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Quantitative analysis of wild type and MeCP2-/y mice hippocampus miRNAs using next generation sequencing

ABSTRACT: To determine whether the miRNA expression profile is altered by MeCP2, we performed Solexa-based RNA sequencing(RNA-seq) to assess global changes in the expression pattern of miRNAs caused by the loss of MeCP2 in mecp2 null (knockout[KO]) mice (Chen et al., 2001). Hippocampus miRNA profiles of 30-day old wild type (WT) and MeCP2-/y mice were generated by deep sequencing using Illumina HiSeq 2000

ORGANISM(S): Mus musculus

SUBMITTER: Zilong Qiu

PROVIDER: E-GEOD-59029 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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MeCP2 suppresses nuclear microRNA processing and dendritic growth by regulating the DGCR8/Drosha complex.

Cheng Tian-Lin TL Wang Zhizhi Z Liao Qiuming Q Zhu Ying Y Zhou Wen-Hao WH Xu Wenqing W Qiu Zilong Z

Developmental cell 20140301 5

Loss- and gain-of-function mutations of the X-linked gene MECP2 (methyl-CpG binding protein 2) lead to severe neurodevelopmental disorders in humans, such as Rett syndrome (RTT) and autism. MeCP2 is previously known as a transcriptional repressor by binding to methylated DNA and recruiting histone deacetylase complex (HDAC). Here, we report that MeCP2 regulates gene expression posttranscriptionally by suppressing nuclear microRNA processing. We found that MeCP2 binds directly to DiGeorge syndrom ...[more]

PMID: 24636259

Similar Datasets

Quantitative analysis of wild type and MeCP2-/y mice hippocampus miRNAs using next generation sequencing

Project description:To determine whether the miRNA expression profile is altered by MeCP2, we performed Solexa-based RNA sequencing(RNA-seq) to assess global changes in the expression pattern of miRNAs caused by the loss of MeCP2 in mecp2 null (knockout[KO]) mice (Chen et al., 2001).

2016-08-08 | GSE59029 | GEO

MeCP2 and H3K27me3 binding in Mecp2-knockout and MECP2-transgenic hippocampus

Project description:MeCP2 globally regulates gene expression in the brain. One example is Growth-differentiation factor 11 (Gdf11), which is down-regulated upon loss of MeCP2 and up-regulated upon gain of MeCP2. To assess if MeCP2 binds near the Gdf11 locus we performed CUT&RUN for MeCP2 in Mecp2-knockout or MECP2-transgenic hippocampus. To assess if a repressive histone modification (H3K27me3) was concordantly changed we profiled H3k27me3 in these same matched tissues.

2023-02-23 | GSE213752 | GEO

MeCP2 and H3K27me3 binding in Mecp2-knockout and MECP2-transgenic hippocampus

Project description:MeCP2 and H3K27me3 binding in Mecp2-knockout and MECP2-transgenic hippocampus

| PRJNA882406 | ENA

Genome-wide Analysis Reveals Mecp2-dependent Regulation of MicroRNAs in a Mouse Model of Rett Syndrome (high-throughput sequencing)

Project description:MicroRNAs (miRNAs) are a class of small non-coding RNAs that function as post-transcriptional regulators of gene expression. Many miRNAs are expressed in the developing brain and regulate multiple aspects of neural development including neurogenesis, dendritogenesis and synapse formation. Rett syndrome (RTT) is a progressive neurodevelopmental disorder caused by mutations in the gene encoding Methyl-CpG binding protein 2 (MECP2). While Mecp2 is known to act as a global transcriptional regulator, miRNAs that are directly regulated by Mecp2 in the brain are not known. Using massively parallel sequencing methods, we have identified miRNAs whose expression is altered in cerebella of Mecp2-null mice before and after the onset of severe neurological symptoms. In vivo genome-wide analyses indicate that promoter regions of a significant fraction of dys-regulated miRNA transcripts, including a large polycistronic cluster of brain-specific miRNAs, are DNA methylated and directly bound by Mecp2. Functional analysis demonstrates that the 3’ untranslated region (UTR) of messenger RNA encoding Brain-derived neurotrophic factor (Bdnf) can be targeted by multiple miRNAs aberrantly up-regulated in absence of Mecp2. Taken together, these results suggest that dys-regulation of miRNAs may contribute to RTT pathoetiology, and also provide a valuable resource to further investigate the role of miRNAs in RTT. Two pooled total RNA samples (4 pairs of wild-type (WT) and Mecp2-null (KO) male mice; postnatal 6-week, the pre-/early-symptomatic stage) were sequenced in a multiplexed configuration (with distinct barcode sequences). And, six samples (two litters, one WT and two KO male mice in each litter; postnatal 8-week, the symptomatic stage) were sequenced individually.

2010-09-29 | E-GEOD-24320 | biostudies-arrayexpress

MeCP2-R270X and MeCP2-G273X ChIP-Seq

Project description:MECP2-R270X transgenic mice (TG) and MECP2-G273X TG mice were generated in the Zoghbi Lab. These mice express the respective truncated form of MeCP2 tagged with GFP at the C-terminus from a transgenic human PAC containing all known regulatory sequences. These transgenes were maintained on a wild-type pure FVB background. For experiments each transgenic line was crossed by Mecp2 null mice (Mecp2 tm1.1Bird) on a pure 129SvEv background and the resulting male F1 hybrid progeny (FVB;129SvEv) that lacked endogenous MeCP2 expression but expressed either transgene (Mecp2 -/y; MECP2-R270X TG or Mecp2-/y; MECP2-G273X TG) were used for ChIP-Seq analysis. Whole brain from either the R270X mice (Mecp2 -/y; MECP2-R270X TG) or the G273X mice (Mecp2 -/y; MECP2-G273X TG) was formaldehyde crosslinked and purified chromatin was immunoprecipitated with anti-GFP antibody (Abcam ab6556). 2 samples: R270X (Mecp2 -/y; MECP2-R270X TG) and G273X (Mecp2 -/y; MECP2-G273X TG) both on an F1 (FVB;129SvEv) hybrid background

2013-03-12 | E-GEOD-36536 | biostudies-arrayexpress

MeCP2-R270X and MeCP2-G273X ChIP-Seq

2013-03-12 | GSE36536 | GEO

Genome-wide Analysis Reveals Mecp2-dependent Regulation of MicroRNAs in a Mouse Model of Rett Syndrome

Project description:This SuperSeries is composed of the following subset Series: GSE24285: Genome-wide Analysis Reveals Mecp2-dependent Regulation of MicroRNAs in a Mouse Model of Rett Syndrome (mm8 chromosomal tiling arrays) GSE24286: Genome-wide Analysis Reveals Mecp2-dependent Regulation of MicroRNAs in a Mouse Model of Rett Syndrome (mm8 promoter tiling arrays) GSE24320: Genome-wide Analysis Reveals Mecp2-dependent Regulation of MicroRNAs in a Mouse Model of Rett Syndrome (high-throughput small RNA sequencing) Refer to individual Series

2010-09-29 | E-GEOD-24329 | biostudies-arrayexpress

Neuronal MeCP2 is expressed at near histone-octamer levels and globally alters the chromatin state

Project description:We report the application of single molecule-based sequencing technology for high-throughput genom-wide mapping of MeCP2 binding and DNA methylation in mouse brain and cerebellum respectively. We find a good correlation between MeCP2 occupancy and methyl-CpG density and depletion of MeCP2 binding at CpG Islands, the majority of which are constitutively hypomethylated. This study provides a comprehensive characterisation of the genome wide distribution of MeCP2. Examination of MeCP2 occupancy in mouse brain and the distribution of methylation in mouse cerebellum.

2010-03-04 | E-GEOD-19786 | biostudies-arrayexpress

Brain-specific transcriptome analysis in MECP2 transgenic monkeys

Project description:We have performed gene expression profiling of the MECP2 transgenic monkey, taking advantage of recently completed genome sequencing for the cynomolgus monkey. We found interesting changes in the pattern of alternative splicing of many genes, including genes coding synaptic proteins (e.g., neurexin-3 and Shank-3) and metabolism-related proteins, as compared to the wild-type monkey. This study provides important information for understanding the impact of disease-related gene on brain development. Examination of transcriptome in brain tissues of wild-type and MECP2 transgenic monkeys.

2015-11-25 | E-GEOD-57974 | biostudies-arrayexpress

Cerebellar gene expression data from Mecp2-null and MECP2-transgenic mice

Project description:We compared gene expression changes in the cerebellum of mice lacking MeCP2 (Mecp2-null) and mice overexpressing MeCP2 (MECP2-transgenic). A group of postnatal neurodevelopmental disorders collectively referred to as MeCP2 disorders are caused by aberrations in the gene encoding methyl-CpG-binding protein 2 (MECP2). Loss of MeCP2 function causes Rett syndrome (RTT), whereas increased copy number of the gene causes MECP2 duplication or triplication syndromes. MeCP2 acts as a transcriptional repressor, however the gene expression changes observed in the hypothalamus of MeCP2 disorder mouse models suggest that MeCP2 can also upregulate gene expression. To determine if this dual role of MeCP2 extends beyond the hypothalamus, we studied gene expression patterns in the cerebellum of Mecp2-null and MECP2-Tg mice, modeling RTT and MECP2 duplication syndrome, respectively. We found that abnormal MeCP2 dosage causes alterations in the expression of hundreds of genes in the cerebellum. The majority of genes were upregulated in MECP2-Tg mice and downregulated in Mecp2-null mice, consistent with a role for MeCP2 as a modulator that can both increase and decrease gene expression. Interestingly, many of the genes altered in the cerebellum, particularly those increased by the presence of MeCP2 and decreased in its absence, were similarly altered in the hypothalamus. Keywords: Comparison of cerebellar gene expression data between Mecp2-null mice and Mecp2-transgenic mice

2009-04-07 | GSE15574 | GEO

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