mice. We found that dietary vitamin D modification has a profound impact on the transcriptome of the neocortex. We identified more than 200 differentially expressed genes whose expression is normalized with vitamin D supplementation, many of which are associated with neuronal morphology. Dietary vitamin D deficiency exacerbated the dysregulation of many of these genes in the Mecp2+/- cortex, but, strikingly, it normalized the expression of many other dysregulated genes, similar to the effect of supplementation.

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Project description:Rett syndrome (RTT, OMIM 312750) is a severe X-linked neurodevelopmental disorder linked to heterozygous de novo mutations in the MECP2 gene. MECP2 encodes methyl-CpG-binding protein 2 (MeCP2), which represses gene transcription by binding to 5-methylcytosine residues in symmetrically positioned CpG dinucleotides. The disorder is almost exclusively diagnosed in females, because males affected by the disease usually die perinatally due to severe encephalopathy. Direct MeCP2 target genes underlying the neuropathogenesis of RTT remain largely unknown.

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