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Transcriptomic analysis of adult mouse hippocampal tissue in control and MeCP2 knockdown conditions

ABSTRACT: Transcriptomic analysis of adult mouse hippocampal tissue in control and MeCP2 knockdown conditions

PROVIDER: PRJNA418773 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6298150_1.fastq.gz	Fastqsanger.gz
	SRR6298150_2.fastq.gz	Fastqsanger.gz
	SRR6298151_1.fastq.gz	Fastqsanger.gz
	SRR6298151_2.fastq.gz	Fastqsanger.gz
	SRR6298152_1.fastq.gz	Fastqsanger.gz

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Transcriptomic analysis of adult mouse hippocampal tissue in control and MeCP2 knockdown conditions

Project description:The overall goal of this study was to clarify the role of MeCP2 in adult cognition. As one of the measures we analyzed gene expression changes associated with MeCP2 loss in the adult hippocampus. The analysis was performed in basal conditions and after exposure to a novel environment. We report gene expression data of mouse adult hippocampal tissue in which MeCP2 has been knockeddown in both conditions.

2018-05-15 | GSE107004 | GEO

Dynamic dysregulation of the transcriptome upon deletion of Mecp2 in adult mice

Project description:Loss of function mutations in methyl Cpg binding protein 2 (MECP2) cause Rett syndrome. Loss of MeCP2 causes global transcriptional dysregulation, but it was unknown whether this transcriptional dysregulation was proximal to Mecp2 function. We deleted Mecp2 from adult mice and performed a time-series RNA-seq experiment to identif what transcripts were altered immediately upon loss of MeCP2.

2024-12-16 | GSE246119 | GEO

Dynamic dysregulation of the transcriptome upon deletion of Mecp2 in adult mice [CUT&RUN]

Project description:Loss of function mutations in methyl Cpg binding protein 2 (MECP2) cause Rett syndrome. Loss of MeCP2 causes global transcriptional dysregulation, but it was unknown whether this transcriptional dysregulation was proximal to Mecp2 function. We deleted Mecp2 from adult mice and performed a time-series CUT&RUN experiment to identify if MeCP2 binding or histone post-translational modficiations are altered immediately upon loss of MeCP2.

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Impaired adult hippocampal neurogenesis in a mouse model of familial hypercholesterolemia: a role for the LDL receptor and cholesterol metabolism in adult neural precursor cells (LDLR Knockdown)

Project description:In familial hypercholesterolemia (FH), mutations in the low-density lipoprotein (LDL) receptor (LDLr) gene result in increased plasma LDL cholesterol. Clinical and preclinical studies revealed an association between FH and hippocampus-related memory and mood impairment. We here asked whether hippocampal pathology in FH might be a consequence of compromised adult hippocampal neurogenesis. We evaluated hippocampus-dependent behaviour and neurogenesis in adult C57BL/6JRj and LDLr-/- mice. Behavioural tests revealed that adult LDLr-/- mice showed reduced performance in a dentate gyrus (DG)-dependent metric change task. This phenotype was accompanied by a reduction in cell proliferation and adult neurogenesis in the DG of LDLr-/- mice, suggesting a potential direct impact of LDLr mutation on NPC. We thus investigated the effects of elevated cholesterol and the function of LDLr in neural precursor cells (NPC) isolated from adult C57BL/6JRj mice in vitro. Exposure of NPC to LDL as well as LDLr gene knockdown reduced proliferation and disrupted transcriptional activity of genes involved in endogenous cholesterol synthesis and metabolism. The LDL treatment also induced an increase in intracellular lipid storage. Functional analysis of differentially expressed genes revealed parallel modulation of distinct regulatory networks upon LDL treatment and LDLr knockdown. Together, these results suggest that high LDL levels and a loss of LDLr function, which are characteristic to individuals with FH, might contribute to a disease-related impairment in adult hippocampal neurogenesis and, consequently, cognitive functions.

2019-09-04 | GSE136797 | GEO

Mediator Med23 regulates adult hippocampal neurogenesis

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Adult hippocampal neurogenesis in aged macaques and humans

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RNA Sequencing on hippocampal tissue after ASO treatment overtime in MECP2 duplication mice

Project description:To understand the response of MECP2-regulated genes to the ASO treatment, we performed RNA-sequencing at multiple timepoints on hippocampal tissue following ASO treatment. It shows that the abnormal transcriptomic profile of hDup mice is significantly rescued 2 weeks after the treatment. Long-term partial rescue of the gene expression was observed at 5 weeks and until 16 weeks after the treatment as the transcriptomic profile does not cluster with the control-ASO treated mice.

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MeCP2 heterochromatin organization is modulated by arginine methylation and serine phosphorylation

Project description:Rett syndrome is a human intellectual disability disorder that is associated with mutations in the X-linked MECP2 gene. Theepigenetic reader MeCP2 binds to methylated cytosines on the DNA and regulates chromatin organization. We have shownpreviously that MECP2 Rett syndrome missense mutations are impaired in chromatin binding and heterochromatinreorganization. Here, we performed a proteomics analysis of post-translational modifications of MeCP2 isolated from adult mousebrain. We show that MeCP2 carries various post-translational modifications, among them phosphorylation on S80 and S421, whichlead to minor changes in either heterochromatin binding kinetics or clustering. We found that MeCP2 is (di)methylated on severalarginines and that this modification alters heterochromatin organization. Interestingly, we identified the Rett syndrome mutationsite R106 as a dimethylation site. In addition, co-expression of protein arginine methyltransferases 1 and 6 lead to a decrease ofheterochromatin clustering. Altogether, we identified and validated novel modifications of MeCP2 in the brain and show that thesecan modulate its ability to bind as well as reorganize heterochromatin, which may play a role in the pathology of Rett syndrome.

2022-10-15 | PXD033696 | Pride

MeCP2 Represses the Activity of Topoisomerase IIβ in Long Neuronal Genes

Project description:A unique signature of neuronal transcriptomes is the high expression of the longest genes in the genome (e.g. >100 kilobases). These genes encode proteins with essential functions in neuronal physiology, and disruption of long gene expression has been implicated in neurological disorders. DNA topoisomerases resolve topological constraints that arise on DNA and facilitate the expression of long genes in neurons. Conversely, methyl-CpG binding protein 2 (MeCP2), which is disrupted in Rett syndrome, can act as a transcriptional repressor to downregulate the expression of long genes. The molecular mechanisms underlying the regulation of long genes by these factors are not fully understood, however, and whether or not they directly influence each other is not known. Here, we identify a functional interaction between MeCP2 and Topoisomerase II-beta (TOP2β) in neurons. We show that MeCP2 and TOP2β physically interact in vivo and map protein sequences sufficient for their physical interaction in vitro. We profile TOP2β activity genome-wide in neurons and detect enrichment at regulatory regions and gene bodies of long neuronal genes, including long genes regulated by MeCP2. Further, we find that knockdown and overexpression of MeCP2 leads to altered TOP2β activity at MeCP2-regulated genes. Our findings uncover a mechanism by which MeCP2 inhibits the activity of TOP2β at long genes in neurons and suggest that this mechanism is disrupted in neurodevelopment disorders caused by mutation of MeCP2.

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