Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

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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Publications

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

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Project description: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 MeCP2 dosage causes MECP2 duplication or triplication syndromes. MeCP2 acts as a transcriptional repressor, however, the gene expression changes observed in the hypothalamus and cerebellum of MeCP2 disorder mouse models suggest that MeCP2 can also upregulate gene expression. In this study, we compared gene expression changes in the amygdalae of mice lacking MeCP2 (Mecp2-null) and mice overexpressing MeCP2 (MECP2-TG). We chose the amygdala because it is a neuroanatomical region implicated in the control of anxiety and social behavior, two prominent phenotypes in MECP2-TG mice, and hypothesized that transcriptional profiling of this particular brain region may reveal expression changes relevant to heightened anxiety-like behavior and abnormal social behavior. A total of 1,060 genes were altered in opposite directions in both MeCP2 mouse models compared with wild-type littermates, with ~60% up-regulated and ~40% down-regulated. Interestingly, we found a significant enrichment of anxiety- and/or social behavior-related genes among the differentially expressed genes. To determine whether these genes contribute to the anxiety and social behavior phenotypes in MECP2-TG mice, we performed genetic and pharmacologic studies and found that a reduction in Crh suppresses anxiety-like behavior, and a reduction in Oprm1 improves social approach behavior. These studies suggest that MeCP2 impacts molecular pathways involved in anxiety and social behavior, and provide insight into potential therapies for MeCP2 disorders. This study is published in Nature Genetics http://dx.doi.org/10.1038/ng.1066. Total amygdala RNA samples were collected from Mecp2-null male mice (n=4), MECP2-transgenic male mice (n=5), and their wild type male littermates at 6 weeks of age (n=4, n=5 for each group respectively).

Dataset Information

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

Publications

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

Similar Datasets

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