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ABSTRACT: Small RNA sequencing of striatum samples of the Huntington's disease mice model BACHD

PROVIDER: PRJNA686706 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13277514.fastq.gz	Fastqsanger.gz
	SRR13277515.fastq.gz	Fastqsanger.gz
	SRR13277516.fastq.gz	Fastqsanger.gz
	SRR13277517.fastq.gz	Fastqsanger.gz
	SRR13277518.fastq.gz	Fastqsanger.gz

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Project description:Striatum of Huntington's disease model mice

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Targeting H3K4 methylation as a therapeutic strategy for Huntington's disease (RNA-seq)

Project description:Transcriptional dysregulation is an early feature of Huntington's disease (HD). We observed gene-specific changes in H3K4me3 at transcriptionally repressed promoters in R6/2 mouse and human HD brain. Genome-wide analysis showed a novel chromatin signature for this mark. Reducing the levels of the H3K4 demethylase SMCX/Jarid1c in primary neurons reversed down-regulation of key neuronal genes caused by mutant Huntingtin (Htt) expression. Finally, reduction of SMCX/Jarid1c in primary neurons from BACHD mice or the single Jarid1 in a Drosophila HD model was protective. Therefore, targeting this epigenetic signature may be an effective strategy to ameliorate the consequences of HD. mRNA-seq in wild type and R6/2 cortex and striatum at 8 and 12 weeks.

2013-07-18 | E-GEOD-48962 | biostudies-arrayexpress

Targeting H3K4 methylation as a therapeutic strategy for Huntington's disease (ChIP-seq)

Project description:Transcriptional dysregulation is an early feature of Huntington's disease (HD). We observed gene-specific changes in H3K4me3 at transcriptionally repressed promoters in R6/2 mouse and human HD brain. Genome-wide analysis showed a novel chromatin signature for this mark. Reducing the levels of the H3K4 demethylase SMCX/Jarid1c in primary neurons reversed down-regulation of key neuronal genes caused by mutant Huntingtin (Htt) expression. Finally, reduction of SMCX/Jarid1c in primary neurons from BACHD mice or the single Jarid1 in a Drosophila HD model was protective. Therefore, targeting this epigenetic signature may be an effective strategy to ameliorate the consequences of HD. ChIP-seq for H3K4me3 in wild type and R6/2 cortex and striatum at 8 and 12 weeks.

2013-07-18 | E-GEOD-48960 | biostudies-arrayexpress

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Project description:Striatum of Huntington's disease model mice [Affymetrix data]

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Mus musculus

Project description:Striatum of Huntington's disease model mice [Illumina data]

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RNAseq of FACS Drd1 and Drd2 receptor expressing medium spiny neurons (direct and indirect medium spiny neurons) from 5-6 month BACHD Huntington's disease model mice, compared to WT littermates

Project description:mRNAseq for baseline transcriptional profiling of D1 and D2 receptor-expressing medium spiny neurons from 5-6 month BACHD mice, compared to respective WT littermates. BACHD iSPN and dSPN RNAseq data has been described in "Impaired TrkB receptor signaling underlies corticostriatal dysfunction in Huntington's disease"; Plotkin et al; 2014; PMID accession number 24991961.

2017-08-31 | GSE103341 | GEO

N17 Modifies Mutant Huntingtin Nuclear Pathogenesis and Severity of Disease in HD BAC Transgenic Mice

Project description:Longitudinal microarray data from BACHD-M-NM-^TN17 mice with wildtype littermate controls Total RNA from cortex and striatum of wildtype and BACHD-M-NM-^TN17 mice collected at 2mo, 7mo, and 11mo was used for microarray on the Illumina MouseRef8v.2 platform.

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Analysis of proteomic consequences of TYROBP deletion in a Huntington's disease mouse model.

Project description:Analysis of proteomic consequences of Tyrobp deletion in a Huntington's disease mouse model. Examination of protein expression alterations in the striatum of mutant huntingtin-Q175 with and without TYROBP (protein tyrosine kinase-binding protein).

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Uninterrupted Mutant Huntingtin CAG-repeat but Not Polyglutamine Length Predicts Striatal Nuclear Pathogenesis and Transcriptionopathy in HD Mice

Project description:Huntington’s disease (HD) is caused by CAG repeat expansion at the N-terminal region of huntingtin (HTT) gene and characterize by neuronal cell loss and neuroinflammation transcriptional profile change in striatum, cortex and other brain regions. Here we reported generation and characterization of BAC-CAG, a novel full length human HD mouse model host over 120 uninterrupted CAG repeats. we performed RNA-seq analysis of the striatum and cortex of BAC-CAG mice at 2m, 6m and 12m of age (N=6 per genotype, sex balanced). We observed an age-dependent transcriptionopathy in the striatum of BAC-CAG mice, with only 7 and 36 significant DE genes in 2m and 6m striatum respectively (FDR<0.1), but 820 DE genes (538 downregulated and 282 upregulated genes) at 12m of age (FDR<0.1). The transcriptomic deficits in this model are highly striatum-selective, as we only detected 4, 3 and 14 DE genes (FDR<0.1) at 2m, 6m and 12m respectively in BAC-CAG cortices compared to WT controls. Remarkably, we found a highly significant positive transcriptome-wide correlation (r=0.62) of DE Z statistics between BAC-CAG vs WT at 12m and Q140 vs WT at 6m (p<1e-200). This result demonstrates a high concordance of both upregulated and downregulated genes in the BAC-CAG striatum compared to that of allelic series KI mice; but RNA-seq studies of BACHD mice at 12m and found only 50 genes significantly differentially expressed (DE) genes (FDR<0.1) in the striatum at 12m of age compared to WT littermates, 31 downregulated and 19 upregulated genes. In the cortex at 12m of age, BACHD only showed 6 significantly downregulated genes and 7 upregulated genes comapred to WT controls (FDR<0.1).

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Transcriptome profiling in knock-in mouse models of Huntington's disease [Striatum_miRNA]

Project description:Huntington's disease (HD) is an autosomal dominant neurodegenerative disorder that is characterized by motor, cognitive, and psychiatric alterations. The mutation responsible for this disease is an abnormally expanded and unstable CAG repeat within the coding region of the gene encoding huntingtin (Htt). Knock-in mouse models of HD with human exon 1 containing expanded CAG repeats inserted in the murine huntingtin gene (Hdh) provide a genetic reconstruction of the human causative mutation within the mouse model. The goal of this study is RNA expression profiling by RNA sequencing (RNA-seq) in 2, 6, and 10 month old knock-in mice with CAG lengths of 20, 80, 92, 111, 140, 175 along with littermate control wild-type animals miRNA expression profiles were obtained via RNA-seq analysis performed on tissue samples from the striatum of 2, 6, and 10 month old knock-in mice with CAG lengths of 20, 80, 92, 111, 140, 175 along with littermate control wild-type animals.

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