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Small-hairpin RNAs cause target-independent microRNA dysregulation in neurons and elicit global transcriptomic changes

ABSTRACT: Small-hairpin RNAs cause target-independent microRNA dysregulation in neurons and elicit global transcriptomic changes

PROVIDER: PRJNA659354 | ENA |

REPOSITORIES: ENA

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Small-hairpin RNAs cause target-independent microRNA dysregulation in neurons and elicit global transcriptomic changes (RNA-seq)

Project description:Small-hairpin RNAs cause target-independent microRNA dysregulation in neurons and elicit global transcriptomic changes (RNA-seq)

| PRJNA659370 | ENA

Small-hairpin RNAs cause target-independent microRNA dysregulation in neurons and elicit global transcriptomic changes (miRNA-seq)

Project description:Small-hairpin RNAs cause target-independent microRNA dysregulation in neurons and elicit global transcriptomic changes (miRNA-seq)

| PRJNA659372 | ENA

Small-hairpin RNAs cause target-independent microRNA dysregulation in neurons and elicit global transcriptomic changes

Project description:This SuperSeries is composed of the SubSeries listed below.

2020-12-31 | GSE156880 | GEO

Small-hairpin RNAs cause target-independent microRNA dysregulation in neurons and elicit global transcriptomic changes (miRNA-seq)

Project description:Small RNA was isolated from neuronal cultures transduced with different shRNA constructs direct against shNogoA with and without mismatches in the seed region

2020-12-31 | GSE156879 | GEO

Small-hairpin RNAs cause target-independent microRNA dysregulation in neurons and elicit global transcriptomic changes (RNA-seq)

Project description:Ribosomal-depleted total RNA was isolated from neuronal cultures transduced with different shRNA constructs direct against shNogoA with and without mismatches in the seed region

2020-12-31 | GSE156878 | GEO

Yra1-bound R loops cause orientation-independent transcription-replication collisions and telomere instability

Project description:Yra1-bound R loops cause orientation-independent transcription-replication collisions and telomere instability

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Histone deacetylation-dependent and -independent transcriptional dysregulation in early-onset polyglutamine disease

Project description:Transcriptional dysregulation is an important early feature of polyglutamine diseases. One of its proposed causes is defective neuronal histone acetylation, but important aspects of this hypothesis, such as the precise genomic topography of acetylation deficits and the relationship between transcriptional and acetylation alterations at the whole-genome level, remain unknown. The new techniques for the mapping of histone posttranslational modifications at genomic scale enable such global analyses and are challenging important assumptions concerning the role of specific histone modifications in gene expression. We examined here the genome-wide correlation of histone acetylation and gene expression defects in a mouse model of early-onset Huntington’s disease. Our analyses identified hundreds of loci that were hypoacetylated for H3K9,14 and H4K12 in the chromatin of these mice. Surprisingly, few genes with altered transcript levels in mutant mice showed significant changes in these acetylation marks and vice versa. Our screen, however, identified a subset of genes in which H3K9,14 deacetylation and transcriptional dysregulation concur. Genes in this group were consistently affected in different brain areas, mouse models and tissue from patients, which suggests a role in the etiology of this pathology. Overall, the combination of histone acetylation and gene expression screenings demonstrates that histone deacetylation and transcriptional dysregulation are two early, largely independent, manifestations of polyglutamine disease and suggests that additional epigenetic marks or mechanisms are required for explaining the full range of transcriptional alterations associated with this disorder. Examination of 2 different histone modifications in the hippocampus of wild-type and HD mice (PrP-htt-N171-82Q (Schilling et al., 1999)). Samples were obtained from 10 week old mice.

2013-06-20 | E-GEOD-44854 | biostudies-arrayexpress

Histone deacetylation-dependent and -independent transcriptional dysregulation in early-onset polyglutamine disease

2013-06-20 | GSE44854 | GEO

AdarΔ7-9 mice: dysregulation of Rps3a

Project description:Editing independent dysregulation of Rps3a1 and its pseudogene Rps3a3 in AdarΔ7-9 mice

| PRJEB31568 | ENA

Tissue-specific dysregulation of DNA methylation in aging

Project description:The normal aging process is a complex phenomenon associated with physiological alterations in the function of cells and organs over time. Although an attractive candidate for mediating transcriptional dysregulation, the contribution of epigenetic dysregulation to these progressive changes in cellular function remains unclear. In this study, we employed the genome-wide HELP assay to define patterns of cytosine methylation throughout the rat genome, and the LUMA assay to measure global levels of DNA methylation in the same samples. We studied both liver and visceral adipose tissue, and demonstrated significant differences in DNA methylation with age at >5% of sites analyzed. Furthermore, we showed that epigenetic dysregulation with age is a highly tissue-dependent phenomenon. The most distinctive loci were located at intergenic sequences and conserved non-coding elements, and not at promoters nor at CG-dinucleotide dense loci. Finally, we demonstrated that changes in methylation occur consistently near genes that are involved in metabolism and metabolic regulation, implicating their potential role in the pathogenesis of age-related diseases. We conclude that different patterns of epigenetic dysregulation occur in each tissue over time and may cause some of the physiological changes associated with normal aging. Direct comparison of DNA methylation in 18 samples belonging to four groups: young liver (n=6), young adipose tissue (n=4), old liver (n=5), old adipose tissue (n=3), isolated from F344*BN rats (young at ~3 months, old at ~18 months). Each microarray consists of a two-color comparison of a methylation-sensitive representation of the genome (HpaII) with an internal methylation-insensitive control/reference (MspI).

2010-05-01 | E-GEOD-17332 | biostudies-arrayexpress

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